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81 publications mentioning rno-mir-155

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-155. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 205
To determine the effects of high glucose on the expression of miR-155 and miR-146a, the HRGECs stimulated with a medium containing 25 mmol/L glucose were cultured at 37°C in 5% CO [2] for 0, 0.5, 1, 2, 4, 8, and 24 h. The expression of both the miR-155 and miR-146a was up-regulated 2 h after the glucose stimulation, peaked after 4 h, and then decreased until 24 h (with a minor increase of the miR-155 expression) relative to the control and the mannitol groups (Figure 6A,B). [score:10]
The miRNA expression profiling of the renal biopsy samples was performed by a microarray analysis; then, in situ hybridization and real-time polymerase chain reaction (PCR) were used to determine the localization and expression of two of the miRNAs significantly up-regulated in human DN kidney samples, miR-155 and miR-146a, in the kidney tissues from type 1 and type 2 DN rat mo dels. [score:8]
Furthermore, the addition of PDTC partially repressed the up-regulated expression of TNF-α and TGF-β1 caused by the activation of NF-κB in the miR-155 and miR-146a over -expressing groups. [score:8]
Thirty-one miRNAs were upregulated by ≥ 2-fold in the DN kidney samples from the DN patients, in which there were two significantly upregulated miRNAs, miR-155 (6.22 ± 2.81-fold) and miR-146a (4.87 ± 1.39-fold). [score:7]
The high glucose -induced up-regulation of TNF-α and TGF-β1 was augmented by the overexpression of miR-155 and miR-146a, thereby increasing renal inflammation and fibrosis and enhancing diabetic GEC injury, which is mediated through the activation of the NF-κB signaling pathway. [score:6]
Under high-glucose conditions, the HRGECs overexpression of miR-155 or miR-146a following the transfection with miR-155 or miR-146a mimics showed an additive effect on the TNF-α and TGF-β1 upregulation. [score:6]
Chemically modified RNA oligonucleotides comprising a sequence complementary to mature miR-155 and miR-146a (miR-155 and miR-146a inhibitors) were used to inhibit the miR-155 and miR-146a activities. [score:5]
In vitro, high glucose induced the over -expression of miR-155 and miR-146a in the HRGECs, which, in turn, increased the TNF-α, TGF-β1, and NF-κB expression. [score:5]
The identification of new and key regulatory miRNAs in DN would be of great importance, and the present study found that among the 32 miRNAs up-regulated in the DN patients, miR-155 and miR-146a were significantly increased and primarily distributed in the GECs, mesangial areas and tubular sections. [score:5]
Surprisingly, some of the candidate targets of miR-155 and miR-146a were involved in the inflammatory responses (data not shown); therefore, we used miR-155 and miR-146a as targets for further study. [score:5]
Furthermore, miR-155 and miR-146a were gradually up-regulated during the development and progression of type 1 and type 2 DN, indicating that they could be activated in a rat DN mo del. [score:5]
Specific miRNAs, such as miR-155 and miR-146a, were initially linked with the inflammatory response by virtue of their potent up-regulation in multiple immune cell lineages by Toll-like receptor ligands, inflammatory cytokines, and specific antigens [15- 17]. [score:4]
A similar trend was observed for miR-155 and miR-146a expression in the development and progression of DN in the rats with type 2 DN (Figure 5A,B). [score:4]
Moreover, data have shown that miR-155 can be up-regulated by TNF-α through NF-κB [36]. [score:4]
Our results demonstrated that miR-155 and miR-146a were up-regulated in the DN patient and experimental animal mo dels and served as a mediator of the glucose -induced TNF-α/TGF-β1-NF-κB pathway. [score:4]
Researchers found that miR-155 directly targets SMAD5 [30] and SMAD2 [31]. [score:4]
The expression of both miR-155 and miR-146a was increased more than fivefold in the kidney samples of the DN patients compared with the controls, and the miR-155 expression was closely correlated with the serum creatinine levels (R = 0.95, P = 0.004). [score:4]
A, B. The expression of miR-155 and miR-146 under high glucose conditions of different times compared with the control and mannitol group; C, D. Quantification of miR-155 and miR-146a mRNA expression levels with different treating methods on HRGECs by a real-time PCR; E, F. Western blot was used to assess the protein levels of TNF-α and TGF-β with the same treating methods in C and D, glucose group is compared with mannitol group; the high glucose + miR155 inhibitor and high glucose + miR155 mimics are compared to high glucose + scrambled miRNA. [score:4]
Quantitative real-time PCR was used to detect the expressions of miR-155 (A) and miR-146a (B) in the kidney of a STZ -induced Type 1 diabetic nephropathy mo del. [score:3]
The linear correlation analysis showed the expression of miR-155 was closely correlated with the serum creatinine level (R = 0.95, P = 0.004). [score:3]
However, the induction by glucose was clearly blunted by the miR-155 and miR-146a inhibitors, suggesting that miR-155 and miR-146a could significantly induce renal inflammation and fibrosis and contribute to HRGEC injury. [score:3]
Taken together, these findings indicate that the increased expression of miR-155 and miR-146a in the DN patients and in the experimental DN animal mo dels was found to contribute to inflammation -mediated glomerular endothelial injury. [score:3]
In comparison with the NPD control group, the expression levels of miR-146a and miR-155 were significantly increased in the type 2 DN rats from week 0 to week 8 and 16 (Figure 5A,B) (serum creatinine and urinary protein excretion were shown in Table 4). [score:3]
Figure 3 Correlation of miR-155, miR-146a expressions and urinary protein excretion, serum creatinine of the DN patients. [score:3]
Lane 1, normal control group; lane 2, high glucose (25 mmol/L); lane 3, high glucose + miR-155/146a mimics (50 nmol/L); lane 4, high glucose + miR-155/146a inhibitor (100 nmol/L); lane 5, high glucose + PDTC (100 umol/L); lane 6, high glucose + miR-155/146a (50 nmol/L) + PDTC (100 μmol/L). [score:3]
To detect the time -dependent changes in the miR-155 and miR-146a expression, the cells cultured with mediums containing 25 mmol/L glucose were cultured at 37°C in 5% CO [2] for 0, 0.5, 1, 2, 4, 8, and 24 h. They were then collected for a real-time PCR. [score:3]
Quantitative real-time PCR for miR-155 and miR146a expression in the human and the rat kidneys. [score:3]
In the present study, therefore, we aimed to clarify the repertoire of miRNAs in the development and progression of DN and the potential regulatory roles of miR-155 and miR-146a in endothelial injury. [score:3]
During the induction and progression of the disease in type 1 and type 2 DN rat mo dels, miR-155 and miR-146a were demonstrated to increase gradually. [score:3]
To explore the biological effect of miR-155 and miR-146a on the HRGECs under high-glucose conditions, the HRGECs were categorized as the normal control (containing 5 mmol/L glucose), mannitol (20 mmol/L mannitol), high glucose (containing 25 mmol/L glucose), high glucose + miR-155 mimic (50 nmol/L), high glucose + miR-155 inhibitor (100 nmol/L), high glucose + Scrambled miRNA (50 nmol/L), high glucose + PDTC (100 μmol/L), and high glucose + miR155 (50 nmol/L) + PDTC (100 μmol/L) groups. [score:3]
In the rats with type 1 DN, the rats were sacrificed after the induction of diabetes at 1, 4, and 8 weeks (serum creatinine and urinary protein excretion were shown in Table 3), and a quantitative real-time PCR was used to show that the expression of miR-155 and miR-146a gradually increased during the progression of the DN (Figure 4A,B). [score:3]
The precise location and expression levels of the miR-155 and miR-146a were determined using in situ hybridization in the patient and control kidney tissue sections stained with Dig-labeled miR-155 and miR-146a riboprobes. [score:3]
Together with our findings from the present study, these results lead us to speculate that miR-155 and miR-146a form a regulatory loop in the TNF-α/NF-κB pathway during DN development. [score:3]
Quantitative real-time PCR was used to detect the expressions of miR-155 (A) and miR-146a (B) in the kidney of the Type 2 diabetic nephropathy mo del. [score:3]
Altered miR-155 and miR-146a expression in type 1 and type 2 DN rat kidneys. [score:3]
According to the set time points, the HRGECs (1 × 10 [5] per well) were transfected with miR-155 and miR-146a mimics, inhibitors, and scramble control after 24 h of starvation in a serum-free medium using Lipofectamine 2000 (Invitrogen) according to the manufacturer’s instructions. [score:3]
Figure 2 The expressions and distribution of miR-155 and miR-146a in the kidneys from DN patients. [score:3]
Our experiments confirmed that high glucose can increase the expression of miR-155 and miR-146a in a time -dependent manner. [score:3]
Figure 5 Expression of miR-155 and miR146a in high-fat and high-sugar diet combined with STZ -induced rat kidney with type 2 diabetic nephropathy. [score:3]
A, B: miR-155 and miR-146a expressions in the kidney of the DN and controls were confirmed by quantitative real-time PCR. [score:3]
The miR-155 and miR-146a expression levels were confirmed by a real-time PCR. [score:3]
The linear correlation analysis revealed that the miR-155 expression was closely correlated with the serum creatinine levels (R = 0.95, P = 0.004) but not with the urinary protein excretion levels (R = 0.336, P = 0.461); there were also no significant correlations between the miR-146a and serum creatinine levels (R = 0.531, P = 0.220) or the urinary protein excretion levels (R = 0.360, P = 0.427) (Figure 3). [score:3]
Aberrant expression of miR-155 and miR-146a between healthy and type 2 diabetic human kidney tissues. [score:3]
Figure 4 Expression of miR-155 and miR146a in the STZ -induced rat kidney with type 1 diabetic nephropathy. [score:3]
In conclusion, the present study provides direct biological evidence for the pathogenic importance of miR-155 and miR-146a in DN. [score:2]
Human renal glomerular endothelial cells (HRGECs) cultured under high-glucose conditions were transfected with miR-155 and miR-146a mimics, and the transforming growth factor (TGF)-β1, tumor necrosis factor (TNF)-α, and nuclear factor (NF)-κB expressions were examined by western blot, real-time PCR, and an electrophoresis mobility shift assay. [score:2]
Compared with the normal controls, the expressions of miR-155 and miR-146a were gradually increased from the time point of week 1 to week 8. *p < 0.05. [score:2]
William Kong el al. found Smad4 can directly bind to the promoter of miR-155 and can be activated through the TGF-β/Smad pathway [35]. [score:2]
Therefore, miR-155 and TGF-β1 may form a positive regulation loop mediated by the SMAD signaling pathway. [score:2]
Taken together, these findings suggest that miR-155 and miR-146a are not only biomarkers but also mediators in the development of DN. [score:2]
Compared with the control group, the expressions of miR-155 and miR-146a were increased at the time points of week 8 and week 16. [score:2]
These findings were further confirmed by a quantitative real-time PCR for miR-155 and miR-146a (Figure 2A,B). [score:1]
A linear correlation analysis was performed between the miR-155 and urinary protein (A); miR-155 and serum creatinine (B); miR-146a and urinary protein (C); and miR-146a and serum creatinine (D). [score:1]
miR-155 and miR-146a were further quantified with a TaqMan quantitative real-time PCR. [score:1]
Furthermore, we investigated the mechanisms by which the nuclear factor (NF)-κB signaling pathway mediates the high glucose -induced expression of miR-155 and miR-146a in cultured human renal glomerular endothelial cells (HRGECs). [score:1]
