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16 publications mentioning gga-mir-122b

Open access articles that are associated with the species Gallus gallus and mention the gene name mir-122b. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

[+] score: 103
Additionally, combined with the results of luciferase reporter assay, the miR-122 could regulate targets expression by repressing target translation or triggering target degradation, For example, the expression of RAD21 might be regulated in triggering target mRNA degradation and TGFβ3 might be regulated in repressing target translation, which indicated the miR-122 has a potential roles in regulating postnatal liver maturation process. [score:22]
Several previous reported target genes of gga-miR-122 involved in cytokinesis and further liver development have also been detected in the present study, including microtubule affinity -regulating kinase 3 (MARK3), mitogen-activated protein kinase kinase kinase 4 (MAP3K4), RAD21 cohesin complex component (RAD21), transforming growth factor beta 3 (TGFβ3), neural precursor cell expressed, developmentally down-regulated 4-like, E3 ubiquitin protein ligase (NEDD4L), and microtubule -associated protein, RP/EB family, member 1 (MAPRE1) [13], which again confirmed the roles of miR-122 in postnatal liver maturation. [score:11]
According to the miRNAs-genes network, several differentially expressed miRNAs including miR-122 and their potential target genes were involved in the regulation of cell cycle [13], which indicated that those differentially expressed miRNAs in our study could regulate the postnatal liver development by influencing the cell cycle pathway. [score:10]
Meanwhile, it can also influence liver polyploidization and further liver maturation, by directly influencing the targets expression of miR-122, which was related to cytokinesis process [13]. [score:6]
For example, miR-122 could contribute to the liver development by regulating the balance between proliferation and differentiation of hepatocytes by targeting CCAAT displacement protein (CUTL1, also known as CDP) 12, 13. [score:5]
These results demonstrated that TGFβ3 or RAD21 were targeted by gga-miR-122-5p and the target predictions of miRNAs were accurate. [score:5]
The gga-miR-122-5p was the highest differentially expressed miRNAs in the present study, and TGFβ3 or RAD21 were the targets of gga-miR-122-5p involved in the cell cycle pathway. [score:5]
The gga-miR-122–5p targets the 3′ Untranslated Regions (3′UTRs) of TGFβ3 or RAD21. [score:5]
By using three different endogenous control miRNAs (U6, 5S, and 18S), the results have all showed that two miRNAs (gga-miR-181b-5p_R + 1 and gga-miR-30b-5p) had significantly lower expression levels in matured livers than the postnatal livers, and the expression level of another four miRNAs (gga-let-7a-5p, gga-miR-2954_R + 2, gga-miR-21-5p, and gga-miR-122-5p) were significantly increased in matured livers (Fig.   3), which were consistent with the miRNA-seq data. [score:5]
Xu H Liver-enriched transcription factors regulate MicroRNA-122 that targets CUTL1 during liver developmentHepatology. [score:4]
Moreover, miR-122 and its target genes, which were related to cytokinesis, have been indicted to regulate the liver cell polyploidization [13]. [score:4]
Note: (a) The overexpression of miR-122–5p was detected at 48 h in miR-122-5p group after transfection. [score:3]
Among those differentially expressed miRNAs, the gga-miR-122 was the highest one. [score:3]
Moreover, gga-miR-122 was the identified differentially expressed miRNAs which proved by miRNAs sequencing with the criteria of P value < 0.05 and the qRT-PCR validation. [score:3]
The significant changes of gga-miR-122-5p expression levels in the gga-miR-122-5p groups showed that our co-transfections were successful (Fig.   5a). [score:3]
Several studies have demonstrated that miR-122 was one of the tissue-specific miRNA and highest expressed miRNAs in liver [19]. [score:3]
