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31 publications mentioning rno-mir-144

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-144. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

[+] score: 222
Correspondingly, in the high glucose media, expression of miR-144 was found to be highest (3.605±0.21) accompanied by a down-regulation of IRS1 (−3.257±0.29), followed by miR-150 (2.904±0.19) and miR-192 (1.989±0.20) which are predicted to target GLUT4 (−2.604±0.25) and CBL (−4.672±0.31) and INSR (1.150±0.28) respectively. [score:8]
miR-29a, miR-144, miR-150, miR-192 and miR-320 showed an up-regulation from that of control samples whereas miR-30d, miR-146a and miR-182 showed down-regulation. [score:7]
This can imply that IRS1 is highly down-regulated in T2D in conjunction with its predicted negative modulator, miR-144 which was up-regulated in T2D. [score:7]
Regulation of IRS1 by miR-144 was further verified by immunocytochemistry and complementarily, the IRS1 protein expression correlated to that of the gene expression studies. [score:6]
Similar to the animal data, miR-144 was again among the highly up-regulated miRNA that showed a linear increase in expression with increasing glycaemic status. [score:6]
miRNAs such as miR-144, miR-29a and miR-192 that were up-regulated in both IFG and T2D patients (Table S8) are predicted to target IRS1, AKT2 and INSR respectively. [score:6]
Here, miR-144 expression is highly up-regulated in T2D and it also seemed to exhibit a linear relationship with increasing glycaemic status (Fig. 5B, 6A). [score:6]
Increased circulating level of miR-144 has been found to correlate with down-regulation of its predicted target, insulin receptor substrate 1 (IRS1) at both mRNA and protein levels. [score:6]
Of the above three, only the expression pattern for miR-144 and its predicted mRNA target, IRS1, are concordant for both IFG and T2D (Fig. 5B, 5C). [score:5]
of pre-miR-144 greatly inhibited IRS1 mRNA level while treatment with anti-miR-144 resulted in increased IRS1 mRNA expression (Fig. 11C). [score:5]
In contrast, miR-192 expression remained close to basal level in the IFG group while miR-144 showed a significant up-regulation against healthy controls but at a lower fold change compared to that in T2D (IFG: 1.385±0.14; T2D: 3.070±0.13). [score:5]
Table S12 shows the bindings sites of miR-144 at the 3′UTR of IRS1 and the different constructs designed to show that miR-144 directly targets IRS1. [score:4]
Of these microRNAs, miR-144 that promotes erythropoiesis has been found to be highly up-regulated. [score:4]
These findings indicate IRS1 forms a direct target of miR-144. [score:4]
In this study, we have also provided evidence that miR-144 directly inhibits IRS1, a key molecule in insulin signaling. [score:4]
In all five sources, miR-144, miR-150, miR-192, miR-29a and miR-320a were found to be highly up-regulated. [score:4]
IRS1 is a direct target of miR-144. [score:4]
0022839.g010 Figure 10Direct inhibitory effect of miR-144 on IRS1. [score:4]
Direct inhibitory effect of miR-144 on IRS1. [score:4]
miR-144 regulates IRS1 mRNA expression. [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]
Among the novel miRNAs (miR-144, miR-146a, miR-150 and miR-182) identified, miR-144 had the highest up-regulation upon T2D in most tissues. [score:4]
Among the eight miRNAs identified, miR-144 remained highly up-regulated in T2D in both cases. [score:4]
miR-144 showed the highest up-regulation among other miRNAs in three tissues namely pancreas (7.94±0.171), adipose (4.34±0.178) and liver (4.26±0.174). [score:4]
Nonetheless, the authors identified a pool of dysregulated miRNAs (∼50 miRNAs) in which some of them such as miR-144, miR-106b, miR-185, miR-30e, miR-589, miR-665 and many more showed similarities in expression as observed in our study (either humans/animals or both). [score:4]
Among these miRNAs, we have identified miR-144 as a direct modulator of IRS1 and hence a potential therapeutic target of T2D. [score:4]
miR-144 and miR-192 were among the highly up-regulated miRNAs in T2D. [score:4]
Previous reports [42]– [44] have also confirmed that miR-144 and IRS1 are expressed in HeLa cells. [score:3]
of pre-miR-144 increased the miR-144 levels by 43 fold and simultaneous reduction in the IRS1 mRNA expression (−1.628±0.18) in HeLa. [score:3]
The eight miRNAs (miR-144, miR-146a, miR-150, mR-182, miR-192, miR-29a, miR-30d and miR-320) which were previously identified in the rat study showed similar expression in the patients' blood miRNAs. [score:3]
To confirm that IRS1 is a target of miR-144, we observed the corresponding changes in IRS1 mRNA level upon treatment with either pre- or anti- miR-144 (Fig. 11B, 11C). [score:3]
Likewise, in anti-miR-144 transfected HeLa and 3T3L1 cells, the relative expression of miR-144 was reduced to 0.019±0.09 and 0.033±0.11 respectively while a significant increase in IRS1 mRNA level was observed (HeLa: 5.607±0.217; 3T3L1: 4.232±0.22). [score:3]
In order to alter miR-144 expression, HeLa and 3T3L1 cells were transfected with pre-miR-144 and anti-miR-144 independently, followed by quantification of the changes in miRNA and mRNA levels (Fig. 11B, 11C). [score:3]
Besides miR-192 [35] and miR-29a [34] which have previously been shown to be implicated in diabetes, we have also observed an approximately linear relationship between miR-144 expression and increasing glycaemic status (from IFG to T2D). [score:3]
Expression of IRS1 in HeLa/3T3L1 cells transfected with pre- or anti- miR-144. [score:3]
We could also experimentally demonstrate that IRS1 is indeed the target of miR-144. [score:3]
