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50 publications mentioning rno-mir-146b

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-146b. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 289
Other miRNAs from this paper: rno-let-7f-1, rno-let-7f-2, rno-mir-141, rno-mir-146a, rno-mir-221
The inhibition of miR-146b-5p in PCCl3 also inhibited migration and invasion, and exogenous overexpression of this miR in TPC-1 and BCPAP cells increased migration and invasion even more. [score:7]
Overexpression of miR-146b-5p in normal rat thyroid cell line (PCCl3) increases migration and invasion, while its inhibition inhibits both processes. [score:7]
Inhibition of miR-146b-5p in PCCl3 and PTC cell lines (highly expressed) was obtained with the use of antagomiR-146b-5p (30nM -Anti-miR [TM] miRNA Inhibitor Product Anti-hsa-miR-146b-5p, AM10105, Applied Biosystems, Foster City, CA, USA), transfected with Lipofectamine 2000. [score:7]
The inhibition of miR-146b-5p in PCCl3 also inhibited migration and invasion, and additional (exogenous) overexpression of this miR in TPC-1 and BCPAP cells increased migration and invasion, without effects on cell morphology or gelatin degradation. [score:7]
The overexpression of SMAD4 in BCPAP cells, a validated target of miR-146b-5p and key protein in the TGF-β signaling pathway, inhibited migration similarly to the effects observed with the antagomiR 146b-5p. [score:7]
The opposite effect was observed after the inhibition of this miR in this cell line and also in human thyroid tumor cell lines which, although bearing different mutations, overexpressed miR-146b. [score:6]
Interestingly, in PCCl3 normal thyroid cells the activation of the oncogenes RET/PTC3 and BRAF upregulated miR-146b-5p expression [31]. [score:6]
The overexpression of SMAD4 in BCPAP cells significantly decreased migration and invasion to a degree very similar to that observed with the antagomiR 146-5p, suggesting that SMAD4 is, indeed, a very important target of miR-146b-5p in those cells, regulating cell migration. [score:6]
Inhibition of miR-146b-5p decreases migration and invasion of the human papillary thyroid carcinoma (PTC) cell lines TPC-1 and BCPAP, whereas its overexpression increases both processes. [score:5]
BCPAP cells express high levels of miR-146-5p, which reduces SMAD4 basal expression [31]. [score:5]
This study aimed to investigate the role of miR-146b-5p on the migratory and invasive behaviors of thyroid cells, using a non tumor rat thyroid follicular cell line (PCCl3) transfected with the miR-146b-5p genomic region, and two PTC cell lines (TPC-1 and BCPAP, bearing distinct oncogenic backgrounds), which express high levels of miR-146b-5p, after miR-146b inhibition by antagomiR and miR-146b overexpression by mimics-miR. [score:5]
Gelatin degradation was inhibited in TPC-1 cells after inhibition of miR-146b-5p, but was unaffected in BCPAP cells, which did not degrade gelatin. [score:5]
Lin F Wang X Jie Z Hong X Li X Wang M Inhibitory effects of miR-146b-5p on cell migration and invasion of pancreatic cancer by targeting MMP16J Huazhong Univ Sci Technolog Med Sci. [score:5]
Experimental procedures were performed with non-tumor rat thyroid follicular cell line (PCCl3) and two PTC cell lines (TPC-1 and BCPAP) after overexpression and inhibition of miR-146b-5p by specific oligonucleotides, mimics-miR and antagomiR, respectively. [score:5]
On the other hand, the inhibition of miR-146b-5p by ~50–60 % using a specific antagomiR also inhibited migration and invasion by approximately 50–60 % (Additional file 4: Figure S4). [score:5]
Briefly, we found that the overexpression of miR-146b-5p in PCCl3 increased migration and invasion, whereas an opposite proportional effect was observed in PTC tumor cell lines after miR-146b-5p inhibition. [score:5]
MiR-146b-5p, which has been positively correlated to the degree of malignancy, is overexpressed in both human PTC cell lines, TPC-1 (spontaneously harboring the RET/PTC-1 mutation) [29] and BCPAP (BRAF [V] [600E] oncogene point mutation) [30]. [score:4]
Statistically significant differences: * P< 0,01 (pBabe SMAD4 versus pBabe ø) MiR-146b-5p, which has been positively correlated to the degree of malignancy, is overexpressed in both human PTC cell lines, TPC-1 (spontaneously harboring the RET/PTC-1 mutation) [29] and BCPAP (BRAF [V] [600E] oncogene point mutation) [30]. [score:4]
For both cell lines, control cells (TPC-1/BCPAP, Mock and Neg) are polarized and show one or two predominant lamellipodia, whereas cells with inhibition of miR-146b-5p (Anti-146B) show a higher number of smaller protrusions in different directions. [score:4]
A specific miR-146b-5p oligonucleotide inhibitor (antagomiR) was used to reduce its expression in both cell lines (Figs.   1a and 2a) before the transwell migration and invasion assays. [score:4]
In contrast, both TPC-1 and BCPAP cells with miR-146b-5p inhibited lost polarity, showing several protrusions in different directions, apparently smaller lamellipodia (Fig.   4). [score:4]
Katakowski M Zheng X Jiang F Rogers T Szalad A Chopp M MiR-146b-5p suppresses EGFR expression and reduces in vitro migration and invasion of gliomaCancer Invest. [score:4]
The same assays were performed after overexpression of miR-146b-5p in both tumor cell lines for 8 h. BCPAP-pBabe SMAD4 and BCPAP-pBabe-puro were seeded (1 × 10 [6] cells), tripsinized and lysed in presence of cocktail proteases inhibitors. [score:4]