Jopling C Liver-specific microRNA-122: Biogenesis and functionRNA Biol. [score:1]
In order to further validate the interaction of gga-miR-122-5p with TGFβ3 or RAD21 in vitro, we constructed luciferase reporter genes with TGFβ3 or RAD21 3′UTRs in psiCHECK [TM]-2 vectors respectively and then co -transfected the vectors and gga-miR-122-5p mimic or miR-NTC into HEK293T cells respectively. [score:1]
24 hours later, 500 ng of vector constructs were co -transfected with either 50 nM of gga-miR-122-5p mimic or miR-NTC (RIBO Bio, Guangzhou, China) using 2.0 μL X-tremeGENE siRNA Transfection Reagent (Roche, USA), and the cells in control group were without any treatment. [score:1]
In our experiment, the gga-miR-122 was significantly increased in matured liver, which could indicate that miR-122 plays crucial roles in postnatal liver maturation. [score:1]
The expression level of gga-miR-122-5p from cells in four groups were measured by qRT-PCR; the methods and data process were described as before. [score:1]
Hsu SH MicroRNA-122 regulates polyploidization in the murine liverHepatology. [score:1]
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[+] score: 34
With the exception of gga-miR-122-5p, which was significantly downregulated, all miRNAs were strongly up-regulated in response to food deprivation. [score:7]
When miR-122-5p is downregulated the hepatic synthesis rate of fatty acids and cholesterol decrease [52], [53], which is in agreement with the finding that this miRNA is downregulated in response to feed deprivation in the liver (Figure 6). [score:7]
This apparent paradox may be explained by a higher constitutive expression in the R+ line of gga-miR-122-5p by other tissues, with subsequent release in plasma. [score:3]
Interestingly, a significant difference between R+ and R− lines (p = 0.03) was observed for gga-miR-122-5p in the feed deprived condition alone and not in the re-fed one (p = 0.82), with gga-miR-122-5p more expressed in the R− line. [score:3]
For example, the three members of the let-7 family (let-7a, let-7f, let-7k) are broadly expressed across tissues [36] and tissue enrichment has been found for miR-499-5p and −3p in heart [37], miR-122-5p in liver [38], miR-202-5p in testis [39] and gga-miR-107-3p in brain tissues [40] (Table 2). [score:3]
Furthermore, it has been reported that a choline- and folate -deficient diet causing nonalcoholic fatty liver disease (NAFLD) determined a different extent of modulation of some miRNAs, including miR-122, in both liver and plasma of divergent strains of mice [59]. [score:3]
This hypothesis is supported by the different plasmatic contents found in the R+ and R− lines of three highly conserved miRNAs with a key regulatory role in energetic metabolism (gga-miR-204, gga-miR-let-7f-5p and gga-miR-122-5p) (Table 2). [score:2]
Conversely, high significance values were found for all miRNAs (gga-miR-122-5p, gga-miR-2188-3p and gga-let-7f-5p) previously identified as differentially abundant between R+ and R- animals (Line). [score:1]
The miRNAs were selected among those found differentially abundant in the Condition comparison (gga-miR-204, gga-miR-2188-5p and gga-miR-365-3p), in the Line comparison (gga-miR-2188-3p, and gga-miR-122-5p) or in both (gga-let-7f-5p). [score:1]
Remarkably, gga-miR-122-5p was confirmed to be significantly more abundant in the R+ animals than in the R− ones despite the high variability observed in the two feeding conditions. [score:1]
Finally, an interesting example is provided by gga-miR-122-5p. [score:1]
However, in plasma, the level of gga-miR-122-5p decreases after feed deprivation only in the R− line. [score:1]
These miRNAs were found to be present in plasma at very different levels of abundance, from an average of 397 normalized counts (gga-miR-122-5p) to an average of 2.1 million normalized counts (gga-miR-2188-5p). [score:1]
