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13 publications mentioning rno-mir-423

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-423. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 362
In the miR-423-5p mimics + siGSTM1 group, GRP78, p-PERK, p-IRE1α and CHOP expression was up-regulated, whereas in the miR-423-5p inhibitors + GSTM1 group, their expression was down-regulated (all P < 0.05). [score:13]
The ROS levels and MDA and GST activities were upregulated, whereas SOD activity was downregulated in the miR-423-5p inhibitors + siGSTM1 group compared to miR-423-5p inhibitors group (all P < 0.05; Figure 5). [score:10]
The miR-423-5p expression in the miR-423-5p mimics group was upregulated compared to the H/R and NC groups whereas expression of GSTM1 mRNA and protein was down-regulated (all P < 0.05; Figure 3A–3B). [score:10]
The following were the 8 groups: (1) the normal control group without H/R treatment; (2) the H/R group (cells with H/R injury); (3) the negative control (NC) group (cells with H/R injury and transfected with nonsense sequence); (4) the miR-423-5p mimics group (cells with H/R injury and transfected with miR-423-5p mimics); (5) the miR-423-5p inhibitor group (with H/R injury and transfected with miR-423-5p inhibitors); (6) the GSTM1 group (cells with H/R injury and transfected with wild type GSTM1 gene); (7) the siGSTM1 group (cells with H/R injury and transfected with siRNA to GSTM1), and (8) the miR-423-5p inhibitor + siGSTM1 group (cells with H/R injury and transfected with miR-423-5p inhibitors and siRNA to GSTM1). [score:9]
Conversely, ROS levels and MDA and GST were down-regulated, whereas SOD activity was up-regulated in the miR-423-5p inhibitors and GSTM1 groups (all P < 0.05). [score:9]
In the miR-423-5p inhibitors group, miR-423-5p was downregulated and both GSTM1 mRNA and protein was up-regulated (all P < 0.05). [score:9]
Our study confirmed that H/R injury of RPETCs induced miR-423-5p, which down-regulated expression of its target gene, GSTM1. [score:8]
Cell proliferation was downregulated in the miR-423-5p mimics and siGSTM1 groups and upregulated in the miR-423-5p inhibitors and GSTM1 group compared to the H/R group (all P < 0.05). [score:8]
In the miR-423-5p inhibitors + siGSTM1 group, GSTM1 mRNA and protein levels were down-regulated compared to the miR-423-5p inhibitors group (Figure 3A–3B). [score:7]
In the miR-423-5p mimics and siGSTM1 groups, ROS levels and MDA and GST activities were up-regulated, whereas SOD activity was downregulated (all P < 0.05). [score:7]
Our study showed that the miR-423-5p inhibitors reduced GRP78 and CHOP expression and increased GSTM1 expression. [score:7]
The miR-423-5p inhibitors are single-stranded RNA with chemical (2-methoxy) modification carried out after synthesis to ensure that specific binding with mature miR-423-5p would inhibit endogenous miR-423-5p expression. [score:7]
This suggested that renal I/R induced miR-423-5p, which subsequently down-regulated GSTM1 expression. [score:6]
In the siGSTM1 group, the miR-423-5p expression was similar to the NC group (P > 0.05), whereas GSTM1 mRNA and protein was down-regulated (all P < 0.05; Figure 3A–3B). [score:6]
In the GSTM1 group, the miR-423-5p expression was comparable to the NC group (P > 0.05), whereas GSTM1 mRNA and protein was up-regulated (all P < 0.05). [score:6]
We observed that miR-423-5p levels were up-regulated and GSTM1 mRNA and protein levels were down-regulated in I/R rats on days 1, 2 and 7 compared to the sham control group (all P < 0.05; Figure 8). [score:6]
