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4 publications mentioning rno-mir-291b

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-291b. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 150
org) analysis tool [22], ~350 miR291b -targeted genes were retrieved with a target prediction score greater than 60; predicted target scores greater than 60 indicate a high likelihood of miRNA binding to a particular target (Supplemental Table  1). [score:9]
While the increase in miR291b expression in non-parenchymal cells is consistent with our data from Kupffer cells after chronic ethanol feeding, induction of miR291b in hepatocytes may also be of pathophysiological significance, as miR291b-3p has been reported to induce hepatocyte apoptosis by downregulating HuR and Bcl-2 expression [28] and also impact glucose and lipid homeostasis in hepatocytes 29, 30. [score:8]
Transfection with a miR291b hairpin inhibitor, but not with a control hairpin, increased Tollip protein expression (Fig.   5B) and normalized LPS-stimulated expression of TNFα mRNA (Fig.   5C). [score:7]
Here we have identified miR291b as an additional miR up-regulated by chronic ethanol that contributes to sensitization of TLR2/4 signaling by decreasing the expression of Tollip, a negative regulator of MyD88 -dependent signaling (Fig.   6). [score:7]
In summary, here we have identified a miR291b -mediated down-regulation of Tollip expression in Kupffer cells from ethanol-fed rats that contributes to the sensitization of TLR2/4 signaling after chronic ethanol (Fig.   6). [score:6]
Expression of miR291b and Tollip, as well as TLR2/4-stimulated TNFα expression can be normalized by treatment of Kupffer cells with HA35. [score:5]
Expression of Tollip protein was lower in Kupffer cells from ethanol-fed rats and increased by HA35 or the presence of a miR291b hairpin inhibitor. [score:5]
Importantly, treatment of Kupffer cells from ethanol-fed rats with either HA35 or a miR291b inhibitor restored Tollip expression and normalized TLR4 sensitivity (Fig.   5). [score:5]
If increased expression of miR291b modulated Tollip expression, then we would expect to see less Tollip protein in Kupffer cells from ethanol-fed rats. [score:5]
Treatment of Kupffer cells from ethanol-fed rats with HA35 ex vivo decreased the expression of miR291b and increased Tollip, reducing the sensitivity of Kupffer cells to TLR2/TLR4 -mediated TNFα expression. [score:5]
Based on these in silico analyses, we predicted that increased expression of miR291b in response to ethanol feeding would decrease the expression of Tollip protein. [score:5]
If the HA35 -mediated reduction in miR291b expression mediated the ethanol -induced increase in the quantity of Tollip protein, then transfection of a miR291b hairpin inhibitor should normalize Tollip protein, as well as TLR4 signaling, in Kupffer cells from ethanol-fed rats. [score:5]
Chronic ethanol feeding increases the expression of miR291b which in turn results in decreased expression of Tollip. [score:5]
In order to confirm a role for CD44 in mediating the impact of HA35 on expression of miR291b, Kupffer cells were nucleofected with scrambled siRNA or siRNA targeting CD44. [score:5]
Short-term ethanol feeding increased expression of miR291b in liver; both hepatocytes and non-parenchymal cells exhibited expression as assessed via in situ hybridization (Fig.   4F). [score:5]
Chronic ethanol feeding decreased the expression of miR291b in Kupffer cells and treatment with HA35 restored expression via a CD44 -dependent mechanism. [score:5]
Importantly, Tollip, a negative regulator of TLR4-MyD88-IRAK signaling 9, 10, was identified as a target of miR291b. [score:4]
If miR291b regulates the expression of Tollip, we hypothesized that it could be a critical mediator of both the sensitization of Kupffer cells from ethanol-fed rats to TLR2/TLR4 signaling, as well as the protective effects of HA35. [score:4]
Figure 5Regulation of Tollip expression by ethanol, HA35 and miR291b in primary cultures of Kupffer cells. [score:4]
Tollip, a negative regulator of the MyD88 -dependent pathway of TLR2 and TLR4 signaling, was identified to have a binding site in its 3′UTR that recognizes miR291b (Fig.   4C) with a target prediction score of 79 in both rat and mouse. [score:4]
However, when CD44 was knocked-down in Kupffer cells, expression of miR291b was not decreased by HA35 treatment (Fig.   4E). [score:4]
org), another bioinformatics tool, also confirmed Tollip as a potential target of miR291b. [score:3]
Expression of miR291b was not sensitive to pre-treatment with HA7, a small-specific sized HA fragment that does not normalize TLR4 signaling in Kupffer cells from ethanol-fed rats [8] (Fig.   4D). [score:3]
Through normalization of expression miR291b, as well as miR181b-3p [8], treatment of HA35 protected from the effects of ethanol in Kupffer cells and PBMCs from patients with AH, suggesting that HA35 has potential as a therapeutic agent for the treatment of ALD. [score:3]