Since insulin -dependent glucose uptake could be compromised by the over expression of miR-144, we further investigated miR-144 and its predicted target, IRS1. [score:3]
B. Relative miR-144 expression in HeLa/3T3L1 cells transfected with either pre- or anti- miR-144 at a concentration of 30 nM. [score:3]
Previous reports [55]– [57] have confirmed that HeLa cells express miR-144 and IRS1. [score:3]
Focusing our interest in miR-144, we next looked into its corresponding IRS1 target at protein level. [score:3]
Hence, miR-144 could serve as a potential therapeutic target in T2D. [score:3]
Moreover, miR-144 was also found to be the most highly expressed miRNA in their T2D samples. [score:3]
Based on the prediction that miR-144 binds to the 3′UTR of IRS1, changes in miR-144 expression should be reflected in IRS1 mRNA levels accordingly. [score:3]
We have also identified eight important miRNAs (miR-144, miR-146a, miR-150, miR-182, miR-192, mir-29a, miR-30d and miR-320) that could participate in the regulation of insulin signaling as well as useful in distinguishing different stages of diabetes progression. [score:2]
These observations together with the luciferase binding assays (Fig. 10) demonstrate that miR-144 functions as a modulator of IRS1 expression. [score:2]
The 3′UTR of IRS1 containing the putative target site for miR-144 was amplified by PCR using gene specific primers. [score:2]
Site-directed mutagenesis of the miR-144 binding sites abolished interactions between miR-144 and IRS1 accordingly. [score:2]
HeLa cells were then used to assess the regulatory function of miR-144 on IRS1 and in addition to that, we also performed the same experiment in an insulin-responsive cell line, 3T3L1 adipocytes. [score:2]
Similar observations were obtained in the immunocytochemistry assay which indicates that inhibition of IRS1 by miR-144 at protein level (Fig. 11D). [score:2]
Seed region if miR-144 is shown in bold italics. [score:1]
Cells transfected with pre-miR-144 exhibited a significant reduction in the luciferase activity which was reduced further when both miR-144 binding sites are present (Fig. 10). [score:1]
Left panel: Non -transfected cells; Middle panel: Pre miR-144 transfected cells showed reduced fluorescence intensity; Right panel: Anti miR-144 transfected cells showed increased fluorescence intensity. [score:1]
Immunocytochemistry was also performed on HeLa cells transfected with either pre miR-144 or anti miR-144 [66]. [score:1]
Predictions: miR-144/ IRS1; miR-146a/ PTPN1; miR-150/ GLUT4 and CBL; miR-182/ FOXO1; miR-192/ INSR; miR-30d/ INS; miR-29a and miR-320/ AKT2. [score:1]
D. IRS1 immunoreactives in HeLa cells transfected with either pre- or anti- miR-144. [score:1]
miR-144 also exhibited an approximately linear relationship with increasing glycaemic status as observed in IFG and T2D patients (Fig. 5B). [score:1]
We have also identified signature miRNAs which could possibly explain the pathogenesis of T2D and the significance of miR-144 in insulin signaling. [score:1]
The plasmid constructs together with pre- or anti- miR-144 were co -transfected into HeLa cells. [score:1]
This result is in conjunction with our hypothesis that miR-144 negatively modulates IRS1. [score:1]
In 3T3L1 adipocytes treated with pre-miR-144, miR-144 levels increased by approximately 80 fold which corresponded to decreased IRS1 mRNA level (−1.737±0.18). [score:1]
To demonstrate that, we constructed independent reporter vectors that contained the different combinations of binding sites of miR-144 at the 3′UTR of IRS1 (Table S12) downstream of a firefly luciferase reporter gene. [score:1]
was also performed on HeLa cells transfected with either pre miR-144 or anti miR-144 [66]. [score:1]
Fragment with both binding sites of miR-144 includes 3′UTR of IRS1 from 3781-4921bp. [score:1]
Likewise, transfection with anti miR-144 showed an increasing pattern of luciferase activity from constructs where only one binding site is present to that where both binding sites are included (Fig. 10). [score:1]
Pre-miR-144 transfected HeLa cells displayed reduced fluorescence intensity for IRS1 (Fig. 11D, middle panel) while the opposite was observed in anti-miR-144 transfected cells (Fig. 11D, right panel). [score:1]
Among the eight miRNAs identified as potential signature miRNAs, miR-144 has shown to be a potential novel key player in T2D. [score:1]
Table S12 Binding sites of miR-144 at 3′UTR of IRS1 and mutated constructs of the binding sites. [score:1]
Fragment with 1 [st] binding site of miR-144 alone includes 3′UTR of IRS1 from 3781-4201bp, while fragment with 2 [nd] binding site of miR144 alone includes 3′UTR of IRS1 from 4501-4921bp. [score:1]
Luminescence for luciferase gene activity in treated samples (pre or anti miR-144) were obtained 48 hours post-transfection. [score:1]
There are two different binding sites of miR-144 at the 3′ UTR of IRS1. [score:1]
0022839.g011 Figure 11 A. Endogenous levels of miR-144 and IRS1 in HeLa/3T3L1 cells as delta threshold cycle (ΔCt) value with respect to 18S rRNA. [score:1]
Employing miRNA microarray and stem-loop real-time RT-PCR, we identify four novel miRNAs, miR-144, miR-146a, miR-150 and miR-182 in addition to four previously reported diabetes-related miRNAs, miR-192, miR-29a, miR-30d and miR-320a, as potential signature miRNAs that distinguished IFG and T2D. [score:1]
Altogether, these results suggest that miR-144 is a modulator of IRS1. [score:1]
A. Endogenous levels of miR-144 and IRS1 in HeLa/3T3L1 cells as delta threshold cycle (ΔCt) value with respect to 18S rRNA. [score:1]