Figure 4(A) Analysis of ER-stress related proteins, GRP78, p-PERK, p-IRE1α and CHOP in (1) normal control, (2) H/R, (3) negative control, (4) miR-423-5p mimics, (5) miR-423-5p inhibitor, (6) GSTM1, (7) siGSTM1 and (8) miR-423-5p inhibitor plus siGSTM1 groups of H/R induced HK-2 cells by western blotting; (B) Relative levels of GRP78, p-PERK, p-IRE1α and CHOP proteins in the 8 experimental groups. [score:5]
FACS analysis of apoptosis in (1) normal control, (2) H/R, (3) negative control, (4) miR-423-5p mimics, (5) miR-423-5p inhibitor, (6) GSTM1, (7) siGSTM1 and (8) miR-423-5p inhibitor plus siGSTM1 groups of H/R induced HK-2 cells by AnnexinV/PI double staining. [score:5]
Figure 9(A) Expression miR-423-5p and GSTM1 mRNA in the renal tissues of I/R, I/R plus miR-423-5p mimics and I/R plus miR-423-5p inhibitors on day 3 by qRT-PCR. [score:5]
Figure 3(A) Levels of miR-423-5p and GSTM1 in (1) normal control, (2) H/R, (3) negative control, (4) miR-423-5p mimics, (5) miR-423-5p inhibitor, (6) GSTM1, (7) siGSTM1 and (8) miR-423-5p inhibitor plus siGSTM1 groups of HK-2 cells by qRT-PCR. [score:5]
Also, cell proliferation in the miR-423-5p inhibitors + siGSTM1 group was lower than the miR-423-5p inhibitors group (Figure 6). [score:5]
These results showed that inhibition of GSTM1 expression by miR-423-5p enhanced ER stress under H/R conditions. [score:5]
In the H/R injury mo del of RPETCs, miR-423-5p mimics and GSTM1 siRNA treatments increased ER stress and oxidative stress, whereas miR-423-5p inhibitors suppressed them. [score:5]
Figure 5(A) FACS analysis of cellular ROS in (1) normal control, (2) H/R, (3) negative control, (4) miR-423-5p mimics, (5) miR-423-5p inhibitor, (6) GSTM1, (7) siGSTM1 and (8) miR-423-5p inhibitor plus siGSTM1 groups of H/R induced HK-2 cells by intracellular DCHF-DA staining. [score:5]
Inhibition of GSTM1 expression by miR-423-5p in H/R induced HK-2 cells. [score:5]
Effects of miR-423-5p mimics and inhibitors on GSTM1 expression in I/R treated rat kidneys. [score:5]
Also, higher rate of apoptosis was observed in the miR-423-5p inhibitors + siGSTM1 group than the miR-423-5p inhibitors group (P < 0.05). [score:5]
Figure 7FACS analysis of apoptosis in (1) normal control, (2) H/R, (3) negative control, (4) miR-423-5p mimics, (5) miR-423-5p inhibitor, (6) GSTM1, (7) siGSTM1 and (8) miR-423-5p inhibitor plus siGSTM1 groups of H/R induced HK-2 cells by AnnexinV/PI double staining. [score:5]
The SOD mRNA and protein levels were lower in the miR-423-5p inhibitors + siGSTM1 group compared to the miR-423-5p inhibitors group (P < 0.05; Figure 5E–5F). [score:4]
SOD mRNA and protein expressions were lower in the miR-423-5p mimics group compared to the miR-423-5p inhibitors group (P < 0.05). [score:4]
The dual-luciferase reporter assay showed that miR-423-5p bound to the 3′UTR of GSTM1 and suppressed its expression. [score:4]
The online bioinformatics software (miRBase Prediction Algorithm) was used to predict target genes which may be regulated by miR-423-5p. [score:4]
These results demonstrated that miR-423-5p negatively regulated GSTM1 expression. [score:4]
In regard to HK-2 cells, the H/R group showed higher miRNA-423-5p expression compared to the normal control group (P < 0.05) with the highest miRNA-423-5p expression at 24 h (Figure 1B). [score:4]
Estimation of proliferation in (1) normal control, (2) H/R, (3) negative control, (4) miR-423-5p mimics, (5) miR-423-5p inhibitor, (6) GSTM1, (7) siGSTM1 and (8) miR-423-5p inhibitor plus siGSTM1 groups of H/R induced HK-2 cells by CCK-8 assay. [score:4]