Expression of miR291b was also found to be increased in the liver of mice in response to short-term ethanol feeding (Fig.   4). [score:3]
Of these miRNAs, HA35 treatment normalized the expression of only 4 miRNAs, including miR291b (Fig.   4B). [score:3]
Treatment of mice with HA35 during ethanol feeding decreased expression of miR291b in both cell types (Fig.   4F). [score:3]
Here, using TargetScan, we identified a miR291b binding site in the Tollip 3′UTR that was associated with decreased Tollip protein quantity in Kupffer cells. [score:3]
Figure 6Mo del illustrating the interactions between HA35 on expression of miR291b and Tollip in Kupffer cells from ethanol-fed rats. [score:3]
Similar to non -transfected cells, when cells were nucleofected with scrambled siRNA, miR291b expression was increased in Kupffer cells from ethanol-fed rats and normalized by treatment with HA35 (Fig.   4E). [score:3]
The reciprocal regulation of miR291b by ethanol and HA35 was confirmed by real-time PCR (Fig.   4D). [score:2]
Making use of 5′, 3′ digoxigenin-tagged Locked nucleic acid (LNA) probe, obtained from Exiqon (Denmark), miR291b was visualized in paraffin-embedded livers from pair- or ethanol-fed mice [45]. [score:1]
Interestingly, miR291b was detected in both non-parenchymal cells and hepatocytes; treatment of mice with HA35 prevented these ethanol -induced increases in both cell types. [score:1]
miR291b –positive cells were counted using Image Pro-Plus software and analyzed. [score:1]
18 h post-nucleofection, Kupffer cells were treated or not with 100 μg/ml HA35 for 5 h and expression of miR291b measured by qRT-PCR and normalized to Hs-SNORD68-11. [score:1]
Here we investigated whether short-term ethanol feeding and/or oral provision of HA35 affected the expression of hepatic miR291b. [score:1]
Paraffin-embedded livers were de-paraffinized followed by in situ hybridization for miR291b using locked nucleic acid probes tagged with digoxigenin at both the 5′and 3′ ends. [score:1]
Further, miR291b was ranked at 15 from 45 miRNAs predicted to bind to Tollip in rat and 11 from 92 miRNAs predicted to bind Tollip in mouse. [score:1]
Sequence alignment between miR291b and Tollip is illustrated. [score:1]
In situ hybridization of micro -RNA 291b in mouse liver using LNA probesMaking use of 5′, 3′ digoxigenin-tagged Locked nucleic acid (LNA) probe, obtained from Exiqon (Denmark), miR291b was visualized in paraffin-embedded livers from pair- or ethanol-fed mice [45]. [score:1]
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[+] score: 35
Notably, we found miR-222, miR-291-3p, miR-183, miR-363-3p, miR-92, miR-19a and miR-145 as down-regulated miRNAs between E11 and E13 and whose expression was negatively correlated with the expression of their predicted targets. [score:10]
Additional support for this hypothesis was provided by the miRNA-TF mRNA network analysis in Figure 8. We found four down-regulated miRNAs (miR-92, miR-183, miR-222 and miR-291-3p) that were predicted to target multiple TFs, which were up-regulated in E13 ENPs. [score:9]
Focusing on the down-regulated miRNAs that had a significant negative correlation in Figure 6, we performed network analysis and identified miR-92, miR-183, miR-222 and miR-291-3p as predicted to target multiple TFs that were up-regulated in E13 ENPs (Figure 8). [score:9]
The number of mRNAs down-regulated between E11 and E13 encoding proteins involved in cell cycle regulation (see additional file 3), and the expression of miR-290, miR-291-3p, and miR-292-3p, are interpreted as an indication of the proliferative phenotype of the E11 ENPs, which likely contain cells that are only a cell division away from neural stem cells. [score:7]
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[+] score: 7
Other miRNAs from this paper: rno-mir-216a, rno-mir-291a, rno-mir-543, rno-mir-760, rno-mir-490
Displaying the most significant KEGG pathways predicted to be targeted by the indicated miRNAs for A) miR-18b-5p, B) miR-291-3p, C) miR-760-5p and D) miR-367-3p. [score:3]
0160318.g005 Fig 5Displaying the most significant KEGG pathways predicted to be targeted by the indicated miRNAs for A) miR-18b-5p, B) miR-291-3p, C) miR-760-5p and D) miR-367-3p. [score:3]
miR-18b-5p and miR-291-3p were identified in the medial habenula. [score:1]
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[+] score: 5
Members of the miR-290-295 cluster (miR-290, miR-291a, miR-292, miR-291b, miR-293, miR-294 and miR-295-1) were the most abundant among known miRNAs that were upregulated in rat PSCs. [score:4]
Some miRNAs, such as miR-291, miR-294 and miR-295, can enhance reprogramming that is induced by OSK factors [22]. [score:1]
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