Determination of the detailed miR-155 and miR-146a mechanisms that cause renal damage in the setting of diabetes could elucidate the pathogenesis of DN and enable improved treatment strategies to be developed. [score:1]
We detected miR-155 expression was closely correlated with serum creatinine levels, Creatinine clearance was used to calculate estimated glomerular filtration rate (eGFR) for detection of kidney dysfunction. [score:1]
miR-155 and miR-146a were primarily localized in the glomerular endothelial cells, the mesangial areas and the tubular sections in kidneys from DN. [score:1]
The role of the NFκB signaling pathway in miR-155 and miR-146a -mediated renal inflammation and fibrosis. [score:1]
When in patients particularly with advanced kidney failure, creatinine clearance usually overestimates the GFR [28], therefore miR-155 may be a good marker for prediction the GFR of the DN. [score:1]
C, D: was performed to determine the distribution of miR-155 and miR-146a in the kidneys from the DN patients. [score:1]
A strong nuclear activation of NF-κB was observed in the cells from the miR-155 and miR-146a group (Figure 6G,H). [score:1]
To confirm the miRNA profiling findings in the human subjects, we used a quantitative real-time PCR to measure the expression of miR-155 and miR-146a in both the human and the rat kidneys. [score:1]
The miR-155 and miR-146a mimics were double-stranded constructs consisting of a guide and passenger strands. [score:1]
Figure 6 Impact of miR-155 and miR-146a on HRGECs. [score:1]
The sequences of the Dig-labeled probes against miR-155 and miR-146a mRNA were as follows: miR-155: 5′-CCCCTATCACGATTAGCATTAA-3′, miR-146a: 5′-AACCCATGGAATTCAGTTCTCA-3′. [score:1]
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[+] score: 190
Other miRNAs from this paper: rno-mir-132, rno-mir-146a
In contrast to the downregulation of the aforementioned genes, miR155 -inhibitor -transfected MSCs resulted in upregulation of Tbx21, Rorc, and SOCS1 expression levels and inhibition of Gata3 and Foxp3. [score:13]
Based on the aforementioned studies it was expected that the mimics of miR-155 would inhibit the expression of MCP-1 in MSCs, while the miR-155 inhibitor would upregulate MCP-1 (Figure 2(b)). [score:10]
In the SMCs and miR155 -suppressed MSCs groups (Figure 3(c)), the expression levels of Tbx21 and Rorc were significantly elevated (p < 0.01 for Tbx21 and p < 0.001 for Rorc), while Gata3 expression was downregulated (p < 0.001) (Figure 3(d)). [score:10]
In addition, miR-155 targets TAK1 -binding protein 2 (TAB2) in MSCs in order to regulate iNOS expression and nitric oxide release, by which T cell proliferation and function were inhibited [18]. [score:8]
Furthermore, inhibition of miR-155 upregulated the expression levels of MCP-1, IL-6, and IL-8 in bone marrow MSCs [34]. [score:8]
MiR155 -mimics -transfected MSCs inhibited the expression of Tbx21, Rorc, and SOCS1, while the expression of Gata3 and Foxp3 was increased. [score:6]
Therefore, it may be possible that MSCs regulate the expression levels of miR-155 target genes in T cells and other immune cells via exosome production. [score:6]
Suppressor of cytokine signaling 1 (SOCS1) is highly expressed in Treg cells [24] and miR-155 has been shown to mediate SOCS1 repression that in turn contributes to Treg cell competitive fitness [25]. [score:5]
Although a vast number of miR-155 target genes have been identified, notably in immune cells and various cancers (reviewed by Mashima [15]), the functions and downstream targets of miR-155 in MSCs are still unknown. [score:5]
In the present study, miR-155 was reported to contribute to the immunosuppressive functions of MSCs by promoting the differentiation of T cells to anti-inflammatory Th2 and Tregs, while concomitantly inhibiting the differentiation to Th1 and Th17 subpopulations. [score:5]
24 h following cell seeding, miR-155 mimic, mimics-nc, miR-155 inhibitor, and inhibitor-nc (Genepharma, Shanghai, China) were transfected in MSCs using Lipofectamine 2000 transfection reagent (Invitrogen, CA, USA) following the manufacturer's instructions. [score:5]
As shown above, miR-155 influence the expression of MCP-1, so we detected the inflammation related gene Tbx21, Gata3, and Rorc expression (Figure 3(e)). [score:5]
The results suggested that high expression of miR-155 can inhibit the migration of SMCs. [score:5]
A study has shown that despite the low levels of basal miR-155 expression in B cells, miR-155 was able to positively regulate antibody -mediated signaling [15]. [score:4]
We further demonstrated that the production of exosomes was increased concomitantly with the upregulation of miR-155 following hypoxia and/or IFN- γ stimulation (data not shown). [score:4]
The findings of the latter study are consistent with the data reported in the present study with regard to reduced Tbx21 and Rorc and the increased Gata3 and SOCS1 mRNA level in MSCs that overexpress miR-155 (Figure 4). [score:3]
The findings indicated that the expression of miR-155 in MSCs may contribute to the differentiation of T cells into Treg cells. [score:3]
Consequently, it was expected that miR-155 may play a role in the immunosuppressive activities of MSCs. [score:3]
Transfection of miRNA-155 Mimic and Inhibitor. [score:3]
and the miR-155 target gene SOCS1 were detected by quantitative real-time PCR (qPCR) in SMCs. [score:3]
miR-155 mimics and/or miR-155 inhibitor and control oligos were transfected in MSCs with lipofectamine 2000 24 h following seeding. [score:3]
MSCs were transfected with miR155 -mimics, miR155 -inhibitor, and control oligos, respectively, and then cocultured with spleen mononuclear cells (SMCs). [score:3]
The results suggested that miR-155 could inhibit the migration of spleen mononuclear cells. [score:3]
In addition, miR-155 was identified in the exosomes from human bone marrow-derived MSCs [36] and was ranked as one of the top 20 miRNAs according to their expression levels in MSC-exosomes [37]. [score:3]
SMCs were loaded on the upper chamber and cultured in medium without serum, whereas the cells in the lower chamber were filled with serum containing medium (negative control, nc) and/or seeded with MSCs -transfected miR155 -mimics and/or miR155 -inhibitor. [score:3]
miR-155 favors the differentiation of T cells into Th2 and Treg cells in MSCs, while it inhibits the differentiation to Th1 and Th17 cells. [score:3]
The results of the qPCR analysis demonstrated abundant expression of miR-155 in MSCs (Figure 2). [score:3]
In this study, we have also shown that different miR-155 levels influence the expression of monocyte chemotactic protein (MCP-1) (Figure 2(b)). [score:3]
3.2. miR-155 Expression in MSCs. [score:3]
Since miR-155 may be an important regulator of the immunosuppressive functions of MSCs, the age of animals and the passage of the MSCs should carefully considered in future studies. [score:3]
The data indicated that miR-155 could promote the transformation of T cells to Th2 cells and inhibit the shift towards Th1 and Th17. [score:3]
For example, the expression levels of miR-146a, miR-155, and miR-132 decreased by 93 ± 3% with increasing donor age [40]. [score:3]
The Effects of MSC miR-155 on the Expression of T Helper Cell-Specific Transcription Factors. [score:3]
MSC miR-155 Inhibits SMCs Migration. [score:3]
miR-155 may be further involved in the maintenance of the MSCs potent immunosuppressive capacity. [score:3]
In summary, the present study demonstrated that alterations of miR-155 levels in MSCs affected the differentiation of T cell subsets in SMCs, indicating that miR-155 may be important for the maintenance of the immunosuppressive functions of MSCs. [score:3]
The SMCs and miR155 -mimics -transfected MSCs coculture groups exhibited significantly lower SOCS1 mRNA levels, while the expression of SOCS1 was significantly elevated compared with the SMCs control group (p < 0.001) (Figure 4(c)). [score:2]
Therefore, the transwell migration assay was used in order to determine whether the miR-155 expression changes in MSCs affected the migration of immune cells. [score:2]
In dendritic cells [13] and macrophages [14], miR-155 has been implicated as a positive regulator of inflammatory cytokine production. [score:2]
In contrast to these findings, the percentage of CD4 [+] FOXP3 [+] Treg cells was significantly lower in SMCs and miR155 -inhibitor -transfected MSCs coculture groups compared with the SMSc control group (1.10 ± 0.02 versus 2.28 ± 0.02, p < 0.001) (Figures 4(a) and 4(b)). [score:2]
In contrast to this decrease in cell number, the number of spleen cells in the miR155 -inhibitor group was significantly higher compared with that noted in the control group (p < 0.01) (Figure 5). [score:2]
In contrast, the percentage of CD4 [+] FOXP3 [+] Treg cells in the SMCs cocultured with miR155 -inhibitor -transfected MSCs was significantly lower compared with that noted in SMCs control group (p < 0.001). [score:2]
The coculture of SMCs with miR155 -overexpressing MSCs (Figure 3(a)) resulted in significantly lower mRNA levels of Tbx21 and Rorc compared with SMCs control samples (p < 0.001 for both Tbx21 and Rorc), whereas the Gata3 level was higher (p < 0.001) (Figure 3(b)). [score:2]
In contrast to these findings, miR-155−/− mice were highly resistant to experimental autoimmune encephalomyelitis (EAE) [17]. [score:1]
However, a comprehensive profiling of the downstream cytokines of miR-155 in MSCs is required in order to understand their effects on different cell populations in SMCs. [score:1]
miR-155 has been considered as an important regulator of the immune response by various studies. [score:1]
This may at least be partially explained by the effect of miR-155 transfected MSCs on the recruitment of immune cells (Figure 5). [score:1]
The present study investigated the role of miR-155 in the immunosuppressive function of MSCs. [score:1]
It was reported that miR-155 and miR-146a were released from dendritic cells within exosomes and were subsequently internalized by recipient dendritic cells in order to reprogram the cellular response to endotoxin [35]. [score:1]
However, the role of miR-155 in the interaction between MSCs and the immune cells remains partially undiscovered. [score:1]
MSC miR-155 Promotes the Differentiation of Treg Cells. [score:1]
Furthermore, miR-155 and miR-146a are present in exosomes and pass between immune cells in mice [35]. [score:1]
Despite these findings, the identification of the targets of miR-155 in MSCs requires further investigation. [score:1]
During hypoxic treatment of MSCs in the presence and/or absence of IFN- γ, miR-155 levels were significantly increased (p < 0.001) (Figure 2(a)). [score:1]
The number of spleen mononuclear cells in the miR155 -mimics group was significantly lower than that in the negative control group (p < 0.01) (Figure 5). [score:1]
In the transwell assay, miR155 -mimics -transfected MSCs exhibited lower levels of SMCs migration, while the miR155 -inhibitor -transfected MSCs demonstrated significantly higher levels of migration, compared with the blank control group (p < 0.01, resp. [score:1]
miR-155 is also considered as a central modulator of T cell responses [16], based on evidence suggesting that miR-155 promoted the development of inflammatory T cells including the Th17 cell and Th1 cell subsets [17]. [score:1]
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3
[+] score: 184
The miR-155 target gene AT1R expression in VSMC was also determined by real time PCR, demonstrating a significant inhibition of AT1R expression compared to that with negative control or non -transfected VSMC (B). [score:8]
For example, miR-155 directly targets angiotensin II type I receptor (AT1R) and inhibits AT1R expression. [score:8]