Our hypothesis is that miR-146-5p contributes to regulate cell migration and invasion through the targeting of SMAD4 in normal and tumor thyroid cell lines. [score:4]
Fig. 3Inhibition of miR-146b-5p decreased gelatin degradation by TPC-1 cells. [score:3]
In both tumor cell lines, our results showed a similar degree of inhibition for migration and invasion, suggesting that the effects of miR-146b-5p are mostly associated with the cytoskeleton, and not necessarily related to increased degradation of ECM. [score:3]
TPC-1 / BCPAP: cell, Mock: cell + transfection agent, Neg: cell + anti-miR negative control, Anti-146b: cell + anti-miR-146b In order to investigate the effects of miR-146b-5p inhibition on cell morphology and actin cytoskeletal reorganization, we stained the F-actin filaments in both tumor cell lines using fluorescent phalloidin, as shown in Fig.   4. We observed that control cells (which express high levels of miR-146b-5p) were elongated, suggesting polarization, featuring one or two predominant lamellipodia. [score:3]
The miR146b-5p has received great attention for being one of the most expressed and positively correlated with tumor aggressiveness and extra-thyroid invasiveness [24– 26]. [score:3]
The overexpression of miR-146b-5p in TPC-I cells led to a slight (not significant) increase in gelatin degradation, whereas BCPAP cells were still not able to degrade gelatin (Additional file 2: Figure S2). [score:3]
Inhibition of miR-146b-5p decreases migration and invasion of the non tumor rat thyroid follicular cell line (PCCl3). [score:3]
The results show that miR-146b-5p inhibition (~70 %) reduced by at least 50 % the migration and invasion capacity of TPC-1 (Fig.   1c and d) and BCPAP (Fig.   2c and d) cells. [score:3]
Bars: 10 μm Interestingly, the overexpression of miR-146b-5p in TPC-1 and BCPAP cells did not affect cell morphology or the F-actin distribution in both cell lines (Additional file 3: Figure S3). [score:3]
In papillary thyroid carcinoma (PTC), miR-146b-5p is highly expressed and positively correlated to the degree of malignancy. [score:3]
Statistically significant differences: * P < 0,01 (BCPAP versus Anti-146b); ** P < 0,01 (Mock versus Anti-146b), *** P < 0,01 (Neg versus Anti-146b)The overexpression of miR-146b-5p in TPC-1 and BCPAP cells (by 11-12x), on the other hand, increased migration and invasion by 2–2.5x in both cell lines (Additional file 1: Figure S1). [score:3]
In BCPAP cell line, no differences between controls and miR-146b-5p -inhibited groups were observed (Fig.   3b). [score:3]
miR-146b-5p positively regulates migration and invasion of thyroid normal and tumor follicular cells (independently from their original mutation, either BRAF or RET/PTC), through a mechanism that involves the actin cytoskeleton but not an increased capacity of matrix degradation. [score:3]
After miR-146b-5p inhibition, TPC-1 and BCPAP migration and invasion were significantly reduced, with cells showing several simultaneous processes and low polarity. [score:3]
The degradation activity of control and treated groups (miR-146b-5p inhibited) are identified as dark areas on gelatin-FITC background. [score:3]
Migration and invasion of PCCl3 were increased 2-3x after miR-146b-5p overexpression (10X) and large lamellipodia were evident in those cells. [score:3]
On the other hand, the high expression of miR-146b-5p in PTC has been positively correlated with the malignancy and aggressiveness in clinicopathological correlative studies [8, 38, 39]. [score:3]
Patnaik SK Kannisto E Mallick R Yendamuri S Overexpression of the lung cancer-prognostic miR-146b microRNAs has a minimal and negative effect on the malignant phenotype of A549 lung cancer cellsPLoS One. [score:3]
The overexpression of miR-146b-5p slightly increased gelatin degradation by TPC-1 cells, having no effect on BCPAP cells gelatinolytic activity. [score:3]
Fig. 4Inhibition of miR-146b-5p alter F-actin cytoskeleton distribution and cell morphology. [score:3]
Exogenous overexpression of miR-146b-5p in both tumor cell lines increased migration and invasion even more, without effects on cell morphology or in the F-actin arrangement. [score:3]
Fig. 5Overexpression of miR-146b-5p promotes migration and invasion of non tumor rat thyroid follicular cell line (PCCl3). [score:3]
Overexpression of miR-146b-5p in a normal rat thyroid cell line (PCCl3) led to increased spreading on the substrate, formation of large lamellipodia, increased migration (without exogenous basement membrane) and invasion (in the presence of basement membrane). [score:3]
The overexpression of miR-146b-5p of PTC cell lines was performed by mimics miR-146b-5p (50nM, MirVana miRNA mimic has-miR-146b-5p, MC10105) transfection. [score:3]
The inhibition of miR-146b-5p significantly reduced this function in those cells, although without any additional disadvantage to the cells to migrate. [score:3]
Statistically significant differences: * P < 0,01 (PCCl3-WT versus PC-CMV-146b); ** P < 0,01 (PC-CMV-ø and PC-CMV-146b) Fig. 6Overexpression of miR-146b-5p enhances cell spreading and formation of large lamellipodia in non tumor rat thyroid follicular cell line (PCCl3). [score:3]
Statistically significant differences: * P < 0,01 (BCPAP versus Anti-146b); ** P < 0,01 (Mock versus Anti-146b), *** P < 0,01 (Neg versus Anti-146b) The overexpression of miR-146b-5p in TPC-1 and BCPAP cells (by 11-12x), on the other hand, increased migration and invasion by 2–2.5x in both cell lines (Additional file 1: Figure S1). [score:3]