Quantitation of the effects of pre- or anti- miR-144 interaction with the 3′ UTR of IRS1. [score:1]
Binding sites of miR-144 at 3′UTR of IRS1 and mutated constructs of the binding sites are listed in Table S12. [score:1]
3′UTR of IRS1 contains two miR-144 binding sites (highlighted). [score:1]
These constructs were then co -transfected with anti- or pre-miR-144 into HeLa cells. [score:1]
miR-144 as an important key player in T2D. [score:1]
HeLa cells cultured in 24-well plates were transfected with 50 nM anti miR-144 or pre miR-144 for 3hrs followed by 200 ng/well pMIR-REPORT constructs for 3 hrs. [score:1]
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[+] score: 189
Kang et al showed that overexpression of miR-144 would inhibit the osteogenic process by targeting Cadherin-11 [17]. [score:7]
To verify the results of microarray, Quantitative polymerase chain reaction (qPCR) was performed to detect the expression level of miR-144-3p during DO process and the results showed that it was significantly downregulated during the distraction period of DO (Figure 1C). [score:6]
In conclusion, miR-144-3p was significantly downregulated during DO process and the anti-miR-144-3p could enhance osteogenesis in vitro and accelerate bone regeneration in vivo through targeting CX-43. [score:6]
For example, miR-144 was significantly downregulated in esophageal carcinoma [11] and osteosarcoma [12] while overexpressed in pulmonary tuberculosis [13], renal cell carcinoma [14], and medulloblastoma [15]. [score:6]
Collectively, these data indicated that miR-144-3p could regulate osteogenesis through suppressing CX-43 expression. [score:6]
To elucidate whether miR-144-3p mediates osteogenesis via suppressing CX-43 expression, a small interfering RNA (siRNA) specifically targeting CX-43 (siCX-43) was designed and its osteogenic effect was investigated. [score:5]
Our results also indicated that miR-144-3p suppressed while its inhibitor promoted osteogenic differentiation of rBMSCs. [score:5]
It was shown that miR-144-3p dramatically suppressed the luciferase activity when compared with control groups and mutations on these binding sites successfully abolished the suppressive effects (Figure 3E–3F). [score:5]
Target genes of miR-144-3p were predicted using online programs: TargetScan (http://www. [score:5]
Taken together, the downregulation of miR-144-3p would play important roles in regulating the calcification in DO and osteogenic differentiation of rBMSCs. [score:5]
Further biological function studies also showed that miR-144-3p inhibitor could contribute to osteoblast in vitro and bone formation in vivo via promoting CX-43 expression. [score:5]
The further staining results of ALP and Alizarin red also demonstrated that miR-144-3p suppressed while its inhibitor could promote osteogenic differentiation (Figure 2C–2D). [score:5]
MiR-144-3p inhibitor attenuated the suppression of osteogenesis induced by CX-43 knockdown. [score:5]
MiR-144-3p inhibitor attenuated the suppressive effect of siCX-43 on osteogenesis. [score:4]
According to the heat map results, miR-144-3p was found to be the most downregulated miRNAs (Figure 1B). [score:4]
MiR-144-3p suppressed while its inhibitor promoted osteogenic differentiation of rBMSCs. [score:4]
In this study, we confirmed that miR-144-3p was significantly downregulated in distraction phase of DO with tensile stimulation. [score:4]
To better understand the molecular mechanism of DO, a panel of miRNAs was screened by a microarray analysis, and miR-144-3p was identified as one of the most downregulated miRNAs by DO. [score:4]
miR-144-3p was downregulated in bone tissues with DO. [score:4]
The rno-miR-144-3p inhibitor lentivirus was purchased from Genepharma Company (Genepharma, China). [score:3]
Therefore, the rapid bone repair would contribute to the reduction of BV/TV at week 4 in miR-144-3p inhibitor group. [score:3]
Bone tissue regeneration was accelerated by miR-144-3p inhibitor modified MSCs in DO animal mo del. [score:3]
The structure of the distracted bone had already repaired as normal at day 44 postoperation in miR-144-3p inhibition group. [score:3]
To further validate whether CX-43 was a bona fide target for miR-144-3p, the binding and the mutated sites into the 3′ UTR of CX-43 were inserted into the pmiR-Glo vector (Figure 3D). [score:3]
Bone healing property was enhanced by miR-144-3p inhibitor therapy. [score:3]
MiR-144-3p was downregulated during DO process and osteogenic differentiation. [score:3]
Result indicated miR-144-3p inhibition could promote mineralization of newly formed bone. [score:3]
We further examined the expression of miR-144-3p during the osteogenic differentiation of rat MSCs derived from bone marrow (rBMSCs), and the results showed that it also was decreased during the osteogenic differentiation of rBMSCs (Figure 1D). [score:3]
Local injection of miR-144-3p inhibitor modified rBMSCs accelerated bone formation in DO animal mo del. [score:3]
Result showed BV/TV within 158-211 as well as 158-1000 were much higher at day 30 but much lower at day 44 post-operation in miR-144-3p inhibition group. [score:3]
The dynamic histomorphometric parameters including MAR and MS/BS were found higher in miR-144-3p inhibition group than that in control group. [score:3]
The hematein & eosin (HE) staining results confirmed that medullary cavity has been recanalized in miR-144-3p inhibitor group, while lots of immature woven bone still could be found within the distraction gap in control group. [score:3]
