PRL/microRNA-183/IRS1 Pathway Regulates Milk Fat Metabolism in Cow Mammary Epithelial Cells

Abstract

The aim of the study was to understand the internal relationship between milk quality and lipid metabolism in cow mammary glands. A serial of studies was conducted to assess the molecular mechanism of PRL/microRNA-183/IRS1 (Insulin receptor substrate) pathway, which regulates milk fat metabolism in dairy cows. microRNA-183 (miR-183) was overexpressed and inhibited in cow mammary epithelial cells (CMECs), and its function was detected. The function of miR-183 in inhibiting milk fat metabolism was clarified by triglycerides (TAG), cholesterol and marker genes. There is a CpG island in the 5′-flanking promoter area of miR-183, which may inhibit the expression of miR-183 after methylation. Our results showed that prolactin (PRL) inhibited the expression of miR-183 by methylating the 5′ terminal CpG island of miR-183. The upstream regulation of PRL on miR-183 was demonstrated, and construction of the lipid metabolism regulation network of microRNA-183 and target gene IRS1 was performed. These results reveal the molecular mechanism of PRL/miR-183/IRS1 pathway regulating milk fat metabolism in dairy cows, thus providing an experimental basis for the improvement of milk quality.

The Association Between Prolactin and Metabolic Parameters in PCOS Women: A Retrospective Analysis

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Epigenetics: New Insights into Mammary Gland Biology

“…In goats, the analysis of the correlation between differentially expressed miRNAs in mammary tissue and the fatty acid composition of milk allowed to determine that the miR-183 level is highly and positively correlated with the fatty acid content in milk and that miR-183 inhibits milk fat metabolism by targeting Mammalian Ste20-like kinase 1 (Mst1) [ 185 ]. Recently, in research undertaken to better understand the internal relationship between milk quality and lipid metabolism in cows, Jiao et al [ 186 ] showed that miR-183 contains a CpG island in its promoter region and that Prl inhibits its expression by methylation of this region. The downregulation of miR-183 in turn leads to the upregulation of the expression of the target gene Irs1 , which ultimately leads to changes in fatty acid metabolism.…”