Literature DB >> 28835435

miR-15b negatively correlates with lipid metabolism in mammary epithelial cells.

Meiqiang Chu1, Yong Zhao1, Shuai Yu1, Yanan Hao1, Pengfei Zhang1, Yanni Feng1, Hongfu Zhang2, Dongxue Ma1, Jing Liu3, Ming Cheng4, Lan Li1, Wei Shen1, Hongfang Cao5, Qiang Li5, Lingjiang Min1.   

Abstract

Mammary epithelial cells are regulated by steroid hormones, growth factors, and even microRNAs. miR-15b has been found to regulate lipid metabolism in adipocytes; however, its effects on lipid metabolism in mammary epithelial cells, the cells of lipid synthesis and secretion, are as yet unknown. The main purpose of this investigation was to explore the effect of miR-15b on lipid metabolism in mammary epithelial cells, along with the underlying mechanisms. miR-15b was overexpressed or inhibited by miRNA mimics or inhibitors; subsequently, lipid formation in mammary epithelial cells, and proteins related to lipid metabolism, were investigated. Through overexpression or inhibition of miR-15b expression, the current investigation found that miR-15b downregulates lipid metabolism in mammary epithelial cells and is expressed differentially at various stages of mouse and goat mammary gland development. Inhibition of miR-15b expression increased lipid content in mammary epithelial cells through elevation of the lipid synthesis enzyme fatty acid synthetase (FASN), and overexpression of miR-15b reduced lipid content in mammary epithelial cells with decreasing levels of FASN. Moreover, the steroid hormones estradiol and progesterone decreased miR-15b expression with a subsequent increase in lipid formation in mammary epithelial cells. The expression of miR-15b was lower during lactation and negatively correlated with lipid synthesis proteins, which suggests that it may be involved in lipid synthesis and milk production. miR-15b might be a useful target for altering lipid production and milk yield.

Entities:  

Keywords:  estradiol; lipid; mammary epithelial cells; metabolism; miR-15b; progesterone

Mesh:

Substances:

Year:  2017        PMID: 28835435     DOI: 10.1152/ajpcell.00115.2017

Source DB:  PubMed          Journal:  Am J Physiol Cell Physiol        ISSN: 0363-6143            Impact factor:   4.249


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