Abstract
Mammary gland development is controlled by several genes. Although miRNAs have been implicated in mammary gland function, the mechanism by which miR-486 regulates mammary gland development and lactation remains unclear. We investigated miR-486 expression in cow mammary gland using qRT-PCR and ISH and show that miR-486 expression was higher during the high-quality lactation period. We found that miR-486 targets phosphoinositide signaling in the cow mammary gland by directly downregulating PTEN gene expression and by altering the expression of downstream genes that are important for the function of the mammary gland, such as AKT, mTOR. We analyzed the effect of β-casein, lactose and triglyceride secretion in bovine mammary gland epithelial cells (BMECs) transfected by an inhibitor and by mimics of miR-486. Our results identify miR-486 as a downstream regulator of PTEN that is required for the development of the cow mammary gland.
Highlights
Bovine mammary glands arise from the ectoderm during embryonic development and continue to develop postnatally through puberty, pregnancy, lactation, and subsequent involution
We found that miR-486 targets phosphoinositide signaling in the cow mammary gland by directly downregulating PTEN gene expression and by altering the expression of downstream genes that are important for the function of the mammary gland, such as AKT, mTOR
To examine whether miR-486 expression depends on the stage of mammary development during the high-milk-quality lactation period (H) (Fig. 1A-1D), the low-milk-quality lactation period (L) (Fig. 1E-1H), and the pregnant period (P) (Fig. 1I-1L), we used in situ hybridization to evaluate the expression of miR-486 in bovine glandular tissue and adipose tissue (Fig. 1A)
Summary
Bovine mammary glands arise from the ectoderm during embryonic development and continue to develop postnatally through puberty, pregnancy, lactation, and subsequent involution. The mammary gland secretes milk, which provides most the nutrient requirements of the newborn offspring during the transition from pregnancy to lactation [2]. Several pathways have been shown to modulate the progression of mammary gland development. More than 100 genes have been shown to modulate various aspects of mammary physiology, from the formation of the fetus to remodeling of the gland during involution [2,3]. MicroRNAs (miRNAs) have been shown to regulate cell processes, and many miRNAs are involved in mammary gland development and tumorigenesis [4]
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