In the present study, miR-144-3p was demonstrated to suppress osteogenic differentiation in vitro, whereas anti-miR-144-3p promoted osteoblast in vitro and accelerated bone formation in vivo. [score:3]
These results suggest that CX-43 is a real target for miR-144-3p in rBMSCs. [score:3]
Result showed that bone remo deling was robust in miR-144-3p inhibition group while lots of regenerated cartilage cells still could be found in the distraction area. [score:3]
Connexin 43 was a real target for miR-144-3p. [score:3]
Our results demonstrated that miR-144-3p suppressed osteoblast and bone formation in distraction osteogenesis, therefore miR-144-3p intervention therapy would be a promising strategy for bone regeneration of DO. [score:3]
Bioinformatic prediction and biological confirmation demonstrated that CX-43 was a real target for miR-144-3p. [score:3]
The knowledge generated from this study improves our understanding of the bone regeneration of DO and explore the potential of miR-144-3p as a promising therapeutic target for bone fracture in clinical practice. [score:3]
In miR-144-3p inhibitor group, less bone tissues were detected in the distraction gap, but the medullary cavity was almost recanalized. [score:3]
More importantly, the bone regeneration ability of miR-144-3p inhibitor was also examined in DO animal mo del. [score:3]
However, ultimate load (B) and energy between (C) were much higher in miR-144-3p inhibition group than that in control group (n=10 each group, [*] P<0.05). [score:3]
All these results demonstrated that the bone healing process was accelerated by miR-144-3p inhibitor therapy. [score:3]
CX-43 was a real target gene of miR-144-3p. [score:3]
Increasing evidence have demonstrated that miR-144 could be identified as regulator of tumorigenesis. [score:2]
2 and 4 weeks after injection, distracted bone were harvested for microCT assays and the results showed that miR-144-3p inhibitor stimulated bone formation at week 2 and week 4 (Figure 5A). [score:2]
MiR-144 also reported to activate Wnt signaling in bladder cancer via targeting EZH2 [16]. [score:2]
To test the therapeutic effect of antagomir-144 on bone regeneration during DO process, stable anti-miR-144-3p modified rBMSCs were established and locally injected into the distraction gap at the end of distraction period. [score:1]
However, tibiae of rats treated with anti-miR-144-3p modified rBMSCs exhibited better mechanical properties than the control group in ultimate load and energy (Figure 6A–6C). [score:1]
Histological analyses indicated that bone structure was almost recovered in anti-miR-144-3p group, while still a lot of immature callus could be found in the control group (Figure 7A–7B). [score:1]
Quantitative Real-Time PCR for osteomarkers and miR-144-3p. [score:1]
Stable anti-miR-144-3p modified rBMSCs. [score:1]
To elucidate the functional characterization of miR-144-3p on osteogenesis, agomir-144 (miR-144-3p mimics) and antagomir-144 (miR-144-3p inhibitor) were transiently transfected into rBMSCs and the osteogenic effects were examined. [score:1]
Fold change of miR-144-3p expression at different time points were calculated through compared to the expression level at day 0. (n=3 each time points, [*] P<0.05 compared to Day 0). [score:1]
Furthermore, the rats with anti-miR-144-3p modified MSCs injection displayed a significant increase in total bone volume (BV)/total tissue volume (TV) at week 2, whereas a slight decrease was observed at week 4 (Figure 5B). [score:1]
According to the results of mechanical testing and bone histomorphometry, bone healing property was enhanced after treated with anti-miR-144-3p modified rBMSCs. [score:1]
However, the studies on the association between miR-144 and osteogenesis remains limited. [score:1]
In this study, another miRNA, miR-144-3p was identified as a crucial miRNA during DO process. [score:1]
Based on the prediction by bioinformatics analyses, Connexin 43 (CX-43) is a promising candidate with potential binding sites in its 3′-UTR for miR-144-3p. [score:1]
Fold change of miR-144-3p expression level at different time points were calculated through compared to the expression level at day 0. (n=3 each time points, [*] P<0.05 compared to Day 0, U6 was used as an internal reference). [score:1]
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[+] score: 95
Other miRNAs from this paper: rno-mir-340-1, rno-let-7b, rno-mir-142, rno-mir-153, rno-mir-340-2
TBI -induced up-regulation of miR-144, miR-153 and miR-340-5p were further confirmed by quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR), and three of their target proteins, calcium/calmodulin -dependent serine protein kinase (CASK), nuclear factor erythroid 2-related factor 2 (NRF2) and alpha-synuclein (SNCA) were found to be concurrently suppressed. [score:8]
In consideration of their correlations with craniocerebral diseases in literature, as well as the involvement of their target genes in cellular component of synaptosome, we would hypothesize that miRNA-miRNA interregulation/interaction among miR-144, miR-153 and miR-340-5p play important roles in the pathophysiological progress of brain injury, especially the development of cognitive dysfunction. [score:7]
miR-144 is well known for its consistent increase in the aging brain, which is usually accompanied by a continuous cognitive decline, and miR-144 deregulation is considered a risk factor for disease development of Alzheimer's disease (AD) [26]. [score:6]
While Nfe212 and Gdf10 are putative targets of miR-144 and miR-153, Crot and Plekha3 are potentially regulated by miR-153 and miR-340-5p, which compelled us to validate the expression of these three miRNAs by miRNA-specific qRT-PCR. [score:6]