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[+] score: 34
Target genes of 14 differentially expressed miRNAs (gga-miR-122-5p, gga-miR-193a-5p, gga-miR-194, gga-miR-215-5p, gga-miR-217-3p, gga-miR-375, gga-miR-1559-3p, gga-miR-1769-3p, gga-miR-1788-3p, gga-miR-1798-5p, gga-miR-2954, gga-miR-3525, and gga-miR-3531-3p) were predicted by using the miRDB and TargetScan programs. [score:7]
In comparison with the S group, the SP group significantly increased gga-miR-3525 (1.783-fold change) expression on day 1 after the infection and gga-miR-193a-5p and gga-miR-122-5p expression on day 3 after the infection (1.719- and 1.860-fold changes, respectively). [score:5]
In addition to VNN1, human has-miR-122-5p targets IL6ST, interleukin 17 receptor (IL-17R), IL21R, tumor necrosis factor superfamily member 10 (TNFSF10), and tumor necrosis factor receptor superfamily member 1B (TNFRSF1B) genes to modulate the host reaction to bacteria and these target genes enriched in immune-related pathways, such as TNF signaling pathway, MAPK pathway. [score:5]
On the other hand, the SP group significantly reduced expression of gga-miR-3525 and gga-miR-122-5p on day 5 post the infection (15.227- and 5.509-fold changes, respectively). [score:3]
A total of 14 differentially expressed miRNAs were detected (gga-miR-2954, gga-miR-215-3p, gga-miR-1798-5p, gga-miR-194, gga-miR-217-3p, gga-miR-1769-3p, gga-miR-1788-3p, gga-miR-1559-3p, gga-miR-3531-3p, gga-miR-215-5p, gga-miR-3525, gga-miR-193a-5p, gga-miR-122-5p, and gga-miR-375). [score:3]
The expression of gga-miR-122-5p increased 1.957-fold in the SP group and decreased 0.792-fold in the P group. [score:3]
To confirm and quantify the differential expression, five miRNAs (gga-miR-215-5p, gga-miR-3525, gga-miR-193a-5p, gga-miR-122-5p, and gga-miR-375) were randomly selected and validated by RT-PCR with six replicates of cecal samples in each group (Figure 3). [score:3]
The gga-miR-122-5p targets the VNN1 in chickens (41). [score:3]
On the other hand, miR-215-3p, miR-194, miR-217-3p, miR-215-3p, miR-193a-5p, miR-122-5p, and miR-375 are more conservative miRNAs in vertebrate animal species. [score:1]
Gga-miR-122-5p decreased 0.782- and 0.501-fold change in the SP and P groups, respectively. [score:1]
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[+] score: 23
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-16-1, hsa-mir-21, hsa-mir-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-9-2, mmu-mir-151, mmu-mir-10b, hsa-mir-192, mmu-mir-194-1, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-122, hsa-mir-10a, hsa-mir-10b, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-210, hsa-mir-214, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-122, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-194-1, mmu-mir-192, 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-16-1, mmu-mir-16-2, mmu-mir-21a, mmu-mir-10a, mmu-mir-210, mmu-mir-214, mmu-mir-199a-2, mmu-mir-199b, mmu-mir-9-1, mmu-mir-9-3, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-365a, mmu-mir-365-1, hsa-mir-365b, hsa-mir-151a, gga-let-7i, gga-let-7a-3, gga-let-7b, gga-let-7c, gga-mir-16-1, gga-mir-194, gga-mir-10b, gga-mir-199-2, gga-mir-16-2, gga-let-7g, gga-let-7d, gga-let-7f, gga-let-7a-1, gga-mir-199-1, gga-let-7a-2, gga-let-7j, gga-let-7k, gga-mir-122-1, gga-mir-122-2, gga-mir-9-2, mmu-mir-365-2, gga-mir-9-1, gga-mir-365-1, gga-mir-365-2, hsa-mir-151b, mmu-mir-744, gga-mir-21, hsa-mir-744, gga-mir-199b, gga-mir-10a, gga-mir-16c, gga-mir-214, sma-let-7, sma-mir-71a, sma-bantam, sma-mir-10, sma-mir-2a, sma-mir-3479, sma-mir-71b, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-let-7k, gga-mir-365b, sma-mir-8437, sma-mir-2162, gga-mir-9-3, gga-mir-210a, gga-mir-9-4, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3, gga-mir-9b-1, gga-mir-10c, gga-mir-210b, gga-let-7l-1, gga-let-7l-2, gga-mir-122b-1, gga-mir-9b-2, gga-mir-122b-2