Figure 6Estimation of proliferation in (1) normal control, (2) H/R, (3) negative control, (4) miR-423-5p mimics, (5) miR-423-5p inhibitor, (6) GSTM1, (7) siGSTM1 and (8) miR-423-5p inhibitor plus siGSTM1 groups of H/R induced HK-2 cells by CCK-8 assay. [score:4]
The levels of GRP78, p-PERK, p-IRE1α and CHOP were higher in the miR-423-5p inhibitors + siGSTM1 group compared to the miR-423-5p inhibitors group (all P < 0.05; Figure 4B). [score:4]
Next, we analyzed the effect of miR-423-5p mimics and inhibitors on the renal function of I/R rats. [score:3]
With a rat mo del of H/R and a rat mo del of I/R injury, the study confirmed the functions of miR-423-5p in the processes of RPETC injury by comparing the expressions and the changes of oxidative stress and ER stress after miR-423-5p treatment. [score:3]
Analysis of miR-423-5p and GSTM1 expression in hypoxia/reoxygenation induced HK-2 cells. [score:3]
This trend was reversed by treating with miR-423-5p inhibitors that increased GSTM1. [score:3]
Also, RPTECs are a vital factor in kidney function and miR-423-5p can regulate renal response to acute injury essential in maintenance of renal function and development of renal injury [2, 12]. [score:3]
These results demonstrated that miR-423-5p inhibition of GSTM1 promote oxidative stress in H/R conditions. [score:3]
Consistent with our data, another study showed that miR-423-5p inhibitors in gastric cancer cells reduced cell proliferation and increased tumor cell invasion [26]. [score:3]
Expression of miR-423-5p and GSTM1 in I/R rat kidney. [score:3]
Inhibition of GSTM1 by miR-423-5p enhances oxidative stress in H/R induced HK-2 cells. [score:3]
However, relative luciferase activity increased in H/R induced HK-2 cells co -transfected with pGL3-GSTM1-WT and miR-423-5p inhibitors (Figure 2C). [score:3]
However, expressions of miR-423-5p and GSTM1 in the H/R and NC groups were similar (both P > 0.05). [score:3]
Inhibition of GSTM1 by miR-423-5p increases cellular apoptosis in H/R induced HK-2 cells. [score:3]
After 3 days, the relative index of renal function and miR-423-5p and GSTM1 expression were determined. [score:3]
, USA) was used to transfect either 50 nM nonsense sequence or 50 nM miR-423-5p mimics, 100 nM miR-423-5p inhibitors, 4 μg pcDNA3.1-GSTM1 plasmids. [score:3]
After I/R treatment of SD rats, miR-423-5p mimics or inhibitors were mixed in a 1: 2 ratio with Entranster™ (Engreen Biosystem Co. [score:3]
Also, when miR-423-5p was inhibited, cell proliferation increased and cellular apoptosis diminished. [score:3]
These results suggested that miR-423-5p inhibition of GSTM1 enhanced apoptosis in HK-2 cells apoptosis in H/R conditions. [score:3]
These results showed that inhibition of GSTM1 by miR-423-5p decreased HK-2 cell proliferation in H/R conditions. [score:3]
Effect of miR-423-5p on GSTM1 expression in I/R rat kidneys. [score:3]
Treatment of rats with miR-423-5p mimics or inhibitors. [score:3]
Inhibition of GSTM1 by miR-423-5p enhances ER stress in H/R induced HK-2 cells. [score:3]
Cell proliferation was similar in H/R, NC and miR-423-5p inhibitors + siGSTM1 groups (P > 0.05). [score:3]
Inhibition of GSTM1 by miR-423-5p decreases cell proliferation in H/R induced HK-2 cells. [score:3]
On the other hand, H/R induced HK-2 cells co -transfected with pGL3-GSTM1-MUT vector and miR-423-5p mimics or miR-423-5p inhibitors demonstrated no change (Figure 2B, 2C). [score:3]
The relative expressions of miRNA-423-5p and GSTM1 mRNA were determined in relation to U6 and glyceraldehyde-3-phosphate dehydrogenase (GAPDH), respectively. [score:3]
In comparison to the H/R group, we observed increased apoptosis in the miR-423-5p mimics and siGSTM1 groups and decreased in the miR-423-5p inhibitors and GSTM1 groups (all P < 0.05; Figure 7). [score:3]