Upregulation of miR155 demonstrated a decrease in AT1R expression and decrease in proliferation, confirming a direct causative role of the low level of miR155 on VSMC to a more synthetic, proliferative phenotype. [score:7]
Furthermore, we demonstrated that overexpression of miR-155 inhibited cell proliferation, confirming that the low expression of miR-155 may be a causative factor in the proliferative VSMC state observed in CKD. [score:7]
To confirm a direct relationship between the levels of miR-155 on target gene AT1R expression, VSMC from CKD rats were transfected with miR-155 mimic or miR negative control for 48 hrs. [score:6]
MiRNAs are known to be important in regulating such differentiation during development, but the low levels of miR-155, 145, and 125b observed in CKD arteries and VSMC and in the circulation of patients with CKD in the present study may lead to further propagation of de-differentiated VSMC, potentiating the development of hypertension, cardiovascular disease and vascular calcification. [score:6]
These results suggest that miR-155 directly controls the AT1R expression and regulate cellular proliferation in VSMC. [score:5]
To determine the effect of CKD on miRNA expression, we isolated VSMC from the aorta of CKD (Cy/+) rats and their normal littermates and determined the expression of miR-125b, miR-145, and miR-155 by real time PCR. [score:5]
Overexpression of miR-155 and AT1R expression in VSMC from CKD rats. [score:5]
Thus, the known upregulation of AT1R in arteries of patients with CKD [35] may be a direct result of low levels of the controlling miRNA-155. [score:5]
To determine if CKD affects the expression of circulating miR-125b, miR-145 and miR-155, we analyzed the expression in stored sera from 90 stage 3–4 CKD patients who had participated in a previous study and consented for future use of their blood samples. [score:5]
For example, in non-CKD patients with cardiovascular disease, miR-145 and miR-155 were found to be lower in patients with coronary artery disease than in those without [7]. [score:5]
Effect of overexpression of miR-155 on AT1R expression and cellular proliferation in VSMC. [score:5]
The miR-155 target gene AT1R expression in VSMC was also determined by real time PCR. [score:5]
Using transfection techniques, we confirmed a direct regulatory effect of miR-155 on AT1R expression in VSMC from CKD rats. [score:5]
Furthermore the decrease in and the tissue artery levels in rats corresponded to altered levels of mRNAs they are known to regulate, either directly or indirectly, and, at least for miR-155, correlated with arterial calcification. [score:4]
AT1R is normally repressed by miR-155, and thus our findings of increased AT1R expression in the arteries and VSMC of CKD animals may represent a defect in ‘regulation’ by the low levels of this miRNA. [score:4]
MiR-155 inhibits human angiotensin type 1 receptor (AT1R) expression and the activation of AT1R receptor mediated signaling cascades in fibroblasts [20]. [score:4]
Upregulation of miR-155 decreases cellular proliferation in VSMC from CKD rats. [score:4]
The expression of RUNX2 was also increased in CKD animals (Figure 2E), with a non-statistical correlation of RUNX2 with miR-125b (r = –0.47, p = 0.07) and miR-155 (r = –0.45, p = 0.08). [score:3]
In spontaneously hypertensive rats, the tissue expression of miR-155 in the aorta is inversely related to blood pressure [22]. [score:3]
Therefore, in the present study we evaluated three “vascular” miRNAs that are known to be expressed in the artery and involved in vascular smooth muscle cell (VSMC) differentiation (miR-145 and 155) [2], [15], [16], inflammatory vascular disease (miR-155) [17]– [19], abnormalities in the angiotensin pathway (miR-155) [20]– [22] and arterial calcification (miR-125b) [23], [24] in patients with CKD. [score:3]
Although many significant correlations were observed, the most consistent observation was with miR-155, whose expression was negatively correlated with vascular calcification. [score:3]
Aortic calcification was determined biochemically and results demonstrated that aorta calcification is increased in CKD rats and the greater the calcification, the lower the miR-155 expression level (r = 0.54, p = 0.04; Figure 2B). [score:3]
Sera were collected from stage 3–4 CKD patients (n = 10), hemodialysis patients (n = 10) and healthy volunteers (n = 8) and total RNA isolated and real time PCR performed to determine the expression of circulating levels of miR-125b (A), miR-145 (B) and miR-155 (C) normalized by U6. [score:3]
Aortic adventitial fibroblasts (often called myofibroblasts) with decreased miR-155 had decreased Angiotensin II receptor expression [21], a finding that parallels our observations. [score:3]
To confirm the role of miR-155 on its target gene AT1R in VSMC, a miR-155 mimic and miR negative control (Applied Biosystems) were used to promote the function of miR-155. [score:3]
miR-155 is also important in inflammation, and is expressed in both activated B and T cells [18], perhaps further adding to the pathogenesis of atherosclerosis. [score:3]
Furthermore, there was a strong negative correlation between the miR-155 and expression of AT1R (r = –. [score:3]
Furthermore, overexpression of miR-155 led to differentiation to a more contractile myofibroblast [21]. [score:3]
was performed to determine the expression of miR-125b, miR-145, miR-155 and miR-210 and normalized by U6 (A). [score:3]
The overexpression of miR-155 in VSMC was confirmed by real time PCR (A). [score:3]
The over expression of miR-155 in VSMC was confirmed by real time PCR of total RNA isolated from miR-155 mimic or negative control transfected VSMC. [score:3]
Thus, low levels of circulating miR-155 may lead to activation of AT1R in patients with CKD, perhaps playing a role in cardiovascular disease and renal fibrosis [35]. [score:3]
Thus, in addition to the effects of miR-155, these results suggest that CKD is associated with decreased VSMC expression and decreased circulating levels of several miRNA that control VSMC differentiation and function. [score:3]
0064558.g001 Figure 1 Sera were collected from stage 3–4 CKD patients (n = 10), hemodialysis patients (n = 10) and healthy volunteers (n = 8) and total RNA isolated and real time PCR performed to determine the expression of circulating levels of miR-125b (A), miR-145 (B) and miR-155 (C) normalized by U6. [score:3]
The results demonstrated that compared to negative control or non- transfected cells, VSMC transfected with miR-155 mimic had more than 1000 fold increase in miR-155 expression (Figure 4A). [score:2]
Furthermore, the AT1R expression in VSMC transfected with miR-155 was significantly decreased compared to that negative control or non -transfected VSMC (Figure 4B). [score:2]
Cultured VSMC from CKD rats had significantly lower expression of miR-125b, miR-145 and miR-155 compared to that from normal rats (Figure 3A). [score:2]
By real time PCR, the expression of miR-125b, miR-145 and miR-155 were lower in thoracic aorta from CKD compared to that from normal rats (all p<0.01; Figure 2A). [score:2]
As shown in Figure 5, cellular proliferation were significantly inhibited at 72 and 96 hrs in VSMC transfected with miR-155 mimic compared to that in miR negative control or non -transfected VSMC. [score:2]
The results demonstrated that the transfection of miR-155 mimic significantly inhibited cellular proliferation at 72 and 96 hrs in VSMC from CKD rats compared to that with negative control or non -transfected VSMC. [score:2]
Target-specific PCR primers (miR-125b, miR-145, miR-155 and miR-210) were obtained from Applied Biosystems. [score:2]
Rat VSMC isolated from CKD rats were transfected with 30 nM of miR-155 mimic or miR negative control. [score:1]
Calcium and vitamin D levels were no longer significant for miR-125b, miR-145 or miR-155. [score:1]
The circulating levels of miR-125b, miR-145 and miR-155 are decreased with progressive eGFR; the ability to detect such miRNA may offer hope of a novel cardiovascular biomarker. [score:1]
There were negative correlations of miR-155 with the presence of calcification miR-155 (r = –0.537, p = 0.04; Figure 2B) and miR-125b and calcification (r = –0.478, p = 0.07), but no relationship with miR-145. [score:1]
Rat VSMC isolated from CKD rats were transfected with 30 nM of miR-155 mimic or miR negative control for 48 hrs. [score:1]
For the human studies, review of circulating miRNAs, the miR-145 and miR-155 indicated the results were not normally distributed, and therefore all of the miRNAs were converted to natural logarithmic values. [score:1]
Taken together, the data strongly supports a role of miR-155 in the aberrant vascular remo deling in CKD. [score:1]
The change in phenotype do a differentiated VSMC is usually accompanied by increased proliferation [31], we therefore examined the effect of miR-155 on proliferation in VSMC from CKD rats. [score:1]
0064558.g004 Figure 4 Rat VSMC isolated from CKD rats were transfected with 30 nM of miR-155 mimic or miR negative control for 48 hrs. [score:1]
A recent study linked low circulating miR-155 levels with increased risk of sudden cardiac death [38], a leading cause of death in ESRD patients. [score:1]
0064558.g005 Figure 5 Rat VSMC isolated from CKD rats were transfected with 30 nM of miR-155 mimic or miR negative control. [score:1]
In addition, one polymorphism in AT1R is likely significant due to alteration in the miR-155 binding site [37]. [score:1]
of 30 nM of miR-155 mimic or negative control was performed using Lipofectamine RNAiMAX reagent (Applied Biosystems) according to the manufacturer’s instructions. [score:1]
Our results are consistent with the study of Neal et al who demonstrated that miRNA levels similarly correlated inversely with decreasing GFR, and also found decreasing miR-155 with decreasing eGFR [50]. [score:1]
In addition, after adjustment, diabetes continued to be associated with miR-145 (β = 1.69, p = 0.02, 95% CI 0.34, 3.04) but not miR-155. [score:1]
Circulating levels of miR-125b, miR-145 and miR-155 are decreased in CKD. [score:1]
[1 to 20 of 59 sentences]
4
[+] score: 109
Biochemical pathways potentially regulated by miRNAs differentially expressed in retina of Aβ -injected rats (Figure 3 and Table 4A) and in serum of AMD patients (Figure 4 and Table 4B) have been identified through the web server DIANA-miRPath v. 3. MiR-27a, miR-146a, and miR-155 (Figure 3 and Table 4A), which were up-regulated in retina of Aβ -injected rats, top scored as associated to TGF-β (p = 1 E-10) and prion diseases (p = 2 E-11) pathways. [score:9]
We found down-regulation of miR-155 in serum of AMD patients and Aβ injected rats; whereas we found up-regulation of miR-155 in the retina of Aβ injected rats, along with miR-27a and miR-146a. [score:7]
With exception of miRNA-155, down-regulated in serum of AMD patients and in serum of Aβ injected rats, six miRNAs (miR-9, miR-23a, miR-27a, miR-34a, miR-146a, miR-126) showed an up-regulation in serum of AMD patients. [score:7]
Furthermore, regulation of prion diseases pathway by miR-27a, miR-146a, and miR-155, reinforces the hypothesis that AMD can be a protein misfolding disease, such as AD, due to deposition of Aβ oligomers in drusen bodies. [score:6]
Increased expression of miR-155 induced formation of neovascular tufts that growth abnormally in vitreous with concomitant retinal microglial activation (Yan et al., 2015); thus, up-regulation of miR-155 in retina of Aβ injected rats might be the triggering factor of retinal inflammation and pro-angiogenic events. [score:6]
Early miR-155 upregulation contributes to neuroinflammation in Alzheimer's disease triple transgenic mouse mo del. [score:6]
In fact, miR-155 and miR-27a can target 42 genes involved in the TGF-β pathway (DIANA-miRPath), while miR-146a can target genes involved in inflammatory pathways (Toll-like receptor, NF-κB, TNF signaling pathways). [score:5]