Temporal expression analysis of miR-199, miR-214, miR-21, miR-210, miR-122, miR-192 and miR-194 in the liver during S. mansoni infectionBetween weeks 6 and 12, female parasites continue to produce ∼300 eggs per day [51], resulting in an increase in the number of granulomas in the liver and the development of fibrosis [45]. [score:4]
However, according to our analysis, although miR-192, miR-122 and miR-194 were down-regulated in the liver during infection, their levels in serum did not change significantly (Fig. 1– 2). [score:4]
As shown in Fig. 2, the levels of miR-192, miR-194 and miR-122 in serum do not change between 4–12 weeks post infection, whereas five of the miRNAs that are up-regulated in the liver are also significantly elevated in serum at 12 weeks post infection (p<0.05), ranging from 2.6 fold (miR-21) to 4.7 fold (miR-214) (Table S2). [score:4]
Among the down regulated miRNAs was the liver-enriched miR-122, which is dysregulated during hepatitis C infection, acetaminophen overdose and hepatocellular carcinoma and is involved in lipid metabolism [49], [50]. [score:3]
A number of reports have demonstrated an increase in miR-122 and miR-192 in plasma or serum upon viral infection as well as chemically induced liver disease [54], [56]. [score:3]
Temporal expression analysis of miR-199, miR-214, miR-21, miR-210, miR-122, miR-192 and miR-194 in the liver during S. mansoni infection. [score:3]
Consistent with the array results, there was an increase in miR-199-5p, miR-199-3p, miR-214, miR-21, miR-210, and a reduction of miR-192, miR-194, miR-365, miR-122 and miR-151 in the liver tissue of S. mansoni infected mice as compared to naïve mice; miR-9 and miR-744 did not display differential expression and were not analysed further (Table 1). [score:2]
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[+] score: 15
For example, miR-122, abundantly expressed in liver, modulates protein metabolism in liver by targeting cationic amino acid transporter 1 [16]; it regulates the synthesis of fatty acids and cholesterol by repressing the expression of aldolase-A, 3-hydroxy-3-methylglutaryl-coenzyme A reductase, and AMP-activated protein kinase [17], [18]. [score:8]
The expression of miR-122 is not changed by GH in male rat liver [45]. [score:3]
We found the same for gga-miR-122 in this study, indicating this miRNA might not be involved in GH regulation of liver metabolism. [score:2]
From many previous reports, miR-122 was known as the most abundant miRNA in liver. [score:1]
But in our study gga-miR-122-5p (previously named gga-miR-122) was identified as the fifth abundant miRNA in primary chicken hepatocytes, similar to the report by Li et al. which found miR-122 was the fourth abundant miRNA in porcine liver [43]. [score:1]
[1 to 20 of 5 sentences]
[+] score: 15
Of particular note, there was a 12-fold up-regulation (five-fold in deep sequencing) of miR-19b-3p, and an eight-fold down regulation (six-fold in deep sequencing) of miR-122-5p between HAbF and LAbF chickens (P < 0.05). [score:5]
For example, the extensive (six- to eight-fold) down-regulation of gga- miR-122-5p was shown by both by deep sequencing and qPCR. [score:4]
Eleven of these (miR-204, miR-19a-3p, miR-19b-3p, miR-30d, miR-26a, miR-122-5p, miR-103-3p, miR-27b-3p, miR-92-3p, miR-142-3p, and miR-17-5p) have been implicated, directly or indirectly, in fat deposition; 9 showed a high fold-change (miR-3535, miR-144-3p, miR-30e-5p, miR-301b-3p, miR-215-5p, miR-200a-3p, miR-133a-3p, miR-133c-3p, and miR-146b-5p). [score:3]
Some of the DEMs identified by deep sequencing (miR-19a-3p, miR-19b-3p, miR-30d, miR-26a, miR-30a-5p, miR-122-5p, miR-103, miR-125b, and miR-17-5p) are known to influence mammalian lipid metabolism. [score:1]
In mice, miR-122 is involved in cholesterol and lipid metabolism, as well as in the replication of hepatitis C virus 26 27. [score:1]