Apoptotic rate was similar in the H/R, NC and miR-423-5p inhibitors + siGSTM1 groups (P > 0.05). [score:3]
A nonsense sequence, miR-423-5p mimics and inhibitors, and siRNA to GSTM1 (siGSTM1) were purchased from GenePharma Co. [score:3]
Increased miRNA-423-5p expression in H/R induced HK-2 cells and I/R treated rats. [score:3]
Increased miRNA-423-5p expression in kidney tissues after acute I/R and hypoxia/reoxygenation induced HK-2 cells. [score:3]
This demonstrated that renal function improved upon miR-423-5p inhibition in I/R rats. [score:3]
Effect of miR-423-5p mimics and inhibitors on renal function of I/R rats. [score:3]
To further explore the consequences of and the negative regulation of GSTM1 by miR-423-5p in RPETC injury, we analyzed of the status of ER stress and oxidative stress. [score:2]
In conclusion, our study demonstrates that miR-423-5p negatively regulates GSTM1 during renal cell injury, thereby affecting the repair process by enhancing oxidative stress and ER stress. [score:2]
These results further showed that negative regulation of GSTM1 by miR-423-5p promoted oxidative stress during renal cell injury. [score:2]
We observed that on day 3, high serum creatinine and urea nitrogen levels in the I/R and I/R + miR-423-5p mimics group and lower serum creatinine and urea nitrogen levels in the I/R + miR-423-5p inhibitors group compared to the sham group (all P < 0.05; Table 2). [score:2]
In addition, miR-423-5p negatively regulated autophagy and cell cycle in hepatocellular carcinoma cells [27]. [score:2]
But, if GSTM1 is regulated by miR-423-5p is not known. [score:2]
This suggested that negative regulation of GSTM1 by miR-423-5p influences cell proliferation and apoptosis during renal injury. [score:2]
On day 3, we observed higher miR-423-5p levels in the rat kidneys of I/R and I/R + miR-423-5p mimics group and lower miR-423-5p levels in the I/R + miR-423-5p inhibitors group compared to the sham group (all P < 0.05; Figure 9). [score:2]
This suggested that miR-423-5p increased ER stress in RPETCs by negatively regulating GSTM1. [score:2]
Further, on day 3, GSTM1 mRNA and protein levels were lower in the I/R and I/R + miR-423-5p mimics groups and higher in the I/R + miR-423-5p inhibitors group compared to the sham group (all P < 0.05; Figure 9). [score:2]
Analysis of miR-423-5p and GSTM1 levels in sham and I/R rat kidneys. [score:1]
Therefore, our study aims to explore the miR-423-5p effect on RPTECs. [score:1]
In this study, cells treated with miR-423-5p mimics demonstrated enhanced ROS and MDA and GST activities, whereas SOD activity was reduced. [score:1]
Figure 1(A) Estimation of miRNA-423-5p levels in kidney tissues of sham and I/R rats by qRT-PCR. [score:1]
Therefore, as described in the methods, we constructed the GSTM1 luciferase reporter vector to analyze the specific binding between miR-423-5p and GSTM1 3 ‘UTR. [score:1]
Figure 8(A) Estimation of miR-423-5p and GSTM1 mRNA levels in the kidneys of sham and I/R group rats on days 1, 3, 7, 14 and 21 by qRT-PCR. [score:1]
The miRBase software was used to predict the binding sites of miR-423-5p in the 3′ UTR with the binding site of miR-423-5p was cloned into pGL3 vector (Promega Corp. [score:1]
The miR-423-5p levels determined tumor cell growth in gastric cancer and predicted heart failure [10, 11]. [score:1]
Note: *denotes P < 0.05 in comparison with the NC group; GSTM1, Glutathione-S-transferase (GST) M1; miR-423-5p, microRNA-423-5p; HK-2 cells, human renal tubular epithelial cells; NC, negative control. [score:1]