The miR-155 can regulate genes involved in the TGF-β signaling pathway (p = 4 E-4), in the apoptosis pathway (p = 1 E-3) and several inflammatory pathways, that are also regulated by the set of miRNAs differentially expressed in Aβ -injected rats and in AMD patients. [score:5]
Furthermore, miR-155 was down-regulated in serum of Aβ -injected rats in comparison to controls (fold change −4.76; p = 0.029). [score:4]
Analysis of serum of Aβ -injected rats revealed that one miRNA out of 13, miR-155 was down-regulated in comparison to control rats, similarly to what was found in serum of AMD patients. [score:4]
Down-regulation of microRNA-155 attenuates retinal neovascularization via the PI3K/Akt pathway. [score:4]
Our results are in accordance to the report by Guedes et al. (2014), showing the up-regulation of miR-155 in hippocampal and cortical brain regions of 3-Tg AD animals as well as in cultured microglia and astrocytes treated with Aβ oligomers. [score:4]
Because miR-155 is associated to blood brain barrier dysfunction (Lopez-Ramirez et al., 2014), the up-regulation of miR-155 in retina of rats injected with Aβ oligomers might also influence the integrity of blood retinal barrier (BRB). [score:4]
Lack of differentially expressed circulating miRNAs in serum of Aβ -injected rats, other than down-regulated miR-155, could be related to variables that characterize miRNA secretion such as aging, duration and type of pathology (Creemers et al., 2012; Weilner et al., 2013). [score:4]
On the contrary, miR-155 was down-regulated, similarly to what found in serum of rats subjected to intravitreal injection of Aβ. [score:4]
Intravitreal injection of Aβ induced the up-regulation of three miRNAs in rat retina: miR-27a, miR-146a, and miR-155 (Table 2 and Figure 1). [score:4]
Analysis of these 13 miRNAs revealed that 7 miRNAs showed a significant up-regulation in serum of AMD patients in comparison to control group (miR-9, miR-23a, miR-27a, miR-34a, miR-146a, miR-155, and miR-126). [score:4]
In conclusion, the modified miRNA levels we found in rat retina (miR-27a, miR-146a, miR-155) and serum of AMD patients (miR-9, miR-23a, miR-34a, miR-126, miR-27a, miR-146a, miR-155) suggest that, among others, miR-27a, miR-146a, and miR-155 have an important role in AMD and could represent suitable biomarkers and appealing pharmacological targets. [score:3]
We found an increased expression of miR-155 in rat retina 72 h after intravitreal injection of Aβ oligomers; this result is in agreement with a previous work by Saxena et al. (2015), who found increased levels of miR-155 in retina of rats 72 h after light -induced retinal damage. [score:3]
The following groups of miRNAs were analyzed: miR-27a, miR-146a, miR-155 miR-9, miR-23a, miR-27a, miR-34a, miR-126,miR-146a, miR-155 miR-155 GraphPad Prism (version 4.0; GraphPad Software, San Diego, CA, USA) was used for statistical analysis and graphical representation of miRNA differential expression data. [score:3]
Incidentally, we showed that changes in circulating levels of some miRNAs (miR-9, miR-23a, miR-27a, miR-34a, miR-126, miR-146a, miR-155) as found in AMD patients are associated to Alzheimer's disease and modulate genes involved in neurodegenerative and inflammatory pathways. [score:3]
Three miRNAs were found to be dysregulated both in AMD patients and in retina of Aβ -injected rats (miR-27a, miR-146a, miR-155). [score:2]
The potential link between AMD and AD is also in line with the deregulation of insulin receptor signaling by miR-27a, miR-146a, and miR-155 (Giuffrida et al., 2012; Gontier et al., 2015; Takach et al., 2015; Han et al., 2016; Sajan et al., 2016; Table 4A). [score:2]
Figure 3 Scatter distribution of pathways regulated by miR-27a, miR-146a, and miR-155. [score:2]
MiR-155 and its angiogenic target gene CCN1 were found to alter vascular and neovascular growth in mice retina (Berber et al., 2017). [score:2]
We have looked at pathways that can be associated to miR-155 (Table 4C). [score:1]
MiR-27a, miR-146a, and miR-155 have been reported to be associated to the inflammatory pathways mTOR, TNFα, HIF signaling, and NF-κB (Romano et al., 2015). [score:1]
[1 to 20 of 27 sentences]
5
[+] score: 94
Other miRNAs from this paper: hsa-mir-155
In our study, we found that overexpression of CCAT1 could inhibit miR-155 expression and enhance the SGK3 expression, which was a direct target gene of miR-155. [score:12]
Moreover, overexpression of CCAT1 increased SGK3 expression, which was the direct target gene of miR-155 (Figure 4C and 4D). [score:8]
Previous study indicated that miR-155 expression was upregulated in the neuropathic pain rats compared to the sham and control group and inhibition of miR-155 decreased the pain thresholds [32]. [score:7]
miR-155 expression was upregulated in the bCCI mo del. [score:6]
LncRNA CCAT1 overexpression could alleviate the pain thresholds partly through regulating miR-155/SGK3 expression. [score:6]
We found that miR-155 expression level was upregulated in the spinal dorsal horn (Figure 5A), DRG (Figure 5B), hippocampus (Figure 5C), and ACC (Figure 5D) compared to sham-operated and nave group rats. [score:5]
Ectopic expression of CCAT1 decreased miR-155 expression in the PC12 cell (Figure 4B). [score:5]
Serum and glucocorticoid regulated protein kinase 3 (SGK3) was indentified as the direct target gene of miR-155. [score:5]
We showed that lncRNA CCAT1 decresaed the expression of miR-155 and enhanced the SGK3 expression in the NGF-differentiated PC12 cell. [score:5]
MiR-155 expression was upregulated in the bCCI mo del. [score:5]
CCAT1 suppressed miR-155 expression in the PC12 cell. [score:5]
The expression of SGK3 was negatively related with miR-155 expression. [score:5]
CCAT1 suppressed the miR-155 expression in the PC12 cell. [score:5]
Next, we determined miR-155 and SGK3 expression in the different regions of the rat nervous system. [score:3]
Real-time PCR was performed to determine the CCAT1 and miR-155 and mRNA expression by using the SYBRW Green PCR Master Mix (Roche, Germany) on the LightCycler 480 system (Roche, Basel, Switzerland). [score:3]
Furthermore, we indicated that the expression of miR-155 was increased in the spinal dorsal horn, DRG, hippocampus, and ACC of rats with bCCI injuries. [score:3]
Figure 5 (A) The expression of miR-155 in the spinal dorsal horn was determined by qRT-PCR. [score:3]
We found that miR-155 expression was increased in the spinal dorsal horn, DRG, hippocampus, and ACC of rats with bCCI injuries. [score:3]
[1 to 20 of 18 sentences]
6
[+] score: 83
Other miRNAs from this paper: rno-mir-21, rno-mir-146a
Previous studies have suggested the involvement of miRNAs in CAG; we further proved that expressions of miR-155 and miR-21 were upregulated and miR-146a was downregulated in gastric tissues of CAG rats. [score:9]
Expression levels of miR-155 and miR-21 were up-regulated significantly in mo del group than in control group and down-regulated significantly in acupuncture group than in mo del group, and there was no significance between acupuncture and control group. [score:9]
To be specific, expressions of miR-155 and miR-21 were downregulated and miR-146a was upregulated after acupuncture treatment. [score:9]
Expression levels of miR-155 and miR-21 were upregulated significantly in the mo del group compared to those in the control group and downregulated significantly in the acupuncture group compared to those in the mo del group, and there was no significance between the acupuncture and control group. [score:7]
These results have suggested that miR-155, miR-21, and miR-146a are potential targets of NF- κB, which are involved in an important signaling pathway in CAG [44], and efficacy of acupuncture in treatment of CAG may take effect by modifying expressions of miR-155, miR-21, and miR-146a via NF- κB pathway, thus to alleviate inflammation reaction of gastric mucosa. [score:5]
And overexpression of miR-155 could negatively regulate release of proinflammatory cytokines, leading to chronic infection [24]. [score:4]
Moreover, miR-155 has been suggested as a crucial effector of immune response in gastric epithelial cell lines and gastric mucosal tissues, which upregulated by activating NF- κB and activator protein-1 pathways [40]. [score:4]
Link et al. observed a gradual increase trend of miR-155 and miR-21 expression in preneoplastic gastric mucosa [22], including CAG stage, indicating that miR-155 and miR-21 were essential to persistent inflammation of gastric mucosa. [score:3]
Additionally, significant improvements of histological changes in CAG rats after altering NF- κB/miR-155/miR-21/miR-146a expression levels are powerful evidence to validate therapeutic roles of NF- κB-miR-155/miR-21/miR-146a signaling in response to acupuncture treatment. [score:3]
However, there is no definite conclusion on downstream targets of NF- κB-miR-155/miR-21/miR-146a signaling. [score:3]
Figure S3 showed that acupuncture may exerts its therapeutic effects via NF- κB-miR-155/miR-21/miR-146a signaling, which including (1) changes of transcription factors (such as NF- κB, which evoked by H. pylori infection, physical damage or chemical damage); (2) changes of miRNAs (miR-155/miR-21/miR-146a); (3) changes of downstream targets (such as TSLP, remain inconclusive). [score:3]
Possible limitations of the study include the fact that exact function of miR-155/miR-21/miR-146a, interaction between NF- κB, miR-155, miR-21, and miR-146a, and existence of NF- κB-miR-155/miR-21/miR-146a signaling and its definite downstream targets in response to acupuncture therapy remain inconclusive, which require further researches in the future work. [score:3]
In conclusion, we proposed that acupuncture may exert its therapeutic effects via NF- κB-miR-155/miR-21/miR-146a signaling, including (1) changes of transcription factors (such as NF- κB); (2) changes of miRNAs (miR-155/miR-21/miR-146a); (3) changes of downstream targets (such as TSLP, remaining inconclusive). [score:3]
What is more, downstream targets of miR-155/miR-21/miR-146a including I-kappa B kinase epsilon, Fas -associated death domain protein [40], and TSLP [43] have been reported. [score:3]
Petrocca et al. showed that chronic gastritis was associated with the alteration of miR-155 [25], which was known to play a major role in regulation of immune response [27] and promote tumor progression [28]. [score:2]
In conclusion, previous researches have indicated that miR-155, miR-21, and miR-146a may function as inflammation regulators in CAG. [score:2]
Previous researches have shown that miR-155, miR-21, and miR-146a were associated with gastritis [22, 24– 26], indicating that miR-155, miR-21, and miR-146a may function as inflammation regulators in CAG. [score:2]
Correlations among miR-155, miR-21, and miR-146a. [score:1]
Therefore, our findings implied that acupuncture may act through transcription factors and subsequent epigenetic changes, such as NF- κB-miR-155/miR-21/miR-146a signaling. [score:1]
The abovementioned findings suggested that miR-155, miR-21, and miR-146a were involved in the pathogenesis of CAG and might play an important role in modulation effect of acupuncture in treatment of CAG. [score:1]
Fold change (RQ = 2 [−ΔΔCt]) values of miR-155, miR-21, and miR-146a were shown in Table 5. Pearson's test results indicated that there were a positive correlation relationship between miR-155 and miR-21 and negative correlation relationships between miR-146a and miR-155/miR-21, respectively. [score:1]
And there were negative correlation relationships between miR-146a and miR-155/miR-21, respectively, indicating antagonism effects of them on CAG. [score:1]
Recently, increasing researches have suggested involvement of miRNAs in different processes of gastric carcinogenesis [21, 22], especially miR-155, miR-21, and miR-146a [22– 24]. [score:1]