Changes in four lipid-related DEMs identified by deep sequencing (gga-miR-122-5p, miR-103-3p, miR-27b-3p, and miR-146b-5p) were confirmed by qPCR. [score:1]
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[+] score: 12
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-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-106a, hsa-mir-16-2, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181a-1, hsa-mir-221, hsa-mir-222, hsa-mir-223, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-23b, hsa-mir-27b, hsa-mir-122, hsa-mir-125b-1, hsa-mir-140, hsa-mir-125b-2, hsa-mir-136, hsa-mir-146a, hsa-mir-150, hsa-mir-206, hsa-mir-155, hsa-mir-181b-2, hsa-mir-106b, hsa-mir-302a, hsa-mir-34b, hsa-mir-34c, hsa-mir-302b, hsa-mir-302c, hsa-mir-302d, hsa-mir-367, gga-let-7i, gga-let-7a-3, gga-let-7b, gga-let-7c, gga-mir-125b-2, gga-mir-155, gga-mir-222a, gga-mir-221, gga-mir-92-1, gga-mir-19b, gga-mir-20a, gga-mir-19a, gga-mir-18a, gga-mir-17, gga-mir-16-1, gga-mir-15a, gga-mir-1a-2, gga-mir-206, gga-mir-223, gga-mir-106, gga-mir-302a, gga-mir-181a-1, gga-mir-181b-1, gga-mir-16-2, gga-mir-15b, gga-mir-140, gga-let-7g, gga-let-7d, gga-let-7f, gga-let-7a-1, gga-mir-146a, gga-mir-181b-2, gga-mir-181a-2, gga-mir-1a-1, gga-mir-1b, gga-let-7a-2, gga-mir-34b, gga-mir-34c, gga-let-7j, gga-let-7k, gga-mir-23b, gga-mir-27b, gga-mir-24, gga-mir-122-1, gga-mir-122-2, hsa-mir-429, hsa-mir-449a, hsa-mir-146b, hsa-mir-507, hsa-mir-455, hsa-mir-92b, hsa-mir-449b, gga-mir-146b, gga-mir-302b, gga-mir-302c, gga-mir-302d, gga-mir-455, gga-mir-367, gga-mir-429, gga-mir-449a, hsa-mir-449c, gga-mir-21, gga-mir-1458, gga-mir-1576, gga-mir-1612, gga-mir-1636, gga-mir-449c, gga-mir-1711, gga-mir-1729, gga-mir-1798, gga-mir-1811, gga-mir-146c, gga-mir-15c, gga-mir-449b, gga-mir-222b, gga-mir-92-2, gga-mir-125b-1, gga-mir-449d, gga-let-7l-1, gga-let-7l-2, gga-mir-122b-1, gga-mir-122b-2
Based on other immune related miRNA studies in mammals [11, 66], differentially expressed miRNAs of their mammalian homologs and their targets are presented in Table 9. MiR-15a, miR-21 and miR-181a have important functions in lymphocytes development and modulations while miR-122 and miR-24 are related to virus infection and miR-146a, induced by macrophages, can activate Toll like receptor (TLR) and expose antigens to interleukin-1 beta. [score:6]
In the current study, miR-122 specifically expressed in chicken lungs compared to tracheae under both infected and non-infected states. [score:2]
MiR-122 can positively affect the viral replication and has become a therapeutic target for the treatment of HCV infection [44]. [score:2]
A liver specific miRNA (miR-122) was shown to be required for Hepatitis C virus (HCV) replication in humans [43]. [score:1]
These data suggest miR-122 might play a more important role in tissue distribution than the responses to AIV infection in chickens. [score:1]
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[+] score: 10
In human, it has been reported that miR-122 may influence spermatozoa-like cells by suppressing TNP2 expression and inhibiting the expression of proteins associated with sperm development [9]. [score:10]
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[+] score: 9
The inhibition of miR-122 expression could reduce plasma cholesterol levels and decrease the synthesis rate of hepatic fatty acids and cholesterol in the mouse liver 12. [score:5]
Another example is miR-122, which is a liver-specific miRNA that regulates hepatic fatty acid oxidation and fatty acid and cholesterol synthesis rates 12 40. [score:2]
In addition, some other miRNAs, such as miR-148a, miR-122, miR-21-5p, Let-7f-5p, miR-26a-5p, miR-126-5p, miR-30d, and miR-10a-5p, were also highly abundant in chicken liver. [score:1]
A previous study demonstrated that miR-148a, miR-122, and miR-21-5p were the most abundant miRNAs in porcine liver 32. [score:1]
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[+] score: 6
Other miRNAs from this paper: gga-mir-29a,