Also, miR-199a-3p, miR-let-7i-5p and miR-423-3p are involved in maintaining renal function and response to renal injury [12]. [score:1]
Figure 2(A) Predicting miR-423-5p binding sites in GSTM1 sequence by miRBase. [score:1]
To detect miR-423-5p and GSTM1 mRNA levels by qRT-PCR, RNA was extracted from the 8 groups of experimental HK-2 cells or the rat kidneys according to the manufacturer’s instructions (Promega Corp. [score:1]
Note: *denotes P < 0.05 compared with the normal control group; # denotes P < 0.05 compared with H/R group; & denotes P < 0.05 compared with miR-423-5p inhibitors group; miR-423-5p, microRNA-423-5p; GSTM1, Glutathione-S-transferase (GST) M1; ER, endoplasmic reticulum; GRP78, 78 kDa glucose-regulated protein; CHOP, C/EBP homology protein; NC, negative control; H/R, hypoxia/reoxygenation. [score:1]
The result showed that the specific binding site of miR-423-5p was presented in the sequence of GSTM1 3′UTR (Figure 2A). [score:1]
Dual luciferase reporter analysis of miR-423-5p binding to GSTM1 3′UTR. [score:1]
Note: *denotes P < 0.05 in comparison with sham or normal control group; I/R, ischemia/reperfusion; qRT-PCR, quantitative real-time polymerase chain reaction; miR-423-5p, microRNA-423-5p. [score:1]
The miR-423-5p -binding site in the pGL3-GSTM1-WT plasmid was mutated to generate the pGL3-GSTM1-mutant-type (MUT) plasmid. [score:1]
This suggested that miRNA-423-5p played a role in renal injury. [score:1]
Therefore, miR-423-5p inhibitors can be potentially therapeutic for RPTEC injury and need to be investigated. [score:1]
In this study, miR-423-5p increased RPETC apoptosis and decreased cell proliferation. [score:1]
Further, the levels of miR-423-5p and GSTM1 mRNA and protein normalized on days 14 and 21 (all P > 0.05; Figure 8). [score:1]
These results confirmed that miR-423-5p specifically bound to GSTM1-3′UTR. [score:1]
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2
[+] score: 18
Other miRNAs from this paper: rno-mir-15b, rno-mir-32, rno-mir-378a, rno-mir-466d, rno-mir-378b
The single miRNA significantly up-regulated at 1 hour (miR-423-5p) remained up-regulated at 6 hours; another 33 miRNAs were significantly up-regulated and another 8 miRNAs were significantly down-regulated at 6 hours. [score:13]
In addition, we validated miR-423-5p, which was the only miRNA up-regulated ≥ 1.5-fold at both 1 and 6 hours of cyclic stretch. [score:4]
In addition, we performed qRT-PCR on miR-423-5p, which was the only miRNA differentially expressed at both 1 and 6 hours, and miR-466f-3p, which was chosen for subsequent investigations. [score:1]
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3
[+] score: 15
In secreted BM-MSC-MVs, the expression of miR-344a, miR-133b-3p, miR-294, miR-423-3p, and miR-872-3p was significantly downregulated in older rats than in younger rats (P < 0.05), and the serum level of these miRNAs exhibited the same patterns. [score:6]
miR-344a, miR-133b-3p, miR-294, miR-423-3p, and miR-872-3p in BM-MSC-MVs from aged rats were downregulated, and the expression of miR-294 and miR-872-3p showed a significant decline (P < 0.05) (Fig.   2c). [score:6]
Lastly, an ABI-Prism 7500 Sequence Detection System (Applied Biosystems, Waltham, MA, USA) and SYBR PrimeScript miRNA RT-PCR Kit (Takara) were used to detect the expression level of specific miRNAs (miR-344a, miR-294, miR-872-3p, miR-133b-3p, and miR-423-3p) and the loading control, miR-191. [score:3]
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4
[+] score: 11
