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miRNA-29a targets COL3A1 to regulate the level of type III collagen in pig

COL3A1 encodes the protein, collagen type III alpha 1, which is an important component of collagen. Collagen can have a considerable effect on the processing quality of meat, and is nutritious. Bioinformatic analysis using Targetscan showed that COL3A1 could be a target gene of miRNA-29a. Moreover,...

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Published in:Gene 2016-10, Vol.592 (1), p.140-147
Main Authors: Chuan-hao, Li, Wei, Chen, Jia-qing, Hu, Yan-dong, Wang, Shou-dong, Wang, Yong-qing, Zeng, Hui, Wang
Format: Article
Language:English
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Summary:COL3A1 encodes the protein, collagen type III alpha 1, which is an important component of collagen. Collagen can have a considerable effect on the processing quality of meat, and is nutritious. Bioinformatic analysis using Targetscan showed that COL3A1 could be a target gene of miRNA-29a. Moreover, we found that Laiwu pigs have higher levels of type III collagen and lower levels of miRNA-29a than Landrace pigs. Therefore, we hypothesized that miRNA-29a suppresses the expression of COL3A1 by targeting its 3′-UTR. miRNA-29a appears to play an inhibitory role in the regulation of COL3A1 in PK15 cells because of the following: (1) overexpression of miRNA-29a resulted in a significant down-regulation of COL3A1 protein levels (2) overexpression of miRNA-29a significantly decreased the level of COL3A1 mRNA. (3) The activity of a COL3A1 luciferase reporter was significant reduced by miRNA-29a. Furthermore, the levels of miRNA-29a and collagen type III in four tissues in Laiwu and Landrace pigs were consistent with the above observations. In this study, we identified COL3A1 as a direct target for miRNA-29a, which will inform further studies of meat quality. •Laiwu pigs have higher levels of type III collagen and lower levels of miRNA-29a than Landrace pigs.•COL3A1 is a direct target for miRNA-29a in pig.•The levels of miRNA-29a and collagen type III in four tissues in pigs were consistent with the observations in PK15 cell.
ISSN:0378-1119
1879-0038
DOI:10.1016/j.gene.2016.07.068