sort by

4 publications mentioning gga-mir-218-1

Open access articles that are associated with the species Gallus gallus and mention the gene name mir-218-1. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 113
Overexpression and knockdown of miR-218-5p in primary hepatocytes significantly up- and down-regulated ELOVL5 expression at both transcriptional and translational levels. [score:11]
To overexpress or knockdown miR-218-5p, chicken hepatocytes were seeded at a density of 1.5 × 105 cells/mL in 6-well plates for 24 h and transfected with miR-218-5p mimics (50 nM) or a negative control (50 nM), miR-218-5p Inhibitors (50 nM) or Inhibitors NC (50 nM) using the TurboFect Transfection Reagent (Thermo Scientific, Waltham, MA, USA) according to the manufacturer’s protocol. [score:8]
The expression level of miR-218-5p, miR-30-5p and miR-19-3p was downregulated by estrogen. [score:6]
Interestingly, we also found that miRNA-218-5p was co-expressed with the host gene SLIT2, which was suppressed by estrogen. [score:5]
Host Gene SLIT2 Inhibition by Estrogen and Co-Expressed with miR-218-5p. [score:5]
This result suggests that the expressions of miR-218-5p and SLIT2 mRNA are co-regulated in chicken liver at different developmental stages. [score:5]
In contrast, miR-218-5p -inhibitor increased ELOVL5 expression at 12, 24, and 48 h (Figure 4E). [score:5]
As shown in Figure 3A, miR-218-5p, miR-30a-5p, miR-30b-5p, miR-30e-5p, miR-19a-3p, and miR-19b-3p were significantly downregulated in 17 β-estradiol treated groups (p < 0.01). [score:4]
These data suggest the possibility that miR-218-5p negatively regulates the expression of ELOVL5 in chicken liver. [score:4]
To verify whether the expression of SLIT2 mRNA was regulated by estrogen, the expression level of SLIT2 and miR-218-5p were investigated in the livers and primary hepatocytes of chickens treated with 17 β-estradiol. [score:4]
Furthermore, we observed that miR-218-5p could directly target ELOVL5. [score:4]
The expression level of miR-218-5p was negatively correlated with the mRNA level of ELOVL5 in the liver at different developmental stages (Pearson correlation r = −0.906, p = 0.034). [score:4]
The correlation coefficient between miR-218-5p and SLIT2 mRNA expression in chicken liver at different developmental stages was 0.83 (p < 0.05) (data not shown). [score:4]
Overexpression of miR-218-5p in chicken hepatocytes significantly decreased ELOVL5 mRNA and protein level (p < 0.05) (Figure 3A,B and Figure 4E). [score:3]
This trend was consistent with expression of miR-218-5p in the liver from 10- to 35-week-old chickens (Figure 5B). [score:3]
Luciferase assay revealed that miR-218-5p significantly reduced the Rluc activity of the wild-type ELOVL5 reporter vector (ELOVL5-UTR-WT) in DF1 cells, whereas point mutations of target sites bound by the seed region of miR-218-5p in the 3′UTR of ELOVL5 did not disturb luciferase activity (Figure 4D). [score:3]
Three miRNA clusters (miR-218-5p, miR-19-3p, and miR-30-5p) from 46 differentially expressed miRNA were found to potentially bind to the 3′UTR of ELOVL5 in the present study (Figure 2B). [score:3]