As a control, we also examined the expression of a miRNA (miR-423-5p) that did not demonstrate altered expression in the Cd-treatment group versus the saline control group according to the microarray analysis, and real-time PCR analysis confirmed there was no significant difference in the expression of miR-423-5p between the saline control and Cd-treatment group (Figure 3H). [score:7]
As an additional validation of the µParaflo™ microRNA microarray assay, the expression of miR-423-5p (rno481159_mir) was examined by real-time PCR since the expression of this miRNA was not significantly altered with Cd treatment. [score:4]
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5
[+] score: 8
Despite tissue- and pathology-specificity of miRNAs expression, we failed to identify miRNAs, such as miR-133a and miR-423-5p, as circulating prognostic biomarkers of cardiac remo delling post-MI [14]. [score:3]
Data were normalized to miR-423-3p for LV and graph shows mean ± SEM values expressed as fold change (2−ΔΔCt). [score:3]
Bauters C Circulating miR-133a and miR-423-5p fail as biomarkers for left ventricular remo deling after myocardial infarctionInt. [score:1]
Up to now, we failed to identify miRNAs, such as miR-133a and miR-423-5p, as circulating prognostic biomarkers of cardiac remo delling post-MI [14]. [score:1]
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6
[+] score: 7
Five differentially expressed microRNAs were randomly selected for validation, including three arterial highly expressed microRNAs (rno-miR-139-3p, rno-miR-423-5p, rno-miR-125b-5p) and two venous highly expressed microRNAs (rno-miR-1-3p, rno-miR-340-3p). [score:7]
[1 to 20 of 1 sentences]
7
[+] score: 4
We found that 14 of the DEmiRNAs identified in our screen can regulate 2927 common putative target genes (Figure 5A), while 9 miRNAs, including miR-1249, miR-1306-3p, miR-32-3p, miR-327, miR-328b-3p, miR-3562, miR-3588, miR-423-5p, and miR-466d, had no common predicted genes. [score:4]
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8
[+] score: 3
Two miRNAs, mmu-mir-324 and mmu-mir-423, lie within genes in which mutations were found, dishevelled 2 (Dvl2) and coiled-coil domain containing 55 (Ccdc55), respectively, though neither mutation identified in these genes is within the miRNA sequence itself. [score:3]
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9
[+] score: 3
Compared to the other 2 groups, 21 miRNAs are upregulated in 6-hour group as shown in the upper portion of Fig. 2, miR-9, miR-204, miR-335, miR-23a, miR-708, miR-146a, miR-325-5p, miR-106b, miR-143, miR-140, miR-376b-3p, miR-7a, miR-541, miR-185, miR-499, miR-127*, miR-320, miR-140*, miR-145*, miR-423*, miR-378. [score:3]
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10
[+] score: 2
In general, the rank order of the expression levels of the measured miRNAs was comparable in mice and rats, with the highest miRNA levels of miR-16-5p and miR-223-3p and the lowest levels of miR-199a-3p, miR-652-3p, miR-423-3p and miR-26b-5p (S1– S3 Figs). [score:1]
In rats we found one significant correlation between the normalized -Ct values of miR-423-3p and the dP/dt [max] values (R = -0.53, P-value = 0.036). [score:1]
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11
[+] score: 2
MiR-423-5p promotes hepatic gluconeogenesis and lipid deposition and induces glucose intolerance, insulin resistance, and hyperglycemia by inhibiting the FAM3A-ATP-Akt pathway in the liver [12]. [score:2]
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12
[+] score: 1
It has also been reported that plasma levels of some miRNAs (mir-1, mir-208, mir-133a, mir-423-5p, mir-499) can be used as biomarkers for myocardial injury [90– 92]. [score:1]
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13