We also detected the alteration in expression of NRF2, the protein of Nfe212 gene which is a putative target of both miR-144 and miR-153, in hippocampus post TBI. [score:5]
In addition, protein levels of CASK, NRF2 and SNCA, which are putative targets of miR-144, miR-153 and miR-340-5p, were found to be consistently suppressed in hippocampus after TBI. [score:5]
miR-144 is overexpressed in AD patients and it may play a mechanistic role in AD pathogenesis via inhibition of ADAM10 protein [26], [27]. [score:5]
A large number of target genes involved in enriched GO terms were targeted by miR-144 and miR-340-5p. [score:5]
Bioinformatics analysis showed 25 potential target genes of miR-144, among which Cask, Etfdh, Nfe212 and Gdf10 garnered our attention because these genes are predicated targets of other altered miRNAs as well. [score:5]
The present study, for the first time, demonstrated consistent up-regulation of miR-144 in the hippocampus at several time points up to 7 days post TBI. [score:4]
In addition to miR-144 and miR-153, miR-340-5p was consistently up-regulated in hippocampus post TBI. [score:4]
Further analysis showed that miR-144 and miR-340-5p share a common target gene Etfdh. [score:3]
Nfe212, another predicted target gene of miR-144, is known for its anti-oxidation trait. [score:3]
Expression levels of miR-144 (A), miR-153 (B) and miR-340-5p (C) assessed by miRNA array and miRNA-specific qRT-PCR. [score:3]
Since their expression patterns after TBI were similar (Figure 5), correlation analyses were carried out for miR-144, -153 and -340-5p. [score:3]
Therefore, we investigated the protein expression of NRF2 in the hippocampus after TBI and found a consistent decrease in NRF2 expression at all five time points post TBI, indicating that TBI -induced cognitive dysfunction might be mediated, at least partially, via miR-144/NRF2 pathway. [score:3]
Our data suggest that miR-144, miR-153 and miR-340-5p could be potential targets for diagnostic and therapeutic purposes against TBI. [score:3]
Interestingly, we found strong positive correlations among the expression patterns of miR-144, miR-153 and miR-340-5p in hippocampus after TBI. [score:3]
Our findings suggest that miRNAs, especially miR-144, miR-153 and miR-340-5p, are important mediators in pathophysiological processes after TBI and might serve as potential targets for intervention against brain damage after TBI. [score:3]
qRT-PCR analysis further confirmed that elevated expression of miR-144, miR-153 and miR-340-5p was rapid and long-lasting. [score:3]
qRT-PCR results showed that expression levels of miR-144, -153 and -340-5p in ipsilateral hippocampus were significantly elevated at all five time points after TBI, compared with that of sham controls (Figure 5). [score:2]
There is a very strong correlation between miRNA array and qRT-PCR results for miR-144 (R [2] = 0.984, P<0.001), miR-153 (R [2] = 0.982, P<0.001) and miR-340-5p (R [2] = 0.958, P<0.001). [score:1]
The correlation analyses showed that miR-144, miR-153 and miR-340-5p have positive interrelated relationships between each other (Figure 6), among which the highest correlation coefficient was obtained between miR-153 and miR-340-5p (R [2] = 0.825, P<0.001) (Figure 6B). [score:1]
However, whether miR-144 is involved in TBI -induced cognitive disorder remains unknown. [score:1]
Correlation between miR-144, miR-153 and miR-340-5p. [score:1]
miR-144 and miR-340-5p are located in chromosome 10, whereas miR-153 is found in chromosome 6. There is no significant similarity found among these 3 miRNA sequences. [score:1]
Correlation analyses between miR-144 and miR-153 (A), miR-153 and miR-340-5p (B) or miR-144 and miR-340-5p (C). [score:1]
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[+] score: 53
Other miRNAs from this paper: rno-mir-29a
To further confirm whether the differential expression of PLA2G4A was directly induced by American ginseng, we performed qRT-PCR analysis to determine whether American ginseng affected the expression of miR-144 and miR-29a, both of which can suppress PLA2G4A expression. [score:10]
The expression of miR-144 and miR-29a has been shown to suppress PLA2G4A transcription or translation or to cut the mRNA so that it is targeted for degradation. [score:9]
Our results suggested that PLA2G4A downregulation might be secondary to the upregulation of miR-144 and miR-29a induced by American ginseng treatment. [score:7]
This inverse correlation might verify our current results, indicating that upregulated miR-29a and miR-144 induced by American ginseng treatment may play a significant role in protecting ovarian function by regulating the response to hormone stimulation and preventing ovarian aging. [score:5]
In this study, we used the same treatment regimens and found that American ginseng significantly reduced PLA2G4A expression and increased miR-144 and miR-29a expression in POF ovarian tissues compared to POF induction alone. [score:4]
However, it is also possible that American ginseng may regulate miR-144 and miR-29a expression to specifically restore PLA2G4A levels. [score:4]
Additionally, the upstream miRNAs miR-29a and miR-144 were downregulated compared to the POF mo del (P < 0.05, Figure 1(a)). [score:3]
Moreover, a recent study showed that follicular thyroid carcinoma tissues had decreased miR-144 expression, resulting in activated mTOR signaling [41], which can accelerate ovarian aging and induce POF [42]. [score:3]
In our previous study, we demonstrated that miR-29a and miR-144 expression decreased in POF ovarian tissues. [score:3]