In gliomas, reduced expression of miR-146b contributes to increase MMP16 and promote metastasis [37]. [score:3]
Statistically significant differences: * P< 0,01 (pBabe SMAD4 versus pBabe ø) A differential overexpression of miR-146b has been observed in different types of cancer, not always correlated with tumor progression or invasion [32– 34]. [score:3]
The results show that cells overexpressing miR-146b-5p (~10 times, Fig.   5a) migrated and invaded about 3 times more than control cells (Fig.   5c and d). [score:3]
Statistically significant differences: * P < 0,01 (TPC-1 versus Anti-146b); ** P < 0,01 (Mock versus Anti-146b), *** P< 0,01 (Neg versus Anti-146b) Fig. 2Inhibition of miR-146b-5p decreases migration and invasion of the PTC cell line BCPAP. [score:3]
Overexpression of miR-146b-5p increases migration and invasion of the PTC cell lines, TPC-1 and BCPAP. [score:3]
The authors showed that miR-146b-5p targets the 3'UTR of SMAD4. [score:3]
Fig. 1Inhibition of miR-146b-5p decreases migration and invasion of the PTC cell line TPC-1. Cells were transfected with an oligonucleotide antagomiR-146b-5p (Anti-146b) (30nM), as described in the section. [score:3]
Bars: 10 μmInterestingly, the overexpression of miR-146b-5p in TPC-1 and BCPAP cells did not affect cell morphology or the F-actin distribution in both cell lines (Additional file 3: Figure S3). [score:3]
Overexpression of miR-146b-5p in TPC-1 and BCPAP cells does not affect morphology and F-actin distribution. [score:3]
Overexpression of miR-146b-5p slightly increases gelatin degradation by TPC-1 cells. [score:3]
In thyroid cancer cells, the targeting of ZNFR3 by miR-146b stimulates Epithelial-to-mesenchymal transition (EMT) [39]. [score:3]
SMAD4, a crucial protein in the canonical TGF-β signaling pathway, was validated as a target of miR-146b-5p in BCPAP, TPC-1 and PCCl3 cells [31]. [score:3]
MiR-146b-5p inhibition reduced gelatin degradation by TPC-1, but not by BCPAP cell lines. [score:2]
The regulatory capacity of miR-146b-5p on tumor invasion, possibly through SMAD4 and the impairment of TGF-β signaling, shows its important role on PTC aggressiveness and invasiveness. [score:2]
Geraldo MV Yamashita AS Kimura ET MicroRNA miR-146b-5p regulates signal transduction of TGF-b by repressing SMAD4 in thyroid cancerOncogene. [score:2]
After miR-146b-5p inhibition, the substrate degradation activity of this cell line was reduced to small focal points during the assay, very different from the control groups (Fig.   3a). [score:2]
Actually, regarding invasiveness, the miR-146b has been considered inhibitory of migration and invasion in several types of tumors, i. e. gliomas, lung cancer, pancreatic cancer, and osteosarcoma [32– 37]. [score:2]
MiR-146b-5p inhibition reduced cell polarization and increased the number of cellular protrusions in TPC-1 and BCPAP cell lines. [score:2]
Subsequently, miR-146b-5p expression was detected from the cDNA product using TaqMan Universal PCR Master Mix No AmpErase UNG (Applied Biosystems) and Taqman miR Assay according to the manufacturer’s instructions (Applied Biosystems, Weiterstadt, Germany) by qPCR. [score:2]
Cells overexpressing miR-146-5p (PC-CMV-146b) and control groups (PC-CMV-ø and PCCl3-WT) were cultured and submitted to transwell migration and invasion assays for 24 h. After this period, miR-146b-5p expression (a) and cell viability (b) were evaluated. [score:2]
Nevertheless, the functional roles of miR-146b appear to affect different cellular processes important for tumor development and are still poorly understood. [score:2]
Recently, using in vitro wound healing assays, Wojtas et al. [40] showed that the overexpression of miR-146b improved migration of HTori-3 and FTC-133 cell lines. [score:2]
MicroRNAs Thyroid Cancer Invasion PTC Cell migration miR-146b Tumor invasiveness is directly related to the ability of tumor cells to migrate and invade surrounding tissues, spreading via blood and lymphatic circulation. [score:2]
Al-Khalaf HH Aboussekhra A MicroRNA-141 and MicroRNA-146b-5p Inhibit the Prometastatic Mesenchymal Characteristics through the RNA -binding Protein AUF1 Targeting the Transcription Factor ZEB1 and the Protein Kinase AKTJ Biol Chem. [score:2]
Deng X Wu B Xiao K Kang J Xie J Zhang X MiR-146b-5p promotes metastasis and induces epithelial-mesenchymal transition in thyroid cancer by targeting ZNRF3Cell Physiol Biochem. [score:2]
TPC-1/BCPAP: cell, Mock: cell + transfection agent, Neg: cell + anti-miR negative control, Anti-146b: cell + anti-miR-146b. [score:1]
Cells were transfected with an oligonucleotide mimics miR-146b-5p (miR-146b) (50nM), as described in the section. [score:1]
Quantitative PCR and miR-146b-5p mature miR quantification. [score:1]
BCPAP: cell, Mock: cell + transfection agent, Neg: cell + anti-miR negative control, Anti-146b: cell + anti-miR-146b-5p. [score:1]
Geraldo MV Fuziwara CS Friguglieti CU Costa RB Kulcsar MA Yamashita AS MicroRNAs miR-146-5p and let-7f as prognostic tools for aggressive papillary thyroid carcinoma: a case reportArq Bras Endocrinol Metabol. [score:1]
Using a non tumor thyroid cell line (PCCl3) we aimed to evaluate if the overexpression of miR-146b-5p influences migration and invasion per se. [score:1]
Forty-eight hours after transfection miR-146b-5p expression (a) and cell viability (b) were evaluated. [score:1]
TPC-1: cell, Mock: cell + transfection agent, Neg: cell + anti-miR negative control, Anti-146b: cell + anti-miR-146b-5p. [score:1]
