Next Article in Journal
Whole-Genome k-mer Topic Modeling Associates Bacterial Families
Next Article in Special Issue
Inhibition of Angiotensin-Converting Enzyme Ameliorates Renal Fibrosis by Mitigating DPP-4 Level and Restoring Antifibrotic MicroRNAs
Previous Article in Journal
Regulation of Mitotic Exit by Cell Cycle Checkpoints: Lessons From Saccharomyces cerevisiae
Previous Article in Special Issue
Circulatory miR-133b and miR-21 as Novel Biomarkers in Early Prediction and Diagnosis of Coronary Artery Disease
Open AccessArticle

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

1
College of Animal Science and Technology, Northeast Agricultural University, Harbin 150030, China
2
School of Nursing, Yangzhou University, Yangzhou 225009, China
3
State Key Laboratory of Livestock and Poultry Breeding, Institute of Animal Science, Guangdong Academy of Agricultural Sciences, Guangzhou 510640, China
4
College of Animal Science and Technology, Yangzhou University, Yangzhou 225009, China
*
Author to whom correspondence should be addressed.
Genes 2020, 11(2), 196; https://doi.org/10.3390/genes11020196 (registering DOI)
Received: 13 January 2020 / Revised: 5 February 2020 / Accepted: 10 February 2020 / Published: 13 February 2020
(This article belongs to the Collection microRNA Omnibus)
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. View Full-Text
Keywords: PRL; miR-183; milk fat metabolism; IRS1; dairy cows PRL; miR-183; milk fat metabolism; IRS1; dairy cows
Show Figures

Figure 1

MDPI and ACS Style

Jiao, P.; Yuan, Y.; Zhang, M.; Sun, Y.; Wei, C.; Xie, X.; Zhang, Y.; Wang, S.; Chen, Z.; Wang, X. PRL/microRNA-183/IRS1 Pathway Regulates Milk Fat Metabolism in Cow Mammary Epithelial Cells. Genes 2020, 11, 196.

Show more citation formats Show less citations formats
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Article Access Map by Country/Region

1
Back to TopTop