In our previous study, we also demonstrated that miR-29a and miR-144 expression decreased in POF ovarian tissues. [score:3]
The changes in the PLA2G4A and miR-29a and miR-144 genes suggest that American ginseng exerts its effect by regulating prostaglandin biosynthesis, ovulation, and preventing ovarian aging. [score:2]
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[+] score: 40
Therefore, we measured the expression of GRP78 mRNA, rno-miR-144, rno-miR-376a, and rno-miR-451 using real-time RT-PCR to examine their expression patterns in the context of LHR downregulation (Fig. 1). [score:6]
In a similar manner, rno-miR-144 and rno-miR-376a expression peaked 12 h after the hCG treatment, and rno-miR-451 expression peaked 24 h after the hCG treatment. [score:5]
We believe that the discrepancy regarding in the expression of miR-144 and 451 between in the in vivo and in vitro experiments (Fig. 1 and 2) can be explained by the presence of blood cells in the in vivo study which express both rno-miR-144 and rno-miR-451 [22], [23]. [score:5]
uk/) revealed that rno-miR-144, rno-miR-376a, and rno-miR-451 can bind to the 3′-UTR of GRP78 mRNA (from bp 2439–2459) and negatively regulate GRP78 expression. [score:4]
Time course of rat GRP78 mRNA, rno-miR-144, rno-miR-376a, and rno-miR-451 expression in rat ovaries induced by PMSG and hCG. [score:3]
The array data along with the bioinformatic analysis provided by MicroCosm Targets, which indicated that several miRNAs bind to the GRP78 mRNA 3′-UTR, led us to focus on rno-miR-144, rno-miR-376a, and rno-miR-451. [score:3]
From these, we narrowed the focus to rno-miR-376a based on the results of the in vitro experiments (Fig. 2) since rno-miR-144 and rno-miR-451 was not induced expression by hCG treatment. [score:3]
In contrast, rno-miR-144 and rno-miR-451 expression decreased significantly after the hCG treatment. [score:3]
Rat GRP78 mRNA, rno-miR-144, rno-miR-376a, and rno-miR-451 expression in primary rat granulosa cells induced by FSH and hCG. [score:3]
Next, we investigated the effects of rno-miR-144, rno-miR-376a, and rno-miR-451 on GRP78 mRNA expression in granulosa cells isolated from DES -treated immature rats (Fig. 2). [score:1]
Total RNA was isolated, and GRP78 mRNA (A), rno-miR-144 (B), rno-miR-376a (C), and rno-miR-451 (D) expression levels were measured using real-time RT-PCR as described in the. [score:1]
Rat GRP78 mRNA (A), rno-miR-144 (B), rno-miR-376a (C), and rno-miR-451 (D) expression levels were measured using real-time RT-PCR as described in the. [score:1]
The amount of rat GRP78 mRNA, rno-miR-144, rno-miR-376a, and rno-miR-451 in the hCG 0 h group was set at 1. Data were normalized to 18S rRNA (for GRP78 mRNA) and 4.5S RNA(H) (for rno-miR-144, rno-miR-376a, and rno-miR451) levels in each sample and represent the mean ±SE of three independent experiments. [score:1]
The amounts of GRP78 mRNA, rno-miR-144, rno-miR-376a, and rno-miR-451 in the hCG 0 h group were set at 1. Data were normalized for 18S rRNA (for GRP78 mRNA) and 4.5S RNA(H) (for rno-miR-144, rno-miR-376a, and rno-miR-451) levels in each sample and represent the mean ±SE of 3 independent experiments. [score:1]
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[+] score: 26
On the other hand, after sciatic nerve denervation, we observed 1 downregulated miRNA (miR-144) and 1 upregulated miRNA (miR-21) in the DRGs (Figure 1). [score:7]
We detected 1 downregulated miRNA (miR-144) and 1 upregulated miRNA (miR-21) after sciatic nerve denervation. [score:7]
In the DRGs, 6 miRNAs (miR-9, miR-320, miR-324-3p, miR-672, miR-466b, and miR-144) were significantly downregulated in the entrapment group and 3 miRNAs (miR-9, miR-320, and miR-324-3p) were significantly downregulated in the decompression group. [score:7]
In the DRGs, 6 miRNAs in the entrapment group (miR-9, miR-320, miR-324-3p, miR-672, miR-466b, and miR-144) and 3 miRNAs in the decompression group (miR-9, miR-320, and miR-324-3p) were significantly downregulated. [score:4]
Although there also appeared to be a decrease of miR-672, miR-466b, and miR-144 in the decompression group, it was not statistically significant in all 3 specimens. [score:1]
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[+] score: 22
Other miRNAs from this paper: rno-mir-30c-2, rno-mir-146b, rno-mir-3586, rno-mir-486
Heqi: Heqi San, MET: metformin Differential miRNA expression contributed to the pathological process in theWe used sequencing and bioinformatics analysis to predict that PTEN was the target gene of rno-miR-144-3p (Table  2). [score:5]
Therefore, we identified the expression of rno-miR-144-3p in different groups, and found that its mRNA expression level was significantly increased in the compared to the control (Fig.   7a). [score:4]
Heqi: Heqi San, MET: metformin We used sequencing and bioinformatics analysis to predict that PTEN was the target gene of rno-miR-144-3p (Table  2). [score:3]
Treatment with either Heqi San or MET led to the decrease of the rno-miR-144-3p expression level in the (Fig. 7a). [score:3]
a The potential role of rno-miR-144-3p, the target gene of PTEN, was elucidated through real time PCR in the and the Heqi -treated group. [score:3]
This revealed that PTEN likely plays a critical role in PCOS pathology, and that it is regulated through rno-miR-144-3p. [score:2]
The potential role of miRNA-144-3p in PCOS pathogenesis. [score:1]
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]
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[+] score: 21