Additionally, our results indicated that there was a positive correlation relationship between miR-155 and miR-21, indicating synergistic effects of these two miRNAs, as what has been reported before [38]. [score:1]
2 [−ΔCt] Values of miR-155, miR-21, and miR-146a. [score:1]
2 [−ΔCt] Values of miR-155, miR-21, and miR-146a Table 4 (and Figure S2) showed 2 [−ΔCt] values of miRNAs obtained from different groups. [score:1]
[1 to 20 of 26 sentences]
7
[+] score: 64
Previous literature has revealed the substantial involvement of miR-155 in both innate and adaptive immunity, including the inhibition of the MyD88 -dependent toll-like receptor pathway [41], immunoglobulin class switching, Th17/IL-17 axis enhancement, and Th1 upregulation with Th2 downregulation [36]. [score:9]
Meanwhile, miR-146a-5p, miR-147b, and miR-155-5p were significantly downregulated from day 7 and were repressed along the disease course, reaching the lowest level of expression at day 15. [score:8]
Firstly, NF- κB upstream factors such as MyD88 [45], TAB2 [46], IKK ε, and RIP1 [35], which are normally inhibited by miR-155, may be overexpressed following the downregulation of miR-155. [score:8]
miR-146a-5p, miR-155-5p, miR-147b, and miR-223-3p were downregulated, while miR-182-5p, miR-183-5p, and miR-9-3p were upregulated. [score:7]
Secondly, the Th1 lineage may be abated after the downregulation of miR-155, which subsequently results in high levels of Th17 axis expression. [score:6]
In accordance with our findings, miR-155 downregulation has also been noted in human subjects with active Behçet's disease [47]. [score:6]
Among the miRNAs studied, miR-146a-5p, miR-155-5p, miR-182-5p, and miR-183-5p are four particularly crucial miRNAs for the following reasons: they all show significant differential profiles in the disease course; they all regulate NF- κB pathway, and miR-146a-5p and miR-155-5p are regarded as potent immunological drivers; they all have been reported in some uveitis mo dels. [score:4]
The downregulation of miR-155 may possibly contribute to EAAU emergence. [score:4]
The expression levels of miR-146a-5p, miR-155-5p, miR-182-5p, and miR-183-5p in iris/ciliary bodies and popliteal lymph nodes are shown in Figure 3. The levels of miR-146a-5p and miR-155-5p in the popliteal lymph nodes reached their lowest point earlier, on day 7, while those in the iris/ciliary body tissue kept decreasing until day 15 after immunization. [score:3]
These contradictory results reflect the fact that multiple targets of the intracellular pathways can be manipulated by miR-155. [score:3]
In contrast, miR-155 was regarded as a positive regulator in both cellular and humoral immune responses in some studies. [score:2]
While the positive contribution of the immune response in clinical and experimental arthritis [42] and multiple sclerosis [43] has been noted, miR-155 knockout mice suffered from an exaggerated autoimmune response in the lungs, indicating its role in the prevention of asthma [44]. [score:2]
miR-155 -deficient mice failed to secrete class-switched immunoglobulins [24] and exhibited diminished production of Th17 cells [25]. [score:1]
The earlier changes of miR-146a-5p and miR-155-5p in the popliteal lymph nodes than in the iris/ciliary bodies also demonstrate the immunoanatomical fact that antigen presentation with T cell maturation has already taken place in the closest draining lymph node. [score:1]
[1 to 20 of 14 sentences]
8
[+] score: 56
This study aimed to assess: a) SIRT1–7 and miR-155 expression in the CC of the aged rat; b) how diet pattern, exercise and atorvastatin modulate SIRT1–7 and miR-155 expression levels and; c) how miR-155 correlates with the eNOS expression levels in the erectile tissue. [score:7]
MiRNA-155 (miR-155) is constitutively expressed in endothelial cells and extremely up-regulated in atherosclerotic plaques [17]. [score:6]
Analysis of microRNA-155 expression also suggests its intervention in the regulation of eNOS expression. [score:6]
Moreover, simvastatin prevented a decrease in eNOS expression, while decreasing miR-155 levels, suggesting miR-155 intervention in the simvastatin -induced increase of eNOS expression [18]. [score:5]
Aiming to elucidate the molecular mechanisms involved in age-related endothelial dysfunction and to unveil potential therapeutic targets, we tested how diet pattern, exercise and atorvastatin modulate the expression of eNOS, inducible NOS (iNOS), endothelin-1, sirtuins (SIRT) and microRNA-155 in the erectile tissue of high-fat fed aged rats. [score:5]
On account of its apparent intervention in the regulation of eNOS expression, miR-155 was quantified in the CC of rats from all the experimental groups (Fig.   6). [score:4]
We found no differences in miR-155 expression between rats under HF diet and controls, but treatments with atorvastatin or atorvastatin coupled with exercise decreased the expression of miR-155 when compared to HF (p = 0.049 and p = 0.011, for HF/ER/S and HF/ER/S/Ex, respectively). [score:4]
In silico analysis suggest that eNOS mRNA may be a direct target of miR-155. [score:4]
Endothelial dysfunction Energy restriction Exercise Atorvastatin Sirtuins microRNA-155 Ageing and obesity increase susceptibility to atherosclerosis and cardiovascular diseases (CVD) [1]. [score:3]
Changes on miR-155 expression in CC nearly opposed the variations found for eNOS, which was expected in view of the predicted affinity of miR-155 to eNOS mRNA [18]. [score:3]
Additionally, it was found that combined exercise, atorvastatin and ER treatments increment expression of both SIRT2 and eNOS while decrease miR-155 levels in the CC of aged rats. [score:3]
Previous evidence supporting that miR-155 promotes atherosclerosis [17] and decreases endothelium -dependent vasorelaxation through targeting eNOS [18], corroborates our data. [score:3]
To the best of our knowledge, no evidence of modulatory effect of atorvastatin, in contrast to simvastatin [18], or exercise on miR-155 has been reported before. [score:1]
Fig. 6Quantification of miR-155 in the CC of rats from all experimental groups. [score:1]
A decrease in miR-155 was found in groups treated with ER and atorvastatin associated or not with exercise, but isolated HF diet or 6 months of ER after HF, did not affect eNOS or miR-155 significantly, suggesting that other contributers, besides diet pattern modification are intervening. [score:1]
[1 to 20 of 15 sentences]
9
[+] score: 47
UNX combined with HSD intake upregulates AT1R, LTCCs leading to increased cardiovascular reactivity and decreased BRS; upregulates miR-25, miR-155 and miR-451 and downregulates miR-99b affecting SERCA2, AKT and AMPK leading to impaired excitation-coupling cycle, fibrosis and hypertrophy culminating in cardiac dysfunction. [score:10]
0180490.g006 Fig 6 UNX combined with HSD intake upregulates AT1R, LTCCs leading to increased cardiovascular reactivity and decreased BRS; upregulates miR-25, miR-155 and miR-451 and downregulates miR-99b affecting SERCA2, AKT and AMPK leading to impaired excitation-coupling cycle, fibrosis and hypertrophy culminating in cardiac dysfunction. [score:10]
miR-99, which regulates the expression of AKT [30] along with miR-155 [31], got downregulated in HSD, UNX and UNX+HSD (Fig 5E). [score:7]
It has been reported that miR-155 downregulates the expression of PTEN, which in turn dephosphorylates p-AKT [31]. [score:6]
miR-155 and miR-451 upregulated in HSD and UNX+HSD rats (Fig 5D). [score:4]
In our study in cardiac tissue, increased level of miR-155 downregulated PTEN, augmenting p-AKT in HSD and UNX+HSD animals. [score:4]
miR-155 was not detected in plasma may be because of its low level of expression. [score:3]
D), E) Relative levels of miR-25, miR-155, miR-451 and miR-99b in heart normalized with sn-RNU5G; F) Relative levels of miR-25, miR-451 and miR-99b in plasma normalized with miR-30e. [score:1]
Roles of miR-25 [14], miR-155 [15] & miR-451 [16] in various murine CVDs have been reported but their role in high salt diet -induced CV complications in uninephrectomized rats is not yet reported. [score:1]
Micro RNAs quantified were hsa-miR-25-3p (Cat# 204361), mmu-miR-155-5p (Cat# 205930), hsa-miR-99b-3p (Cat# 204064) and mmu-miR-451(Cat# 204734) and normalized with RNU5G (a small nuclear RNA) in heart and hsa-miR-30e-5p (Cat# 204714) in plasma. [score:1]
[1 to 20 of 10 sentences]
10
[+] score: 41
Upregulation or downregulation of miRNAs previously implicated in aGvHD pathogenesis such as the miR-17-92 cluster, miR-29a, miR-29b, miR-146a, or miR-155 did not reach significance in the NanoString analysis. [score:7]
These miRNAs were not among the significantly differentially expressed miRNAs as detected by the NanoString analyses, but we clearly observed higher expression levels of miR-146a and miR-155 in skin tissue, but not in intestines, liver, and lung, by qRT-PCR. [score:5]
Importantly, miR-155 is shown to repress Socs1 expression leading to increased proinflammatory cytokine production (32), which could correlate with the higher expression levels of inflammatory cytokines in skin observed in this study. [score:5]
Particular miRNAs associated with aGvHD include miRNAs that enhance T-cell activation, such as miR-155 (4, 10), miR-142 (11), miR-29a, miR-29b, and the miR-17-92 cluster (12), and miRNAs that repress T-cell activation, such as mir-146a (13), which is also upregulated in T regulatory cells (Tregs) (14). [score:5]
Figure 4 Upregulation of miR-146a and miR-155 in skin but not liver, lung, and intestines during aGvHD. [score:4]
We found clear upregulation of miR-146a and miR-155, but not of miR-29a, miR-29b, miR-19b, or miR-20a in skin (Figure 4A and data not shown). [score:4]
The expression of miR-146a and miR-155 is induced by lipopolysaccharide, which in the context of aGvHD is released as a consequence of breached epithelial barriers during pretransplantation irradiation. [score:3]
Differential Expression of miR-146a and miR-155 in Skin. [score:3]
miR-155 is involved in a number of inflammatory responses, and its expression is induced by inflammatory cytokines. [score:3]
The miR-17-92 cluster, miR-146a, and miR-155 have been previously implicated in aGvHD, where they are shown to regulate different aspects of T cell allo-activation (4, 10, 12, 13, 30) or T helper cell differentiation (31). [score:2]
[1 to 20 of 10 sentences]
11
[+] score: 36
Other miRNAs from this paper: rno-mir-199a
In the tissue of the corpus cavernosum, a significant downregulation of the miRNA-199 in the AD group and non-significant downregulation in the A and D groups compared to the C group were observed, whereas the miR-155 analysis demonstrated non-significant gene downregulation in the experimental groups compared to group C (Figure 4). [score:8]
Fichtlscherer et al. (28) studied plasma expression of some microRNAs known to be associated with endothelium and inflammation using quantitative PCR in patients with stable coronary disease comparing results with healthy volunteers and found significant hypoexpression of miR-199a and miR-155 in diabetics and males. [score:7]
They found an increase in ET-1 and its type B receptors as an effect of alcohol exposure, correlating the suppression of ET-1 expression by miR-199 in hepatic endothelial cells with miR-199 and miR-155 in human endothelial cells, thus indicating that these miRNAs may function as negative regulators of ET transcription control. [score:6]
Figure 4. When analyzing the blood microRNA profile, a significant downregulation of miR-155 was found in group AD and non-significant downregulation was observed in the other experimental groups compared to the C group. [score:6]
Figure 4. When analyzing the blood microRNA profile, a significant downregulation of miR-155 was found in group AD and non-significant downregulation was observed in the other experimental groups compared to the C group. [score:6]