To evaluate the possibility that ELOVL5 expression is negatively regulated by candidate miRNA under normal physiological conditions, miR-218-5p and ELOVL5 mRNA in chicken liver at different developmental stages were detected by qPCR. [score:3]
The double luciferase reporter assay performed by pcDNA3.1 and psiCheck2 vector system indicated a direct targeting interaction between miR-218-5p and the 3′UTR of ELOVL5. [score:3]
The results showed that the expression of miR-218-5p increased before 20 weeks of age and decreased after 20 weeks of age, whereas that of ELOVL5 mRNA tended to have the opposite change (Figure 4B). [score:3]
To investigate whether miR-218-5p was decreased due to the host gene SLIT2, resulting in the upregulation of ELOVL5 after 20 weeks of age in the liver of laying hens, miR-218-5p and ELOVL5 mRNA in chicken liver at different developmental stages were detected using qPCR. [score:3]
To determine if miR-218-5p targets the ELOVL5 3′UTR, DF1 cells were seeded in 12-well plates in triplicate and transfected with a wild-type or mutant construct in serum-free DMEM medium. [score:3]
The results showed that the expression of SLIT2 and miR-218-5p decreased significantly with the increase of estradiol concentration in vitro and in vivo (p < 0.01 and p < 0.05) (Figure 5C–H). [score:3]
The correlation coefficient between miR-218-5p and ELOVL5 mRNA in chicken liver at different developmental stages was −0.906 (p = 0.034) in the present study (data not shown). [score:2]
To verify the direct binding between miR-218-5p and ELOVL5, a 3′UTR fragment with seed region binding site was inserted into the 3′UTR of a Renilla luciferase (Rluc) gene of the psiCHECK-2 vector (Figure 4A). [score:2]
Verification of the Interaction between miR-218-5p and ELOVL5. [score:1]
A mutant 3′UTR of ELOVL5 reporter was generated by mutating the seed region of the miR-218-5p binding sites by overlapping extension PCR, named psiCHECK2-ELOVL5-3′UTR-Mut (Figure S4). [score:1]
In addition, the expression level of miR-218-5p and ELOVL5 were measured in 16 liver tissue samples at peak- and later laying-period (35–55 weeks old). [score:1]
The putative miR-218-5p -binding sites at ELOVL5 3′UTR are evolutionarily conserved across species (Figure 4A). [score:1]
Results indicated that miR-218-5p was inversely correlated with ELOVL5 in laying hens (r = −0.97, p < 0.001) (Figure 4C). [score:1]
Among them, we found the seed sequences of miR-218-5p, miR-19a-3p, miR-19b-3p, miR-30a-5p, miR-30b-5p, miR-30d-5p, and miR-30e-5p were complementary with the 3′UTR of ELOVL5 (Figure 3A). [score:1]
The 3′UTR of ELOVL5 containing a miR-218-5p binding site was amplified from chicken genome DNA by PCR, and cloned into the XhoI–NotI site of the psiCHECK-2 vector (Promega, Maddison, WI, USA), named psiCHECK2-ELOVL5-3′UTR-WT. [score:1]
Two miRNA (miR-124a-3p and miR-124b) and four miRNA clusters (miR-19-3p, miR-218-5p, miR-124-3p, and miR-30-5p) shared by three databases were found to be potentially combine the 3′UTR of ELOVL5, respectively (Figure 2A,B and Figure S3). [score:1]
The DNA sequence encoding the miR-218-5p precursor was PCR amplified from chicken genomic DNA. [score:1]
miR-218-5p was found to be encoded from the intron 14 of slit guidance ligand 2 (SLIT2) gene in the chicken genome (Figure 5A). [score:1]