In the present study, although we did not observe altered expression of miR-99a or miR-144, we found that miR-99a-3p and miR-144-3p were significantly down-regulated in NAFLD rats and constructed a series of miRNAs- mRNAs regulatory pairs. [score:7]
Among these DEMs, miR-33, miR-33-5p, miR-33-3p, miR-144-3p and miR-99a-3p were down-regulated in NAFLD, whereas miR-200b, miR-200b-3p, miR-200b-5p, miR-200c-3p and miR-349 were up-regulated. [score:7]
We also observed that NAFLD-related genes Apln, Vcan, Cd36 and Cyp7a1 were targets of miR-99a-3p and miR-144-3p 26, 27, 31, 32. [score:3]
By integrated analysis, we observed 14 decreased miRNAs (such as miR-33, miR-33-5p, miR-33-3p, miR-144-3p, and miR-99a-3p) and constructed 459 miRNA and mRNA regulatory pairs in NAFLD rats. [score:2]
In addition, miR-144 might contribute to the pathogenesis of NASH in morbidly obese subjects [30]. [score:1]
Decreased miR-144 could enhance TNF-α and IFN-γ production, which might contribute to the progression of NAFLD in rats [29]. [score:1]
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[+] score: 19
Other miRNAs from this paper: rno-mir-27a, rno-mir-28, rno-mir-34a, rno-mir-153, rno-mir-155
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]
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[+] score: 19
Su et al. showed that miR-144 regulates hematopoiesis and vascular development by repressing expression of meis1 in zebrafish 44. [score:5]
Pathways derived from changes that we confirmed in the blood of irradiated rats are shown in Fig. 4. To our knowledge this is the first time that miR-144-3p, 144-5p, and 19a-3p are upregulated in rat blood 2 week after irradiation of the thorax. [score:4]
In summary miR-144 plays a role in inflammation, immune response and suppression of cell growth, processes that are activated by radiation. [score:3]
MiR-144 is overexpressed in peripheral blood mononuclear cells from patients with pulmonary tuberculosis (TB) and regulated anti-TB immune response in T cells 42. [score:3]
In summary, similar to miR-144, miR-142-5p regulates cell growth and inflammation. [score:2]
Hassan et al. found increase in miR-144 in human bronchial epithelial (HBE) cells exposed to cigarette smoke extract and cadmium. [score:1]
Besides the current study, elevation of miR-144 was also reported in many non-cancer studies 42 43. [score:1]
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[+] score: 14
Nine miRNAs (miR-21, miR-24, miR-214, miR-132, miR-195, miR-210, miR-144, miR-150 and miR-34a) were found in exosomes obtained from rats subjected to RIPC, but only miR-24 was significantly upregulated ([#] P < 0.05, n = 4). [score:4]
b, c Flow cytometric analysis of the uptake of exosomes by H9c2 cells at various time points We further determined the expression of nine miRNAs (miR-24, miR-21, miR-214, miR-132, miR-195, miR-210, miR-144, miR-150 and miR-34a) in both RIPC-EXO and EXO (Fig.   3a). [score:3]
A recent study by Li et al. [16] showed that cardioprotection elicited by RIPC was associated with the elevation of circulating miR-144 bound to Argonaute 2. In contrast, in our study, miR-144 expression was hardly altered in RIPC-EXO. [score:3]
Wang X Loss of the miR-144/451 cluster impairs ischaemic preconditioning -mediated cardioprotection by targeting Rac-1Cardiovasc. [score:3]
Since the subject of our study was IRI, we selected nine miRNAs that have been reported to be involved either in oxidative stress (such as miR-150 and miR-21) 14, 15 or in cardiomyocyte apoptosis (such as miR-195, miR-132, miR-140, miR-144, miR-24, miR-214 and miR-34a) 16– 21 in our investigation and, using quantitative PCR (qPCR), explored whether RIPC could modify the expression level of these nine miRNAs in plasma exosomes. [score:1]
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[+] score: 8
The expression levels of miR-376b-3p and miR-137-3p were downregulated, but miR-144-3p was upregulated on the 14th day compared to the 3rd day after injury (Figure  3C). [score:8]
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[+] score: 7
Moreover, our data showed that miR-451 and miR-144 were specifically expressed in hematopoietic tissues e. g., spleen and bone marrow (refer to the original dataset for details). [score:3]
These data support the hypothesis that there are no distinct differences in miRNA profiles between these major organs and peripheral blood cells with some exceptions, such as miR-451 and miR-144, and that expression profiles for the majority of miRNAs were not markedly affected by remaining peripheral blood. [score:3]
As shown in Figure 1, blood-cell–specific miRNAs (e. g., miR-451 and miR-144) [21] were clearly evident in nonperfused samples, but not in perfused samples. [score:1]
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[+] score: 7
Levels of miR-144, miR-451, and miR-770 were significantly down-regulated in CCA rats (p < 0.05 vs. [score:4]
Some alteration in miRNA expression following cocaine exposure may persist for a long time, even still being evident after a long-term abstinence from cocaine administration, such as miR-144, miR-451 and miR-770 in this study. [score:3]
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[+] score: 7
Other microRNAs to have been reported to be related to depression are miR-34 acting as a regulator of CRF signaling, miR-134 and miR-124a levels were significantly downregulated after treatment with duloxetine and miR-144 was found to have an increased expression in both lithium- and valproate -treated animals (Haramati et al., 2011; Hansen and Obrietan, 2013; Pan and Liu, 2015). [score:7]
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[+] score: 6