[+] score: 1
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-20a, hsa-mir-22, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-98, hsa-mir-101-1, hsa-mir-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-15b, mmu-mir-101a, mmu-mir-126a, mmu-mir-130a, mmu-mir-133a-1, mmu-mir-142a, mmu-mir-181a-2, mmu-mir-194-1, hsa-mir-208a, hsa-mir-30c-2, mmu-mir-122, mmu-mir-143, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-181a-1, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-15b, hsa-mir-122, hsa-mir-130a, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-142, hsa-mir-143, hsa-mir-126, hsa-mir-194-1, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-208a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-15a, mmu-mir-16-1, mmu-mir-16-2, mmu-mir-18a, mmu-mir-20a, mmu-mir-22, mmu-mir-26a-1, mmu-mir-26b, mmu-mir-29c, mmu-mir-98, mmu-mir-326, rno-mir-326, rno-let-7d, rno-mir-20a, rno-mir-101b, mmu-mir-101b, hsa-mir-1-1, mmu-mir-1a-2, hsa-mir-181b-2, mmu-mir-17, mmu-mir-19a, mmu-mir-181a-1, mmu-mir-26a-2, mmu-mir-19b-1, mmu-mir-181b-1, mmu-mir-181c, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-101-2, hsa-mir-26a-2, hsa-mir-378a, mmu-mir-378a, hsa-mir-326, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, mmu-mir-181b-2, rno-let-7a-1, rno-let-7a-2, rno-let-7b, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7f-1, rno-let-7f-2, rno-let-7i, rno-mir-15b, rno-mir-16, rno-mir-17-1, rno-mir-18a, rno-mir-19b-1, rno-mir-19a, rno-mir-22, rno-mir-26a, rno-mir-26b, rno-mir-29c-1, rno-mir-30c-1, rno-mir-30c-2, rno-mir-98, rno-mir-101a, rno-mir-122, rno-mir-126a, rno-mir-130a, rno-mir-133a, rno-mir-142, rno-mir-143, rno-mir-181c, rno-mir-181a-2, rno-mir-181b-1, rno-mir-181b-2, rno-mir-194-1, rno-mir-194-2, rno-mir-208a, rno-mir-181a-1, hsa-mir-423, hsa-mir-18b, hsa-mir-20b, hsa-mir-451a, mmu-mir-451a, rno-mir-451, ssc-mir-122, ssc-mir-15b, ssc-mir-181b-2, ssc-mir-19a, ssc-mir-20a, ssc-mir-26a, ssc-mir-326, ssc-mir-181c, ssc-let-7c, ssc-let-7f-1, ssc-let-7i, ssc-mir-18a, ssc-mir-29c, ssc-mir-30c-2, hsa-mir-484, hsa-mir-181d, hsa-mir-499a, rno-mir-1, rno-mir-133b, mmu-mir-484, mmu-mir-20b, rno-mir-20b, rno-mir-378a, rno-mir-499, hsa-mir-378d-2, mmu-mir-423, mmu-mir-499, mmu-mir-181d, mmu-mir-18b, mmu-mir-208b, hsa-mir-208b, rno-mir-17-2, rno-mir-181d, rno-mir-484, mmu-mir-1b, ssc-mir-15a, ssc-mir-16-2, ssc-mir-16-1, ssc-mir-17, ssc-mir-130a, ssc-mir-101-1, ssc-mir-101-2, ssc-mir-133a-1, ssc-mir-1, ssc-mir-181a-1, ssc-let-7a-1, ssc-let-7e, ssc-let-7g, ssc-mir-378-1, ssc-mir-133b, ssc-mir-499, ssc-mir-143, ssc-mir-423, ssc-mir-181a-2, ssc-mir-181b-1, ssc-mir-181d, ssc-mir-98, ssc-mir-208b, ssc-mir-142, ssc-mir-19b-1, hsa-mir-378b, ssc-mir-22, rno-mir-126b, rno-mir-208b, rno-mir-133c, hsa-mir-378c, ssc-mir-194b, ssc-mir-133a-2, ssc-mir-484, ssc-mir-30c-1, ssc-mir-126, ssc-mir-378-2, ssc-mir-451, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, mmu-mir-378b, mmu-mir-101c, hsa-mir-451b, hsa-mir-499b, ssc-let-7a-2, ssc-mir-18b, hsa-mir-378j, rno-mir-378b, mmu-mir-133c, mmu-let-7j, mmu-mir-378c, mmu-mir-378d, mmu-mir-451b, ssc-let-7d, ssc-let-7f-2, ssc-mir-20b-1, ssc-mir-20b-2, ssc-mir-194a, mmu-let-7k, mmu-mir-126b, mmu-mir-142b, rno-let-7g, rno-mir-15a, ssc-mir-378b, rno-mir-29c-2, rno-mir-1b, ssc-mir-26b
Sharbati-Tehrani et al., [67] have reported 4 new miRNAs (miR-326, miR-423-3p, miR-484 and miR-451,) that could not be identified in our study, which could be attributed to the use of very specialized tissues (Jejunium, spleen, ileum and kidney) for their study. [score:1]
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