[1 to 20 of 35 sentences]
2
[+] score: 5
Last but not least, expression levels of 10 miRNAs can be perturbed in animals when fed with high-fat diet (miR-142–5p and miR-101) [74– 78], or with obesity or obesity-related diseases (miR-10a, miR-218, miR-429, miR-200a, miR-200b, miR-451, miR-142–3p, and miR-454) [77, 79– 85], which indicates that they could be potentially related to adipogenesis. [score:5]
[1 to 20 of 1 sentences]
3
[+] score: 5
In this study, FADS1 was targeted by miR-365-3p, miR-218-5p, miR-181a-5p, miR-181b-5p, miR-29a-3p, and miR-23b-3p, whereas FADS2 was targeted by miR-30c-1-3p. [score:5]
[1 to 20 of 1 sentences]
4
[+] score: 5
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-mir-15a, hsa-mir-18a, hsa-mir-33a, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-107, mmu-mir-27b, mmu-mir-126a, mmu-mir-128-1, mmu-mir-140, mmu-mir-146a, mmu-mir-152, mmu-mir-155, mmu-mir-191, hsa-mir-10a, hsa-mir-211, hsa-mir-218-1, hsa-mir-218-2, mmu-mir-297a-1, mmu-mir-297a-2, hsa-mir-27b, hsa-mir-128-1, hsa-mir-140, hsa-mir-152, hsa-mir-191, hsa-mir-126, hsa-mir-146a, mmu-let-7a-1, mmu-let-7a-2, mmu-mir-15a, mmu-mir-18a, mmu-mir-103-1, mmu-mir-103-2, mmu-mir-342, hsa-mir-155, mmu-mir-107, mmu-mir-10a, mmu-mir-218-1, mmu-mir-218-2, mmu-mir-33, mmu-mir-211, hsa-mir-374a, hsa-mir-342, gga-mir-33-1, gga-let-7a-3, gga-mir-155, gga-mir-18a, gga-mir-15a, gga-mir-103-2, gga-mir-107, gga-mir-128-1, gga-mir-140, gga-let-7a-1, gga-mir-146a, gga-mir-103-1, gga-mir-218-2, gga-mir-126, gga-let-7a-2, gga-mir-27b, mmu-mir-466a, mmu-mir-467a-1, hsa-mir-499a, hsa-mir-545, hsa-mir-593, hsa-mir-600, hsa-mir-33b, gga-mir-499, gga-mir-211, gga-mir-466, mmu-mir-675, mmu-mir-677, mmu-mir-467b, mmu-mir-297b, mmu-mir-499, mmu-mir-717, hsa-mir-675, mmu-mir-297a-3, mmu-mir-297a-4, mmu-mir-297c, mmu-mir-466b-1, mmu-mir-466b-2, mmu-mir-466b-3, mmu-mir-466c-1, mmu-mir-466e, mmu-mir-466f-1, mmu-mir-466f-2, mmu-mir-466f-3, mmu-mir-466g, mmu-mir-466h, mmu-mir-467c, mmu-mir-467d, mmu-mir-466d, hsa-mir-297, mmu-mir-467e, mmu-mir-466l, mmu-mir-466i, mmu-mir-466f-4, mmu-mir-466k, mmu-mir-467f, mmu-mir-466j, mmu-mir-467g, mmu-mir-467h, hsa-mir-664a, hsa-mir-1306, hsa-mir-1307, gga-mir-1306, hsa-mir-103b-1, hsa-mir-103b-2, gga-mir-10a, mmu-mir-1306, mmu-mir-3064, mmu-mir-466m, mmu-mir-466o, mmu-mir-467a-2, mmu-mir-467a-3, mmu-mir-466c-2, mmu-mir-467a-4, mmu-mir-466b-4, mmu-mir-467a-5, mmu-mir-466b-5, mmu-mir-467a-6, mmu-mir-466b-6, mmu-mir-467a-7, mmu-mir-466b-7, mmu-mir-467a-8, mmu-mir-467a-9, mmu-mir-467a-10, mmu-mir-466p, mmu-mir-466n, mmu-mir-466b-8, hsa-mir-466, hsa-mir-3173, hsa-mir-3618, hsa-mir-3064, hsa-mir-499b, mmu-mir-466q, hsa-mir-664b, gga-mir-3064, mmu-mir-126b, gga-mir-33-2, mmu-mir-3618, mmu-mir-466c-3, gga-mir-191
Out of the 26 miRNA/host gene pairs with coordinated expression, 11 have been found to be coordinately expressed in both, human and mouse [19], [27], [59], [61]– [64], [67]– [69], [71], [73]– [79]: mir-103/ PANK3, mir-107/ PANK1, mir-126/ EGFL7, mir-128-1/ R3HDM1, mir-140/ WWP2, mir-211/ TRPM1, mir-218-1/ SLIT2, mir-218-2/ SLIT3, mir-27b/ C9orf3, mir-33/ SREBF2, and mir-499/ MYH7B. [score:5]
[1 to 20 of 1 sentences]