Similarly, several downregulated microRNAs were associated with genes participating in cell death process, such as yy1 (miR-294) [34], the pro-apoptotic factor bim (miR-144), the pro-apoptotic blcap (miR-294), which stimulates apoptosis independently of p53 and NF-κB [35], and the anti-apoptotic factor Bcl-XL (miR-342) (Figure 7, networks 1, 3 and 4). [score:4]
In contrast, microRNAs that were detected in the present study but not in previous studies (Table 4) include the Exiqon miR-plus probes as well as several newly released microRNAs, for which no previous data have been published, and more interestingly, the miR-451 cluster and miR-144, which are both important gene regulators of erythrocyte homeostasis and cardiomyocyte ischemia [23], [24]. [score:2]
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[+] score: 6
Recently, miRNA-144, 145, and 214 are identified to be down-regulated in primary neurons responding to sciatic nerve transection, and miR-145 inhibited neurite growth of dorsal root ganglia (DRG) neuron through Slit-Robo-srGAP signaling pathway [13]. [score:6]
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[+] score: 5
For example, ectopic expression of miR-144 and -451 augmented cardiomyocyte survival, which was further improved by overexpression of miR-144/451 in response to simulated myocardial I/R injury [12]. [score:5]
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[+] score: 5
miRNA expression profiling is challenging as mature miRNAs are; i) short single stranded RNAs (22–24 nts); ii) their CG content varies between 33% of hsa-miR-144 and 89% of hsa-miR-4665-3p resulting in a wide range of Tms; iii) miRNAs only represent a small fraction of the cellular RNA; iv) miRNA target sequence is contained in its precursors (i. e. pri- and pre-miRNAs); and v) miRNAs are redundant and exist in families where individual members can differ by just a single nucleotide 27. [score:5]
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[+] score: 4
Stretch-sensitive down-regulation of the miR-144/451 cluster in vascular smooth muscle and its role in AMP-activated protein kinase signaling. [score:4]
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[+] score: 3
Genome-wide analysis of miRNA expression reveals a potential role for miR-144 in brain aging and spinocerebellar ataxia pathogenesis. [score:3]
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[+] score: 2
[1] [,] [12–14] Several candidate humoral factors of RIc have been proposed, including stromal cell-derived factor-1α, [15] nitrite/nitric oxide, [16] interleukin-10, [17] microRNA-144, [18] apolipoprotein A-I [19] and alpha-ketoglutarate -dependent dioxygenase Egln1. [score:1]
[15–19] Cell-derived factor-1α, [15] nitrite/nitric oxide, [16] interleukin-10, [17] microRNA-144 [18] were shown to be involved in cardioprotection; however, RIc cardioprotection cannot be fully explained by any of the identified factors acting alone. [score:1]
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[+] score: 2
Namely, pregnant rats fed SO and FO diets during the first 12 days of pregnancy showed significant lower expression of miR-449c-5p, miR-134–5p, miR-188, miR-32, miR130a, miR-144–3p, miR-431, miR-142–5p, miR-33, miR-340–5p, miR-301a, miR-30a, miR-106b, and miR-136–5p, as compared with OO, LO, and PO diets. [score:2]
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[+] score: 1
Murphy CP, Li X, Maurer V, Oberhauser M, Gstir R, Wearick-Silva LE, et al. MicroRNA -mediated rescue of fear extinction memory by miR-144-3p in extinction-impaired mice. [score:1]
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[+] score: 1
Katsuura, for example, and co-workers have shown that naturalistic stress in healthy students caused significant elevation of miR-144/144* and miR-16 in blood [37]. [score:1]
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[+] score: 1
Among the 21 miRNAs altered at 24 hours, 5 (miR-144, miR-136, miR-148b-5p, miR-342-5p, miR-23a*) showed persistent changes by 7 days after CCI (Figure 1C, D). [score:1]
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[+] score: 1
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-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, rno-mir-155, mmu-mir-142b, mmu-mir-497b, rno-mir-148a, rno-mir-15a, rno-mir-193b
For example, the cluster mmu-mir-144~451 is overlapped by a full length cDNA 'AK158085.1', whose 5'/3' ends coincides with ditags. [score:1]
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[+] score: 1
Among potential humoral factors identified in plasma-derived dialysate only three were reported to have a cardioprotective effect: nitrite [35], microRNA-144 [36] and stromal derived factor-1α [37]. [score:1]
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[+] score: 1
For example, rno_circRNA_003295 is potentially able to interact with rno-miR-206-3p, rno_circRNA_002441 with miR-144-3p, and rno_circRNA_012846 with rno-miR-10a-5p. [score:1]
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[+] score: 1
The eight circulating miRNAs, miR-29a, miR-34a, miR-375, miR-103, miR-107, miR-132, miR-142-3p and miR-144, and the two tissue-specific miRNAs, miR-199a-3p and miR-223, were identified to be significantly altered in T2D across a meta-analysis of controlled profiling studies [51]. [score:1]
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[+] score: 1
Of the plasma HTE miRNAs, only miR-144 is known to be blood cell specific [5] and is involved in erythrocyte homeostasis [42]. [score:1]
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