Our findings improve the understanding of the functional role of miR-146b-5p in thyroid gland oncogenesis. [score:1]
This study also shows that the role of miR-146b-5p is independent of the cell’s capacity to degrade ECM. [score:1]
In this study, we demonstrate that miR-146b-5p stimulates the migratory and invasive behavior of PTC cell lines. [score:1]
TPC-1/BCPAP: cell, Mock: cell + transfection agent, Neg: cell + mimics-miR negative control, miR-146b: cell + mimics miR-146b-5p. [score:1]
Statistically significant differences: * P < 0,01 (TPC-1/BCPAP versus miR-146b); ** P < 0,01 (Mock versus miR-146b), *** P > 0,01 (Neg versus miR-146b). [score:1]
PCCl3-WT: normal thyroid follicular cell line, PC-CMV-ø: cell transfected with an empty vector, PC-CMV-146b: cell transfected with the miR-146-5p genomic region. [score:1]
The degradation activity of control and treated groups (miR-146b-5p) were identified as dark areas on gelatin-FITC background. [score:1]
PCCl3 were transfected with a pcDNA3.1 plasmid containing the genomic region of miR-146b-5p (PC-CMV-146b) or the pcDNA3.1 empty vector (PC-CMV- ø as control), as previously described [31]. [score:1]
We transfected the cells with a pcDNA3.1 plasmid containing the genomic region of miR-146b-5p (PC-CMV-146b) [31]. [score:1]
PCCl3: cell, Mock: cell + transfection agent, Neg: cell + anti-miR negative control, Anti-146b: cell + anti-miR-146b-5p. [score:1]
TPC-1/BCPAP: cell, Mock: cell + transfection agent, Neg: cell + mimics-miR negative control, miR-146b: cell + mimics-miR-146b. [score:1]
TPC-1 / BCPAP: cell, Mock: cell + transfection agent, Neg: cell + mimics miR negative control, miR-146b: cell + mimics-miR-146b. [score:1]
For miR expression analysis, the TaqMan microRNA Reverse Transcription kit and RT Primers provided with the miR-146b-5p Taqman miR Assay (PN4373178; Applied Biosystems) were used according to the manufacturer’s instructions to cDNA synthesis from total RNA (10 ng). [score:1]
Forty-eight hours after transfection miR-146b-5p expression (A, D) was evaluated. [score:1]
Sixty-four hours after transfection miR-146b-5p expression (A) was evaluated. [score:1]
PCCl3-WT: non tumor rat thyroid follicular cell line, PC-CMV-ø: cell transfected with an empty vector, PC-CMV-146b: cell transfected with the miR-146-5p genomic region. [score:1]
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2
[+] score: 68
24-Hour Acute ZT06 Expression 24-Hour Chronic ZT06 Expression 2-Week chronic ZT06 Expression rno-miR-142-5p Over rno-miR-126a-5p Under rno-miR-146a-5p Under rno-miR-150-5p Over rno-miR-30b-5p Under rno-miR-24-3p Under rno-miR-335 Under rno-let-7b-5p Over rno-miR-130a-3p Over rno-miR-15b-5p Over rno-miR-99a-5p Over rno-miR-127-3p Under rno-miR-133a-3p Under rno-miR-10a-5p Over rno-miR-672-5p Over rno-miR-l-3p Under rno-let-7c-5p Over rno-miR-193-3p Over rno-miR-142-5p Under rno-miR-146b-5p Under rno-miR-150-5p Over Of the three ZT06 groups that illustrated differential expression of miRNAs due to CD, emphasis was placed on the two-week chronic ZT06 group due to the differential expression of miRs 146a and 146b, and miR-127 (Figures 5A-5B and 6A). [score:11]
24-Hour Acute ZT06 Expression 24-Hour Chronic ZT06 Expression 2-Week chronic ZT06 Expression rno-miR-142-5p Over rno-miR-126a-5p Under rno-miR-146a-5p Under rno-miR-150-5p Over rno-miR-30b-5p Under rno-miR-24-3p Under rno-miR-335 Under rno-let-7b-5p Over rno-miR-130a-3p Over rno-miR-15b-5p Over rno-miR-99a-5p Over rno-miR-127-3p Under rno-miR-133a-3p Under rno-miR-10a-5p Over rno-miR-672-5p Over rno-miR-l-3p Under rno-let-7c-5p Over rno-miR-193-3p Over rno-miR-142-5p Under rno-miR-146b-5p Under rno-miR-150-5p Over Differentially expressed miRNAs based on Illumina sequencing in all the circadian-disrupted samples and their links to breast cancer development and circadian rhythms. [score:10]
In view of the previously discussed results, it seems that CD results in a cascade of interrelated activity that revolves around increased NF-κB activity and expression of BCL6, with aberrant CD -induced downregulation of miR-127 and miR-146b potentially contributing to this cascade. [score:6]
In breast cancer cells, increased promoter methylation of miR-146b results in inhibition of the negative feedback loop and increased expression of STAT3 [53]. [score:5]
The activation of miR-146b results in the attenuation of NF-κB activity, which in turn, results in the subsequent inhibition of STAT3 expression [34, 53]. [score:5]
A. Mean relative expression of miR-146a based on Illumina sequencing, * p-adjusted < 0.1, N = 6. B. Mean relative expression of miR-146b based on Illumina sequencing, * p-adjusted < 0.1, N = 6. C. Western immunoblotting images of phospho-NFκB (p65) and β-actin from a 6% SDS-PAGE gel for the two-week chronic ZT06 group. [score:5]
Figure 5 A. Mean relative expression of miR-146a based on Illumina sequencing, * p-adjusted < 0.1, N = 6. B. Mean relative expression of miR-146b based on Illumina sequencing, * p-adjusted < 0.1, N = 6. C. Western immunoblotting images of phospho-NFκB (p65) and β-actin from a 6% SDS-PAGE gel for the two-week chronic ZT06 group. [score:5]
In healthy cells, the gene encoding miR-146b is a direct target of STAT3, and as STAT3 levels increase, it results in the activation of miR-146b [34, 53]. [score:4]
As mentioned, miRNA146b levels were downregulated in the circadian-disrupted samples and NF-κB activity was also increased (Figure 5). [score:4]