Mean (±standard error) of microRNA-155 and -199 expression in blood samples of the groups studied. [score:3]
[1 to 20 of 6 sentences]
12
[+] score: 34
The results of luc reporter assays are summarized in Figure 10, C and D. The data showed that miR-143 and miR-155 down-regulated the WT2 c-Maf 3′-UTR, and miR-301a down-regulated the WT3 c-Maf 3′-UTR (Figure 10C, n = 6, P < 0.05). [score:6]
Expression of five miRNAs was shown in the transitional zones of both E14.5 and P0 lenses (Figure 11); however, expression of miR-155 was not established in the mouse lens (data not shown). [score:5]
Expression of the lens-differentiation factor c-Maf was predicted to be regulated by multiple miRNAs and experimentally validated for three miRNAs, including miR-143, miR-155, and miR-301a, in lens cells. [score:4]
To determine whether the aforementioned miRNAs identified in rat lens explant system are also expressed during mammalian lens development in vivo, we conducted ISH analysis of miR-9, miR-143, miR-155, miR-301a, miR-381, and miR-455 in E14.5 and newborn (P0) lenses. [score:4]
The current data suggest that multiple miRNAs, including miR-9, miR-137, miR-155, miR-301a, miR455, and miR-543 (Figure 7A and Figure 8A), regulate c-Maf expression through its 3′-UTR. [score:4]
The miR-143, miR-155, and miR-301a down-regulated expression of c-Maf evaluated in cultured lens cells through the 3′-UTR luciferase reporter assays. [score:3]
Although we confirmed these data for lens cells, we could not identify expression of miR-155 in mouse E14.5 and P0 lenses. [score:3]
The miR-155 has been identified to regulate c-Maf in T cells (Rodriguez et al. 2007; Suzuki et al. 2011) and was linked to multiple genes within the Ras/MAPK cascade disrupted in chronic myeloid leukemia (Machova Polakova et al. 2013). [score:2]
In case of c-Maf, an additional connection to miR-155 was shown in T cells (Rodriguez et al. 2007; Suzuki et al. 2011) and was included in Figure 8A. [score:1]
Similar analysis of “late” group, including c-Maf, Ets1, N-Myc, Nfat5, and Nfib, yielded 10 miRNAs: miR-20b, miR-145, miR-152, miR-155, miR-181a, miR-203, miR-222, miR-301a, miR-324-5p, and miR-351, with multiple connections. [score:1]
Ten miRNAs, miR-20b, miR-145, miR-152, miR-155, miR-181a, miR-203, miR-222, miR-301a, miR-324-5p, and miR-351. [score:1]
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13
[+] score: 30
We found that the expression levels of other two miRNAs (i. e., miR-150 and miR-155) were up-regulated only in the vesicular-fraction, while the expression of both miR-21 and miR-33 was found to be up-regulated in RNA isolated from vesicles enriched pellets and down-regulated in the RNA isolated from vesicles -depleted sera. [score:14]
The expression of miRNA associated with infection and inflammation [i. e., miR-150 (P = 0.01) and miR-155 (P = 0.04)] is up-regulated through day 2 and 4, and declines at day 6 (Fig. 6, middle row). [score:6]
However, the expression of miRNAs associated to infection and inflammation (i. e., miR-150 and miR-155) is unchanged in the VDS fraction (Fig. 7, middle row), while the expression of regeneration -associated miRNAs [i. e., miR-21 (P = 0.01) and miR-33 (P = 0.02)] is significantly reduced in the VDS RNAs. [score:5]
On the other hand, miR-150 and miR-155 were found up-regulated only in the VEP fractions, while miR-21 and miR-33 were found differentially regulated across the two populations. [score:5]
[1 to 20 of 4 sentences]
14
[+] score: 20
Other miRNAs from this paper: rno-mir-21, rno-mir-146a, rno-mir-223
In a mo del of endotoxemia in mice, it has been reported that exosomal miR-146a inhibits while miR-155 promotes the inflammatory response in some contexts [29]. [score:3]
The changes seen in the expression of miR-146a and miR-155 may reflect part of the functional adaptations after a chronic exposure to high sucrose, in this case probably related to the innate immune response. [score:3]
Although, it has been recently reported by Li and collaborators that miR-155 is overexpressed in the plasma from patients with atherosclerosis and may have a key role in the anti-inflammation activity of macrophages, attenuating foam cell formation [28]. [score:3]
The plasma levels of miR-155 from the animals fed with sucrose had a nonsignificant tendency to be 40% downregulated when compared to the control group (p = 0.066). [score:3]
Accordingly Chen and collaborators showed that miR-155 and C/EBP β constitute a bistable system for the regulation of adipogenesis [26]. [score:2]
We also found lower levels of miR-155 in plasma EVs, correlated with total plasma levels. [score:1]
In inflammation, evidence so far presented on miR-155 function indicates that it is likely to be pro- rather than anti-inflammatory [27]. [score:1]
The miR-155 levels in the EVs had lower levels in the sucrose drink animals than in the control group (p < 0.05). [score:1]
Such is the case of miR-21, miR-146a, miR-155, and miR-223 [9– 11]. [score:1]
Thus, the alternated increase of miR-146a and reduction miR-155 in plasma EVs could be part of the miRNA -mediated modulation of the inflammatory response. [score:1]
The relative abundance of miRNAs present in plasma EVs was miR-223 > miR-21 > miR-155 > miR-146a (Figure 3). [score:1]
[1 to 20 of 11 sentences]
15
[+] score: 19
Other miRNAs from this paper: rno-mir-27a, rno-mir-28, rno-mir-34a, rno-mir-144, rno-mir-153
H [2]S reduced miR-34a expression in hepatocytes of the young rats but has no effect in old ratsTo further study the mechanism of H [2]S on Nrf-2 expression in the liver after I/R, we detected the expression of many miRNAs including miR-34a, miR-28, miR-155, miR-27a, miR-144 and miR-153, which may be involved in regulating the expression of this transcription factor [28]. [score:10]
To further study the mechanism of H [2]S on Nrf-2 expression in the liver after I/R, we detected the expression of many miRNAs including miR-34a, miR-28, miR-155, miR-27a, miR-144 and miR-153, which may be involved in regulating the expression of this transcription factor [28]. [score:8]
The levels of miRNAs (miR-34a, miR-28, miR-155, miR-27a, miR-144 and miR-153) were quantified with a TaqMan PCR kit. [score:1]
[1 to 20 of 3 sentences]
16
[+] score: 18
Other miRNAs from this paper: rno-mir-29c-1, rno-mir-34a, rno-mir-200b, rno-mir-29c-2
The up-regulation of miR-200b, as well as of other miRNAs, including miR-155, is correlated with the development and progression of methyl -deficient diet-triggered NAFLD in mice [33]. [score:5]
Besides, as a new finding, the miR-155 was also observed to be up-regulated (Figure 5b). [score:4]
Pogribny I. P. Starlard-Davenport A. Tryndyak V. P. Han T. Ross S. A. Rusyn I. Beland F. A. Difference in expression of hepatic microRNAs miR-29c, miR-34a, miR-155, and miR-200b is associated with strain-specific susceptibility to dietary nonalcoholic steatohepatitis in miceLab. [score:3]
Effects of DZNep on the Hepatic Expression of miR-200b and miR-155. [score:3]
TaqMan microRNA assays (Applied Biosystems, Life Technologies, Carlsbad, CA, USA) were used for relative quantification of the mature miR-200b (hsa-miR-200b; 002251) and miR-155 (hsa-miR-155; 000479) expression levels, as described [36]. [score:2]
However, further experiments are required to investigate the potential mechanisms that could link EZH2, miR-200b/miR-155 expression, with in vitro and in vivo NAFLD. [score:1]
[1 to 20 of 6 sentences]
17
[+] score: 17
To replicate the findings obtained using TLDA array plate, we selected three miRNAs that were upregulated (mir-124, miR-218, miR-29a) and three, miRNAs that were downregulated (miR-146a, miR-200c, miR-155) based on their highest degree of significance by chronic CORT treatment and re-analyzed their expression individually by qPCR. [score:9]
When most significantly upregulated or downregulated miRNAs (for example, miR-124, miR-218, miR-146a and miR-155) were further analyzed, we found that these miRNAs had at least three simple GR elements (Supplementary Figure 1). [score:7]
We confirmed this finding by analyzing the six most significant CORT -induced altered miRNAs (miR-218, miR-124, miR-29a, miR-146a, miR-200c, miR-155) by qPCR. [score:1]
[1 to 20 of 3 sentences]
18
[+] score: 16
Scheme of miR-155-PLBr and shPLBr expressing vectors as well as of a luciferase PLB cDNA reporter gene plasmid (A) and luciferase expression in HEK293 cells co -transfected with either PLB silencing or non-silencing control plasmids (B). [score:5]
The lower activity of the heart-specific CMV-MLC0.26 promoter [43] driving the expression of miR155-PLBr compared to the highly active U6 promoter used for shPLBr delivery is the most reasonable explanation for the observed differences between the two expression systems. [score:4]
Hence, the miR-155 scaffold does not affect the inhibitory activity of amiRs. [score:3]
To develop an improved vector system for modulation of cardiac Ca [2+] homeostasis by silencing PLB, an siRNA sequence directed against the rat PLB [11] was embedded into the native environment of the miR-155 stem loop structure (amiR155-PLBr) and placed under control of the CMV-MLC0.26 promoter, which is specifically active in cardiac cells [43], [49]. [score:2]
The amiRNAs represent a type of shRNAs in which a siRNA sequence is embedded into a native microRNA scaffold [30], most commonly into that of miR-30 [30], [31] or miR-155 [32], [33]. [score:1]
pamiR155-Con and pamiR155-Luc were digested with SalI/ BglII and the miR155-Con and miR155-Luc containing fragments were inserted into SalI/ BglII digested pscAAV-amiR155-PLBr to replace amiR155-PLBr. [score:1]
[1 to 20 of 6 sentences]
19
[+] score: 16
Although miR-155 and miR-126 have been demonstrated to promote intestinal inflammation in IBD by inhibiting the expression of NF- κB inhibitor I κB α [59, 60], they are not the miRNA targets in HPM treatment on Tianshu and Qihai of experimental CD rats, indicating that HPM has specificity in terms of gene regulation. [score:10]
However, only 3 miRNAs are significantly upregulated in blood samples of UC subjects, of which miR-155 is the most highly expressed [46]. [score:6]
[1 to 20 of 2 sentences]
20
[+] score: 13
MiR-16 inhibited apoptosis of ESCC cells by downregulating RECK and SOX6 [9]; miR-208 [8] and miR-155 [11] promoted ESCC or hepatocellular carcinoma cell proliferation by targeting SOX6. [score:8]
In hepatocellular carcinoma, SOX6 activates p21WAF1/CIP1 (p21) expression in a p53 -dependent manner, and miR-155 targeting of SOX6 facilitated cell proliferation [11]. [score:5]
[1 to 20 of 2 sentences]
21
[+] score: 12
Wu C. Wang R. Li X. Chen J. Preoperative serum microRNA-155 expression independently predicts postoperative cognitive dysfunction after laparoscopic surgery for colon cancerMed. [score:3]
Moreover, serum expression of miRNA-155 was shown by multiple logistic regression analysis to be an independent predictive indicator for postoperative cognitive impairment after surgery [43]. [score:3]
Quinn S. R. Mangan N. E. Caffrey B. E. Gantier M. P. Williams B. R. Hertzog P. J. McCoy C. E. O’Neill L. A. The role of ETS2 transcription factor in the induction of microRNA-155 (miR-155) by lipopolysaccharide and its targeting by interleukin-10J. [score:3]
Tili E. Michaille J. J. Cimino A. Costinean S. Dumitru C. D. Adair B. Fabbri M. Alder H. Liu C. G. Calin G. A. Modulation of miR-155 and miR-125b levels following lipopolysaccharide/ TNF-α stimulation and their possible roles in regulating the response to endotoxin shockJ. [score:2]
Woodbury M. E. Freilich R. W. Cheng C. J. Asai H. Ikezu S. Boucher J. D. Slack F. Ikezu T. miR-155 is essential for inflammation -induced hippocampal neurogenic dysfunctionJ. [score:1]
[1 to 20 of 5 sentences]
22