Finally, in the two-week chronic ZT06 group, both miR-146a and miR-146b, which belong to the same gene family, were downregulated (Tables 1 & 2). [score:4]
The basis of the link between miRNA activity and CD -induced breast cancer seems to be an interconnected web of increased NF-κB activity and BCL6 expression, likely linked to and promoted by the CD -induced decrease in miR-127 and miR-146b. [score:3]
Increased STAT3 levels are linked to lower expression of miR-146b and increased NF-κB activity, both of which were present in the two-week chronic ZT06 group (Figure 5). [score:3]
Together with previous literature that has shown that CD results in increased miRNA promoter methylation, this indicates that the aberrant NF-κB activity and STAT3 levels could potentially be a consequence of miR-146b promoter methylation due to increased levels of DNMT1 [18, 54]. [score:1]
Interestingly, STAT3 has also been identified as part of a negative feedback loop with miR-146b. [score:1]
Verification of potential circadian-relevant targets through luciferase reporter experiments, incorporation of the CD schemes into xenograft mo dels, and further investigation of the dynamic of miR-127 and miR-146b activity in cancer cells are all logical extensions of the present study. [score:1]
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3
[+] score: 30
Of the 30 miRNAs they found upregulated in traumatic spinal cord injury, miR-223, miR-214, miR-20b-5p, miR-17, miR-146a, miR-199a-3p, miR-221-3p, miR-146b, and miR-145 were also upregulated in our study, and among the 16 downregulated miRNAs in traumatic spinal cord injury, miR-34a and miR-338 were also downregulated after ventral combined with dorsal root avulsion in our study. [score:13]
The upregulation of miR-146b-5p and miR-31a-3p and the downregulation of miR-324-3p and miR-484 were observed. [score:7]
On the 14th day after injury, 25 miRNAs, including miR-31a-3p, miR-17-5p, miR-146b-5p, miR-154-3p, and miR-363-3p, were upregulated (Figure  2C), and 18 miRNAs were downregulated, including miR-433-3p and miR-496-3p (Figure  2D). [score:7]
The qRT-PCR analysis confirmed that miR-146b-5p and miR-31a-3p were significantly upregulated in the ipsilateral spinal cord compared to the contralateral spinal cord on the 14th day after injury (Figure  3A). [score:3]
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4
[+] score: 23
Although the mechanism of miR-146 -mediated tumor suppression is still unclear, EGF-R was identified as a target of this miR [42]. [score:5]
Increased miR-146 and a subsequent decline of EGF-R expression are associated with decreased proliferation, and inhibited invasion and migration of tumor cells in breast, pancreatic and gastric cancer [43, 44]. [score:5]
The rejuvenating effects of miR-146 on fibroblasts are associated with inhibition of IL-6 expression [40], a key mediator of the senescence -associated secretory phenotype [41]. [score:5]
Mouse miR-146 knockout mo dels strongly support a role for miR-146 as a tumor suppressor for myelo-lymphoid cells [45]. [score:4]
Meanwhile, miR-146 may appears to act as a tumor suppressor for many solid and hematological malignancies [42]. [score:3]
Both IL-6 and EGF-R were negatively modulated by CDC-EVs in our study, supporting the simplistic idea that CDC-EVs may act as a source of miR-146 as one possible anti-oncogenic mechanism. [score:1]
[1 to 20 of 6 sentences]
5
[+] score: 22
miR-21-5p, miR-34a-5p, miR-146b-5p, miR-149-3p, miR-224-5p, miR-451-5p, miR-1949, miR-3084a-3p, and miR-3084c-3p were more abundantly expressed and demonstrated a two-fold or greater increased expression in the Cd-treatment group. [score:5]
miR-21-5p, miR-34a-5p, miR-146b-5p, miR-149-3p, miR-224-5p, miR-451-5p, miR-1949, miR-3084a-3p, and miR-3084c-3p demonstrated more abundant expression and a two-fold or greater significant increase in expression with Cd treatment. [score:5]
Additionally, miR-146-5p expression was increased in human renal cortices with documented severe kidney injury or fibrosis [44]. [score:3]
We used real-time PCR to confirm the increased expression of miR-21-5p, miR-34a-5p, mir-146b-5p, miR-224-5p, miR-3084a-3p, and miR-3084c-3p in the renal cortices from Cd -treated animals versus the saline controls. [score:3]
The expression of miR-146-5p was shown to be increased with fibrosis in a mouse mo del of folic-acid -induced kidney injury, and in mouse mo dels of ischemia/reperfusion injury and unilateral urethral obstruction -induced fibrosis [44]. [score:3]
Selected miRNAs that demonstrated a statistically significant (p ≤ 0.05) altered expression using µParaflo™ microRNA microarray were validated using the following TaqMan [®] Advanced miRNA assays: miR-21-5p (rno481342_mir), miR-34a-5p (rno481304_mir), miR-146b-5p (rno480941_mir), miR-224-5p (rno481010_mir), miR-3084a-3p (rno481040_mir), miR-3084c-3p (rno481313_mir), and miR-455-3p (rno481396_mir). [score:2]
As shown in Figure 3, real-time PCR demonstrated a significant increase in the Cd -treated group for the following miRNAs: a 2.7-fold increase in miR-21-5p (Figure 3A), a 10.8-fold increase in miR-34a-5p (Figure 3B), a 2-fold increase in miR-146b-5p (Figure 3C), a 10.2-fold increase in miR-224-5p (Figure 3D), a 2.4-fold increase in miR-3084a-3p (Figure 3E), and a 3.3-fold increase in miR-3084c-3p (Figure 3F). [score:1]
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6
[+] score: 16
Seven miRNAs i. e. rno-miR-146b, -132, -21, -503, -199a-5p, -214 and -34a were found to be significantly up-regulated in diseased animals with a fold change ≥0.5 with significant p-value ≤0.01. [score:6]
The seven miRNAs i. e. rno-miR-146b, -132, -21, -503, -199a-5p, -214 and -34a were determined as significantly up-regulated in PKD as depicted in Figure 3. [score:4]
Moreover, Fn1 was predicted to be a putative target of miR-146b (5 programs) and miR-503, -214, -31, -34a, -199a-5p, and -132 (2 programs). [score:3]
The implications of miR-146a (but not miR-146b) have been shown in chronic renal inflammation [48], human renal cell carcinoma [49] and retinoic acid induction in acute promyelocytic leukemia [50]. [score:1]
The figure shows high abundance of transcripts of rno-miR-146b, -199a-5p, -214 and -31 in PKD/Mhm (cy/+) rat mo del as observed on microarrays. [score:1]
0053780.g004 Figure 4 The figure shows high abundance of transcripts of rno-miR-146b, -199a-5p, -214 and -31 in PKD/Mhm (cy/+) rat mo del as observed on microarrays. [score:1]
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7
[+] score: 15
We performed network analyses using top 10 identified miRNAs (up-regulated: let-7i, let-7c, let-7a, miR-124, miR -145, miR-143, miR-34a, miR-466; down-regulated: miR-21, miR-146b) to predict their potential target transcripts. [score:9]
A: microRNA let-7i was up regulated; miR-146b and miR-21 were down regulated 3 weeks post-irradiation vs. [score:3]
C: microRNAs miR-466b and miR-21 were up regulated; miR-146b was down regulated 26 weeks post-irradiation vs. [score:3]
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8
[+] score: 12
Other miRNAs from this paper: rno-mir-30c-2, rno-mir-144, rno-mir-3586, rno-mir-486
In contrast, the expression level of rno-miR-146b-5p was decreased in the (Fig. 8b), and treatment with either Heqi San or MET increased its expression level (Fig. 8b). [score:5]
Heqi: Heqi San, MET: metformin We then used the bioinformatics analysis to identify certain differences in miRNA between the control group and PCOS groups, and some of the identified miRNAs involved in the P13K/AKT pathway are listed in Table  3. Accordingly, we selected four miRNAs (rno-miR-30c-2-3p, rno-miR-146b-5p, rno-miR-486 and rno-miR-3586-3p) and determined their expression levels in the different groups. [score:3]
Heqi: Heqi San, MET: metformin We then used the bioinformatics analysis to identify certain differences in miRNA between the control group and PCOS groups, and some of the identified miRNAs involved in the P13K/AKT pathway are listed in Table  3. Accordingly, we selected four miRNAs (rno-miR-30c-2-3p, rno-miR-146b-5p, rno-miR-486 and rno-miR-3586-3p) and determined their expression levels in the different groups. [score:3]
Through a bioinformatical analysis, we predicted the related gene function and pathway of the pathological mechanism of PCOS and found miRNAs that are likely to be critical in PCOS occurrence, including rno-miR-144-3p, rno-miR-30c-2-3p, rno-miR-486, rno-miR-3586-3p and rno-miR-146b-5p. [score:1]
[1 to 20 of 4 sentences]
9
[+] score: 12
[5– 7] Certain noncoding RNA molecules (microRNAs), such as miR-9, miR-22 (Gene ID: 407004), and miR-146 (Gene ID: 406938), have been reported to modify target gene expressions by targeting their mRNA 3′untranslated regions (UTR). [score:9]
In retrospect, such miRNAs as miR-9, miR-27 (Gene ID: 407018), miR-140 (Gene ID: 406932), and miR-146 have been indicated to be abnormally expressed in OA patients. [score:3]
[1 to 20 of 2 sentences]
10
[+] score: 11
Other miRNAs from this paper: rno-mir-146a
Particularly, for the analysis of the expression of mir146 (used here as target gene) in the epileptogenic process, the U6snRNA has been used as a reference gene, also, without previous validation [22], [39]– [42]. [score:5]
It remains unclear how the induction of mir146 expression may contribute to the etiopathogenesis of TLE. [score:3]
In fact, mir146 is overexpressed in all epilepsy associated condictions tested, including PILO and electrical stimulation TLE mo dels and human TLE with hippocampal sclerosis [22], [39]– [42]. [score:3]
[1 to 20 of 3 sentences]
11
[+] score: 10
Other miRNAs from this paper: rno-mir-19b-1, rno-mir-19b-2, rno-mir-183
Moreover, in AA rats, both miR-146b-5p and -183-5p showed a significant decrease in the visceral adipose tissue, and miR-146b-5p was significantly downregulated in the PBMCs and hepatocytes. [score:4]
In PBMCs, miR-146b-5p may be associated with the immaturity of the neonatal immune system because it is strongly upregulated in umbilical cord blood granulocytes and T lymphocytes compared to their peripheral blood cell counterparts (54). [score:3]
For instance, miR-146b-5p is involved in the TLR pathway by targeting TNF, FOS, mitogen-activated protein kinase (MAPK)14, MAPK3, RELA and CCL5 in adipocytes, hepatocytes and PBMCs. [score:3]
[1 to 20 of 3 sentences]
12
[+] score: 9
Among the miRNAs differentially expressed in Liu's study, rno-miR-132-3p, rno-miR-146b-5p, rno-miR-223-3p, rno-miR-21-5p, and rno-miR-214-3p were upregulated, which was just the same as our findings. [score:6]
In addition, as predicted by the bioinformatics databases, SLC4A1 was the potential target gene of rno-miR-34b, rno-miR-146b, rno-miR-214, rno-miR-223, and rno-miR-351. [score:3]
[1 to 20 of 2 sentences]
13
[+] score: 9
Among the four down-regulated miRs, changes in miR-146b-5p and miR-208b-3p expression levels were obvious. [score:6]
The literatures of miR-208 on cardiovascular diseases were more than miR-146. [score:3]
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14
[+] score: 9