[+] score: 11
In the mo del group, 17 miRNAs were downregulated, including miR-1, miR-133, miR-29, miR-126, miR-212, miR-499, miR-322, miR-378, and miR-30 family members, whereas the other 18 miRNAs were upregulated, including miR-21, miR-195, miR-155, miR-320, miR-125, miR-199, miR-214, miR-324, and miR-140 family members. [score:7]
Among these differentially expressed miRNAs, miR-1, miR-133, miR-29, miR-126, miR-499, miR-30, miR-21, miR-195, miR-155, miR-199, miR-214, and miR-140 have been reported to be related to MI [25– 36], while the other miRNAs have not been reported directly in MI. [score:4]
[1 to 20 of 2 sentences]
23
[+] score: 11
Other miRNAs from this paper: rno-mir-21, rno-mir-146a
And it has been reported that acupuncture can down-regulate the expression of miR-21, NF-γB p65 and miR-155 and up-regulate the expression of miR-146a in rats with CAG [16]. [score:11]
[1 to 20 of 1 sentences]
24
[+] score: 9
Though there was no difference of miR-155 in the expression between the two groups of our study, we found that the targets of miRNAs were enriched in the biological function of inflammatory response. [score:5]
Hu et al. [12] reported that the miR-155 level in serum and urine was significantly increased in patients with nephrolithiasis and proposed that miR-155 might influence the nephrolithiasis pathophysiological process by regulating inflammatory cytokines expression. [score:4]
[1 to 20 of 2 sentences]
25
[+] score: 9
In adults, ethanol causes systemic release of miR-155 and miR-27a to regulate TLR4 signaling and monocyte activation state, respectively [60, 61]. [score:2]
We found that ethanol increases miR-155 levels by 6.7-fold in our MV preparations (100 nm–1 μm) from BV2 microglia (Fig.   5c). [score:1]
In order to determine if this ethanol effect showed specificity for let-7b, we assessed two additional relevant pro-inflammatory miRNAs, miR-155 and miR181c. [score:1]
c Ethanol caused a robust increase in miR-155 in BV2 microglial MVs. [score:1]
The miR-155 has been shown previously to be increased by 2.5-fold in plasma MVs in response to ethanol [24]. [score:1]
d miR-155 binding to Ago2 was increased in HEC media MVs after ethanol treatment. [score:1]
Ethanol did not, however, increase the binding of HMGB1 with miR-155 (not shown), though miR-155 binding to Ago2 binding was increased as expected (Fig.   5f). [score:1]
let-7b, miR-155, and miR181c were assessed as described above. [score:1]
[1 to 20 of 8 sentences]
26
[+] score: 8
It has been reported that the expression of miR-146a, miR-155, and miR-132 is upregulated in monocytes after exposure with TNF-α [38], but our study showed only the expression miR-146a was increased in T cells after chronic exposure to TNF-α. [score:8]
[1 to 20 of 1 sentences]
27
[+] score: 7
However, it should be noted that although miRNAs-including miR-352 in this paper and other miRNAs found in previous studies, such as miR-100, miR-155, miR-329, and miR-495- are important factors controlling FSS -induced collateral vessel growth 15– 17, the mechanism by which miRNAs expression is regulated remains unclear. [score:4]
More recently, several studies have demonstrated that a different miRNA expression profile is induced in collateral vessels of mice following femoral artery occlusion, and several miRNAs such as miR-100, miR-155, miR-329 and miR-495 were found to be important factors that control collateral vessel growth 15– 17. [score:3]
[1 to 20 of 2 sentences]
28
[+] score: 7
For example, miR155 expression is up-regulated in Kupffer cells and contributes to ethanol -induced stabilization of TNFα mRNA [23]. [score:6]
These data add to a growing number of miRNAs involved in the response to macrophages to ethanol, including miR155 [23] and miR181b-3p [8]. [score:1]
[1 to 20 of 2 sentences]
29
[+] score: 7
The relative expression level of miR-134, miR-155, miR-30c and miR-630 in breast cancer cells respectively was detected by qRT-PCR. [score:3]
a The relative expression level of miR-134, miR-155, miR-30c and miR-630 in breast cancer cells respectively was detected by qRT-PCR. [score:3]
We used miRwalk database to identify potential miRNAs that bind to 3′ UTR of CTHRC1 and identified miR-134, miR-155, miR-30c and miR-630 as possible candidates (Additional file 4: Figure S2A). [score:1]
[1 to 20 of 3 sentences]
30
[+] score: 7
Other miRNAs from this paper: rno-mir-21, rno-mir-126a, rno-mir-192, rno-mir-210, rno-mir-126b
Saikumar et al. [22] demonstrated that kidney miR-21 and miR-155 were upregulated after IRI, while blood miR-21 and miR-155 were downregulated. [score:7]
[1 to 20 of 1 sentences]
31
[+] score: 7
Hu et al. (2014) reported serum and urinary levels of miR-155 were significantly elevated in patients with nephrolithiasis, and miR-155 might influence pathophysiology of nephrolithiasis via regulating inflammatory cytokines expression. [score:4]
However, the expressions of miR-155 were not significantly different between the two groups of our present study. [score:3]
[1 to 20 of 2 sentences]
32
[+] score: 6
Other miRNAs from this paper: rno-mir-93, rno-mir-96, rno-mir-143, rno-mir-206
Suppression of microRNA-155 attenuates neuropathic pain by regulating SOCS1 signalling pathway. [score:4]
MiR-155 modulates the progression of neuropathic pain through targeting SGK3. [score:2]
[1 to 20 of 2 sentences]
33
[+] score: 6
Dexamethasone down-regulates the expression of microRNA-155 in the livers of septic mice. [score:6]
[1 to 20 of 1 sentences]
34
[+] score: 5
Okoye et al. have recently documented that murine CD4 [+]CD25 [+]Foxp3 [+]Treg release miRNA-containing exosomes, that transfer Let-7b, Let-7d and miR-155 into Th1 cells, contributing to suppressing Th1 activation and inflammation in murine colitis [10]. [score:3]
Forrest AR Induction of microRNAs, mir-155, mir-222, mir-424 and mir-503, promotes monocytic differentiation through combinatorial regulationLeukemia. [score:2]
[1 to 20 of 2 sentences]
35
[+] score: 5
346A showed antisense complementarity with miR-155 and the expression levels of both UCRs were significantly reduced after the overexpression of miR-155 in leukemia cells. [score:5]
[1 to 20 of 1 sentences]
36
[+] score: 5
Interestingly, among these miRNAs, miR-155 [19] and miR-429 [23] were shown to directly target HIF-1α mRNA 3’UTR, and found to be involved in HIF-1α negative-feedback loop. [score:4]
Moreover 18S rRNA has also been previously used as an endogenous control by Bruning et al [19] in their study on miR-155 interaction with Hif-1α. [score:1]
[1 to 20 of 2 sentences]
37
[+] score: 5
Other miRNAs from this paper: rno-mir-7b
Two microRNAs, mir-155 and mir-7b, in particular, have been shown to decrease c-Fos protein levels by suppressing the translation of its mRNA transcript into protein (48, 49). [score:5]
[1 to 20 of 1 sentences]
38
[+] score: 5
Other deregulated biological processes included ‘blood vessel development’ (Mir-155, Mir-17-5p and Mir-130a) (FDR = 6x10 [-4]), 'lung development' (Mir-17-5p and Mir-27a) (FDR = 4x10 [-4]), and ‘cell motion’ (Mir-103) (FDR = 8x10 [-4]) (S3 Table). [score:3]
A heatmap built from nominally significant miRNAs between SHVT and NA detected by sRNA-seq are shown in S3 Fig. When comparing the direct sequencing of the samples with the bioinformatic prediction, 28 miRNA species overlapped, from which Mir-27a, Mir-103, Mir-17-5p, Mir-130a, and Mir-155 were nominally significant although the abundance of the latter was observed to be opposite to the one deduced by GSEA (Table 2). [score:2]
[1 to 20 of 2 sentences]
39
[+] score: 5
They showed an upregulation of miR-155 in the hippocampi of children with mesial temporal lobe epilepsy [20]. [score:4]
A study by Abou-Zeid et al. concentrated on the role of miR-155. [score:1]
[1 to 20 of 2 sentences]
40
[+] score: 5
Other miRNAs from this paper: rno-mir-20a, rno-mir-126a, rno-mir-132
Moreover, STDP was reported to attenuate atherosclerotic lesions in ApoE(-/-) mouse mo del via reducing the aortic expression of miR-21a, miR-132, miR-126a, miR-155 and increasing expression of miR-20a [16]. [score:5]
[1 to 20 of 1 sentences]
41
[+] score: 4
Other miRNAs from this paper: mmu-mir-155, mmu-mir-451a, rno-mir-451, mmu-mir-451b
To generate the miHTT-155 and miSNP67T-155 constructs, their guide sequences targeting HTT transcripts were embedded into the engineered murine pre-miR-155 backbone of pcDNA6.2-GW/EmGFP-miR (Invitrogen, Carlsbad, CA, USA) by annealing complementary oligonucleotides (Qiagen, Valencia, CA, USA) followed by ligation into the linearized pcDNA6.2 plasmid. [score:3]
Both miHTT and miSNP67T constructs were previously designed in the engineered mmu-miR-155 precursor, named miHTT-155 and miSNP67T-155 (Figure 1a). [score:1]
[1 to 20 of 2 sentences]
42
[+] score: 4
miR-146a and miR-155 displayed similar expression between groups C-C and C-HF of our study (see Supplemental Table 4; padj-values > 3.0E-01). [score:3]
miR-146a and miR-155 appeared to play specific roles in brain inflammatory responses (Cardoso et al., 2016). [score:1]
[1 to 20 of 2 sentences]
43
[+] score: 4
Other miRNAs from this paper: rno-mir-125b-1, rno-mir-125b-2, rno-mir-134, rno-mir-146a
It is remarkable that several significantly up-regulated brain miRNAs– miR-125b, miR-146a and miR-155–may contribute to so many of the observed deficits in AD including increased glial cell proliferation, altered synaptogenesis, deficits in neurotrophism, altered cytokine signalling and non-homoeostatic activation of innate immunity and inflammatory signalling [60– 62]. [score:4]
[1 to 20 of 1 sentences]
44
[+] score: 4
Moreover, decreased miR-155 and increased miR-27a in the disc may be associated with apoptosis [14, 15], whereas up-regulation of miR-10b and miR-21 is linked to NP cell proliferation [16, 17]. [score:4]
[1 to 20 of 1 sentences]
45
[+] score: 4
For instance, recent reports have indicated that both APC and MMR gene expression is regulated by miRs (e. g. miR-135 and miR-155, respectively) [10], [16]. [score:4]
[1 to 20 of 1 sentences]
46
[+] score: 4
For example, miR-21, miR-210 and miR-155 reduce pro-apoptotic signaling in response to a hypoxic environment and are consistently over-expressed in a variety of human tumors (Table 1). [score:3]
We found that hypoxia related microRNA had the most significant fold changes, with miR-210, miR-155 and miR-21 being amongst the top. [score:1]
[1 to 20 of 2 sentences]
47
[+] score: 4
Other miRNAs from this paper: hsa-mir-155
Furthermore, miR-K10a and its variants also target TGF-β type II receptor [28] while miR-K11 is an ortholog of cellular miR-155 [26], [34], which is implicated in cancer [66]. [score:3]
These results are not surprising because miR-K11 is a functional ortholog of miR-155, a human oncogenic miR [26], [34]. [score:1]
[1 to 20 of 2 sentences]
48
[+] score: 4
Wu H Huang T Ying L MiR-155 is involved in renal ischemia-reperfusion injury via direct targeting of FoxO3a and regulating renal tubular cell pyroptosisCell Physiol Biochem. [score:4]
[1 to 20 of 1 sentences]
49
[+] score: 4
miRNA-155 upregulation and complement factor H deficits in Down's syndrome. [score:4]
[1 to 20 of 1 sentences]
50
[+] score: 3
Tongxinluo inhibits vascular inflammation and neointimal hyperplasia through blockade of the positive feedback loop between miR-155 and TNF-α. [score:3]
[1 to 20 of 1 sentences]
51
[+] score: 3
For example, bone marrow progenitor cell-released HGF inhibited miRNA-155 -induced fibrosis, thereby exerting an anti-fibrotic effect [53]. [score:3]
[1 to 20 of 1 sentences]
52
[+] score: 3