NF-kappaB -dependent induction of microRNA miR-146, an inhibitor targeted to signaling proteins of innate immune responses. [score:5]
Expression of microRNA-146 in rheumatoid arthritis synovial tissue. [score:3]
For miR-146 and U6, 4.0 μg (tissue) or 2.0 μg (cell) of total RNA were reverse-transcribed into cDNA by polyA polymerase according to the manufacturer's instructions (All-in-one™ miRNA qRT-PCR Detection Kit, GeneCopoeia, USA). [score:1]
[1 to 20 of 3 sentences]
15
[+] score: 9
Several microRNAs involved in inflammation have also been shown to undergo changes in expression following astrocyte activation in vitro [101], including the upregulation of miR-146 and the downregulation of miR-455, which is in agreement with our results. [score:9]
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16
[+] score: 7
A step-wise linear regression analysis revealed that variation in miR124, miR21, and miR146 accounted for a significant proportion of the variation in IGF-1 mRNA expression, and that miR21 and miR124 accounted for variation in BDNF mRNA expression, suggesting that both BDNF and IGF-1 regulation involves a network of miRNAs. [score:6]
The change in miR146 appeared, in contrast, to fade over days, with the only significant increase observed in the dorsal region of shocked rats at 1 day. [score:1]
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17
[+] score: 7
MiR-320 was down-regulated, while miR-21, miR-146b and miR-491 were up-regulated after IR injury [16]. [score:7]
[1 to 20 of 1 sentences]
18
[+] score: 7
For example, miR-223 regulates TLR-triggered IL-6 and IL-1β production by targeting Signal transducer and activator of transcription (STAT3) [19] and miR-146 exerts negative feedback regulation of TLRs and cytokine receptor signaling via targeting IL-1 receptor -associated kinase (IRAK)1 and TNF receptor -associated factor (TRAF)6 [20]. [score:7]
[1 to 20 of 1 sentences]
19
[+] score: 7
Other miRNAs from this paper: rno-mir-146a, rno-mir-155
NF-κB -dependent induction of microRNA miR-146, an inhibitor targeted to signaling proteins of innate immune responses. [score:5]
MicroRNA-146 represses endothelial activation by inhibiting pro-inflammatory pathways. [score:2]
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20
[+] score: 6
Katakowski M. Buller B. Zheng X. Lu Y. Rogers T. Osobamiro O. Shu W. Jiang F. Chopp M. Exosomes from marrow stromal cells expressing mir-146b inhibit glioma growth Cancer Lett. [score:5]
Another study showed that the administration of exosomes containing miRNA-146 from MSCs reduced brain tumors [32]. [score:1]
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21
[+] score: 6
Treatment with triptolide enhanced expression of five miRNAs (rno-miR-146b-5p, rno-miR-20b-5p, rno-miR-142-3p, rno-miR-223-3p, and rno-miR-21-5p), while that of five other miRNAs (rno-miR-668, rno-miR-203-3p, rno-miR-382-5p, rno-miR-344b-3p, and rno-miR-30b-3p) was significantly downregulated (Tables 3 and 4, and Figure 8). [score:6]
[1 to 20 of 1 sentences]
22
[+] score: 5
Taganov K. D. Boldin M. P. Chang K. J. Baltimore D. NF-κB -dependent induction of microRNA miR-146, an inhibitor targeted to signaling proteins of innate immune responsesProc. [score:5]
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23
[+] score: 5
Interestingly, among the miRNAs found to be upregulated in exosomes in response to cytokines, several of them including miR-146a, miR-146b, miR-195, miR-290a-3p, miR-362-3p and miR-497 are known to be involved in cell death [29- 34]. [score:4]
MIN6B1 cells were transiently transfected for 48 h or 72 h using Lipofectamine 2000 [TM] (Invitrogen) according to manufacturer’s instructions with pMSCV-miR146 (or pMSCV-control plasmid) or with oligo-cel-miR-238 (containing the mature sequence of C. elegans miR-238). [score:1]
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24
[+] score: 4
Several miRNAs are demonstrated that associated with OA development and modulation such as miR-18a (chondrocyte differentiation), miR-27b (controlling the expression of MMP-13), miR-34a (prevention of cartilage degradation), miR-140 and miR-222 (controlling cartilage homeostasis), miR-146 (promotion of inflammatory OA), miR146a (OA cartilage pathogenesis), miR-675 (cartilage repair) [30, 31]. [score:4]
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25
[+] score: 4
miR-144, miR-146, miR-182 and miR-192 showed a lower expression compared to the other miRNAs in the three insulin target tissues as well as in the pancreas. [score:4]
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26
[+] score: 4
Recently, Li et al. reported that 16 miRNAs including miR-34, miR-199a-5p, miR-221, miR-146b, and miR-214 showed progressive up-regulation in rat with hepatic fibrosis caused by dimethylnitrosamine [30]. [score:4]
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27
[+] 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]
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28
[+] score: 4
Because, for example, let-7i and miR-146b has been reported to down regulate TLRs [30], [35], and miR-125b has been reported to suppress TNF-α [30]. [score:4]
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29
[+] score: 3
Other miRNAs from this paper: rno-mir-346, rno-mir-146a, rno-mir-192
mir-146 expression in RA patients. [score:3]
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30
[+] score: 3
Other miRNAs from this paper: rno-mir-146a, bta-mir-146b, bta-mir-146a
CD3 [+] (the TCR coreceptor) T cells express miR-146 in synovial tissues of people with rheumatoid arthritis [34]. [score:3]
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31
[+] score: 3
Stanczyk and colleagues reported that the expression of miR-146 is increased in rheumatoid arthritis synovial fibroblasts [30]. [score:3]
[1 to 20 of 1 sentences]
32
[+] score: 3
Other miRNAs from this paper: rno-mir-146a, rno-mir-206
Except miR-146, Saos-2 and chondrosarcoma overexpressed these contributory miRNAs. [score:3]
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33
[+] score: 2
For assessing the efficacy of the transfection system, the TRAF6 3′-UTR plasmid and the rno-mir negative control plasmid or has-miR-146b plasmid were also cotransfected into cells. [score:1]
In addition, gain of position miR (has-miR-146b) decreased the relative luciferase activity in the 3′-UTR (TRAF6) group, confirming that the transfection system was functional. [score:1]
[1 to 20 of 2 sentences]
34
[+] score: 2
Other miRNAs from this paper: rno-mir-146a, rno-mir-203a, rno-mir-203b, rno-mir-155
MiR-146, miR-155 and miR-203 regulate arthritic inflammatory response and joint destruction 31. [score:2]
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35
[+] score: 2
Others have been linked to the regulation of vascular smooth muscle cells; these include miR-145, let-7d, miR-24, miR-26a, and miR-146 [13]. [score:2]
[1 to 20 of 1 sentences]
36
[+] score: 2
miR-125b, miR-146, miR-150, miR-199a, miR-21, miR-129, miR-341 and miR-451 have been confirmed to play an important role in the different developmental stages of the cardiovascular system (4– 18). [score:2]
[1 to 20 of 1 sentences]
37
[+] score: 2
Li JW MicroRNA-146b inhibition augments hypoxia -induced cardiomyocyte apoptosisMol Med Rep. [score:2]
[1 to 20 of 1 sentences]
38
[+] score: 2
Other miRNAs from this paper: rno-mir-10a, rno-mir-10b, rno-mir-26a, rno-mir-26b, rno-mir-146a
Moreover, the endocannabinoid system has come under scrutiny given that several microRNAs such as miR26, miR146, and miR10 are responsible for its gene regulation [28, 29]. [score:2]
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39
[+] score: 2
Differential regulation of microRNA-146a and microRNA-146b-5p in human retinal pigment epithelial cells by interleukin-1β, tumor necrosis factor-α, and interferon-γ. [score:2]
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40
[+] score: 2
With regard to fracture nonunion, we recently profiled miRNAs in nonunion of the rat femur and identified five miRNAs, miR-31a-3p, miR-31a-5p, miR-146a-5p, miR-146b-5p, and miR- 223-3p that were associated with the development of nonunion [14]. [score:2]
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41
[+] 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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42
[+] score: 2
The results were summarized in Figure 2. Integrating the results of Figure 1, the miR-146b, miR-486-3p, and miR-499a, which were detected both in the intact comparison and no-T2D comparison but not in HFD comparison, might involve both the progresses of T2D fed with normal diets and fat metabolism fed with HFD. [score:1]
Among the 24 specific miRNAs, 13 of them, such as miR-182/196a/381/499a/99a [6], miR-183 [6, 23], miR-409 [23], miR-146b [6, 24], miR-143 [6, 24], miR-148a [24, 25], miR-204 [5], and miR-9 [6], have been reported to involve in T2D process in mouse or rat. [score:1]
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43
[+] score: 2
The following miRNAs, also present in the VTMs list of Fig 5, were found by RT-PCR to be dysregulated in mouse lung tissue: miR-21, miR-146, miR-20, miR-302, miR-19, miR-98, let-7a, miR-15a. [score:2]
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44
[+] score: 1
On the other hand, the response of certain miRNAs (e. g. miR-146 and miR-134) following SE contrasts with results from other studies, probably due to specificities of the H-PILO or technical limitations inherent in the use of a large-scale experimental approach. [score:1]
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45
[+] score: 1
Bdnf has a large, 2.9 kb 3′UTR with multiple seed binding sites for several miRNAs differentially affected by TBI, miR-15b, miR-146b, miR-17-5p (all increased) and miR-181c (decreased). [score:1]
[1 to 20 of 1 sentences]
46
[+] score: 1
STAT3 Activity and Function in Cancer: Modulation by STAT5 and miR-146b. [score:1]
[1 to 20 of 1 sentences]
47
[+] score: 1
Additionally, four miRNAs (miR-138, miR-146b, miR-301a, and miR-92b) were common between our data and those of Kan et al. in human temporal lobe epilepsy [22]. [score:1]
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48
[+] score: 1
In addition, the neural progenitor cells isolated by LCM exhibited increases in miR-146a, miR-146b, miR-210, miR-19b and miR-378 and decreases in miR-128, miR-291a-3p, and miR-139-5p (Fig. 3A to 3C), which are consistent with the array data findings. [score:1]
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49
[+] score: 1
This may also explain why miRNAs previously reported in islets upon in vitro cytokine exposure, such as miR-146 and miR-34a, were not confirmed in our study [25]. [score:1]
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50
[+] score: 1
Recently, some miRNAs, such as miR-146 [29], -34c [30], -30 [31], -532-3p [32] and let-7g [33], have been reported involved in Dox -induced cardiotoxicity. [score:1]
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