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-17, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-32, hsa-mir-33a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-106a, mmu-let-7g, mmu-let-7i, mmu-mir-27b, mmu-mir-30a, mmu-mir-30b, mmu-mir-126a, mmu-mir-9-2, mmu-mir-135a-1, mmu-mir-137, mmu-mir-140, mmu-mir-150, mmu-mir-155, mmu-mir-24-1, mmu-mir-193a, mmu-mir-194-1, mmu-mir-204, mmu-mir-205, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-143, mmu-mir-30e, hsa-mir-34a, hsa-mir-204, hsa-mir-205, hsa-mir-222, mmu-let-7d, mmu-mir-106a, mmu-mir-106b, hsa-let-7g, hsa-let-7i, hsa-mir-27b, hsa-mir-30b, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-137, hsa-mir-140, hsa-mir-143, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-126, hsa-mir-150, hsa-mir-193a, hsa-mir-194-1, mmu-mir-19b-2, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-mir-200a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-15a, mmu-mir-23a, mmu-mir-24-2, mmu-mir-29a, mmu-mir-31, mmu-mir-92a-2, mmu-mir-34a, rno-mir-322-1, mmu-mir-322, rno-let-7d, rno-mir-329, mmu-mir-329, rno-mir-140, rno-mir-350-1, mmu-mir-350, hsa-mir-200c, hsa-mir-155, mmu-mir-17, mmu-mir-25, mmu-mir-32, mmu-mir-200c, mmu-mir-33, mmu-mir-222, mmu-mir-135a-2, mmu-mir-19b-1, mmu-mir-92a-1, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-7b, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-106b, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-30e, hsa-mir-375, mmu-mir-375, mmu-mir-133b, hsa-mir-133b, rno-let-7a-1, rno-let-7a-2, rno-let-7b, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7f-1, rno-let-7f-2, rno-let-7i, rno-mir-7b, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-17-1, rno-mir-19b-1, rno-mir-19b-2, rno-mir-23a, rno-mir-24-1, rno-mir-24-2, rno-mir-25, rno-mir-27b, rno-mir-29a, rno-mir-30c-1, rno-mir-30e, rno-mir-30b, rno-mir-30d, rno-mir-30a, rno-mir-30c-2, rno-mir-31a, rno-mir-32, rno-mir-33, rno-mir-34a, rno-mir-92a-1, rno-mir-92a-2, rno-mir-106b, rno-mir-126a, rno-mir-135a, rno-mir-137, rno-mir-143, rno-mir-150, rno-mir-193a, rno-mir-194-1, rno-mir-194-2, rno-mir-200c, rno-mir-200a, rno-mir-204, rno-mir-205, rno-mir-222, hsa-mir-196b, mmu-mir-196b, rno-mir-196b-1, mmu-mir-410, hsa-mir-329-1, hsa-mir-329-2, mmu-mir-470, hsa-mir-410, hsa-mir-486-1, hsa-mir-499a, rno-mir-133b, mmu-mir-486a, hsa-mir-33b, rno-mir-499, mmu-mir-499, mmu-mir-467d, hsa-mir-891a, hsa-mir-892a, hsa-mir-890, hsa-mir-891b, hsa-mir-888, hsa-mir-892b, rno-mir-17-2, rno-mir-375, rno-mir-410, mmu-mir-486b, rno-mir-31b, rno-mir-9b-3, rno-mir-9b-1, rno-mir-126b, rno-mir-9b-2, hsa-mir-499b, mmu-let-7j, mmu-mir-30f, mmu-let-7k, hsa-mir-486-2, mmu-mir-126b, rno-let-7g, rno-mir-15a, rno-mir-196b-2, rno-mir-322-2, rno-mir-350-2, rno-mir-486, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
Similarly, miR-133b, miR-137, miR-155, and miR499 were exclusively expressed in the caudal region of the mouse epididymis but were wi dely distributed throughout the rat and/or human epididymis (S4 Table). [score:3]
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53
[+] score: 3
Other miRNAs from this paper: hsa-let-7a-2, hsa-let-7c, hsa-let-7e, hsa-mir-15a, hsa-mir-16-1, hsa-mir-21, hsa-mir-22, hsa-mir-23a, hsa-mir-24-2, hsa-mir-100, hsa-mir-29b-2, mmu-let-7i, mmu-mir-99b, mmu-mir-125a, mmu-mir-130a, mmu-mir-142a, mmu-mir-144, mmu-mir-155, mmu-mir-183, hsa-mir-196a-1, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-200b, hsa-mir-148a, mmu-mir-143, hsa-mir-181c, hsa-mir-183, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-181a-1, hsa-mir-200b, mmu-mir-298, mmu-mir-34b, hsa-let-7i, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-130a, hsa-mir-142, hsa-mir-143, hsa-mir-144, hsa-mir-125a, mmu-mir-148a, mmu-mir-196a-1, mmu-let-7a-2, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-mir-15a, mmu-mir-16-1, mmu-mir-21a, mmu-mir-22, mmu-mir-23a, mmu-mir-24-2, rno-mir-148b, mmu-mir-148b, hsa-mir-200c, hsa-mir-155, mmu-mir-100, mmu-mir-200c, mmu-mir-181a-1, mmu-mir-29b-2, mmu-mir-199a-2, mmu-mir-199b, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-181c, hsa-mir-34b, hsa-mir-99b, hsa-mir-374a, hsa-mir-148b, rno-let-7a-2, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7i, rno-mir-21, rno-mir-22, rno-mir-23a, rno-mir-24-2, rno-mir-29b-2, rno-mir-34b, rno-mir-99b, rno-mir-100, rno-mir-124-1, rno-mir-124-2, rno-mir-125a, rno-mir-130a, rno-mir-142, rno-mir-143, rno-mir-144, rno-mir-181c, rno-mir-183, rno-mir-199a, rno-mir-200c, rno-mir-200b, rno-mir-181a-1, rno-mir-298, hsa-mir-193b, hsa-mir-497, hsa-mir-568, hsa-mir-572, hsa-mir-596, hsa-mir-612, rno-mir-664-1, rno-mir-664-2, rno-mir-497, mmu-mir-374b, mmu-mir-497a, mmu-mir-193b, mmu-mir-466b-1, mmu-mir-466b-2, mmu-mir-568, hsa-mir-298, hsa-mir-374b, rno-mir-466b-1, rno-mir-466b-2, hsa-mir-664a, mmu-mir-664, rno-mir-568, hsa-mir-664b, mmu-mir-21b, mmu-mir-21c, mmu-mir-142b, mmu-mir-497b, rno-mir-148a, rno-mir-15a, rno-mir-193b
Among them are two polycistronic transcripts (miR-15a~16-1 and miR-193b~365-1), and two expressing single miRNAs (miR-148a and miR-155). [score:3]
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54
[+] score: 3
Other genes regulates by this miRNA are the UDP-Glucose Ceramide Glucosyltransferase (UCGC) and acyl-CoA synthetase long-chain family member 3. Besides, regulation of syntaxin 5 by miR-155-5p is of critical importance. [score:3]
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55
[+] score: 3
Other miRNAs from this paper: rno-mir-146a, rno-mir-146b
Modulation of hippocampal gene expression of microRNA-146a/microRNA-155-nuclear factor-kappa B inflammatory signaling by troxerutin in healthy and diabetic rats. [score:3]
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56
[+] score: 3
Other miRNAs from this paper: ocu-mir-155
The existence of miRNAs for angiotensin receptors, for example, miR-155 [56] further erodes the value of mRNA levels as indicators of angiotensin receptor protein expression. [score:3]
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57
[+] score: 3
Other miRNAs from this paper: mmu-mir-155, hsa-mir-155
A conserved miRNA binding site for miR155 lies in the 3′UTR as determined by TargetScan. [score:3]
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58
[+] score: 3
Expressions of tumor necrosis factor alpha and microRNA-155 in immature rat mo del of status epilepticus and children with mesial temporal lobe epilepsy. [score:3]
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59
[+] score: 3
Murine macrophages incubated with paclitaxel had significantly increased expression of miR-155, miR-147, miR-146a and miR-132 30. [score:3]
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60
[+] score: 3
Bioinformatics analyses and cellular mo deling from the same group identified two additional microRNAs, miR-155 and miR-105, that target the 3′UTR of NPPA. [score:3]
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61
[+] score: 3
To test whether the anti-inflammatory effects of D-4F are related to miR expression, expression of miRs (miR-124a, miR-126, miR-146a, miR-153, miR-155) related to inflammation, BBB integrity and DM were measured in the ischemic brain of control and D-4F treated T1DM stroke rats. [score:3]
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62
[+] score: 3
miR-155 and miR-132 expression levels were also demonstrated to be increased in the total liver as well as in isolated hepatocytes and the Kupffer cells of alcohol-fed mice (9). [score:3]
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63
[+] score: 3
Other miRNAs from this paper: rno-mir-21, rno-mir-25, rno-mir-204
Zhou et al. [6] reported that miR-155 alleviated myocardial injury in septic rats by inhibiting JNK-related inflammatory signaling. [score:3]
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64
[+] score: 3
Emerging data support that micro -RNA, including miR-22 [23], miR-34a [24], miR-155 [25], miR-221/222 [26], is important for the multiple functions of statins, which is independent of HMG-CoA reductase inhibition. [score:3]
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65
[+] score: 3
miR-21, miR-155 and miR-221/222 have recently been shown to regulate AngII signaling in cardiac fibroblasts [14– 16] and in endothelial cells [17], while miR-29 regulates fibrotic pathways [18]. [score:3]
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66
[+] score: 2
Resveratrol decreases the levels of miR-155 in THP-1 and modulating JunB and JunD, key regulators in carcinogenesis [31]. [score:2]
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67
[+] score: 2
Other miRNAs from this paper: rno-mir-146a, rno-mir-203a, rno-mir-146b, rno-mir-203b
MiR-146, miR-155 and miR-203 regulate arthritic inflammatory response and joint destruction 31. [score:2]
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68
[+] score: 2
Other miRNAs from this paper: rno-mir-34a, rno-mir-98, rno-mir-146a, rno-mir-187
Expressions of tumor necrosis factor alpha and microrna-155 in immature rat mo del of status epilepticus and children with mesial temporal lobe epilepsy. [score:2]
[1 to 20 of 1 sentences]
69
[+] score: 2
Studies report the presence of both M1 and M2 macrophages in cardiac hypertrophy: the proinflammatory M1 macrophages express miR-155 microRNA and thereby increase the hypertrophic phenotype of cardiac tissue, while M2 macrophages are considered to be cardioprotective [14, 49, 50]. [score:2]
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70
[+] score: 2
NF-kB-regulated exosomal miR-155 promotes the inflammation associated with arsenite carcinogenesis. [score:2]
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71
[+] score: 2
Other miRNAs from this paper: rno-mir-10b, rno-mir-191a, rno-mir-1, rno-mir-191b
miR-1, miR-10b, miR-155, and miR-191 are novel regulators of BDNF. [score:2]
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72
[+] score: 2
Particularly, it has been shown that some microRNAs (miRNAs) (e. g., miR-155, miR-146, miR-150) control the development and responses of the immune system [14]. [score:2]
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73
[+] score: 1
Other miRNAs from this paper: rno-mir-132, rno-mir-146a
Kong H, Yin F, He F, Omran A, Li L, Wu T, Wang Y, Peng J. The effect of miR-132, miR-146a, and miR-155 on MRP8/TLR4 -induced astrocyte-related inflammation. [score:1]
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74
[+] score: 1
Other miRNAs from this paper: rno-mir-27a
Banerjee N. Talcott S. Safe S. Mertens-Talcott S. U. Cytotoxicity of pomegranate polyphenolics in breast cancer cells in vitro and vivo: Potential role of miRNA-27a and miRNA-155 in cell survival and inflammationBreast Cancer Res. [score:1]
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75
[+] score: 1
MiRNA from stressed, control, stress + prazosin, and control + prazosin rats were analyzed for changes in miR-142-5p, miR-150, miR-155, and miR-203. [score:1]
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76
[+] score: 1
A number of miRNAs have been identified to be involved in cardiac cell survival and death, such as miR-155, miR-874 and miR-200a-5p 8– 10. [score:1]
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77
[+] score: 1
One of the 18 was recognized in the newly released miRBase-v20 (rno-miR-155-5p). [score:1]
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78
[+] score: 1
The miRNAs miR-1, miR-155, and miR-208 have significant effects on the RAAS [14]. [score:1]
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79
[+] score: 1
Another study indicated that miR-155 and -223 increased significantly in mice prefrontal cortex after inflammatory pain induced by facial carrageenan injection [14]. [score:1]
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80
[+] score: 1
TCA cycle intermediates including citrate, succinate, 2-oxoglutarate and fumarate are positively correlated with miR-143, miR-126-3p, miR-146a, miR-150 and miR-155. [score:1]
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81
[+] score: 1
Anti-Warburg effect of rosmarinic acid via miR-155 in gastric cancer cells. [score:1]
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