4.7 Article

MRCKα is a novel regulator of prolactin-induced lactogenesis in bovine mammary epithelial cells

Journal

ANIMAL NUTRITION
Volume 10, Issue -, Pages 319-328

Publisher

KEAI PUBLISHING LTD
DOI: 10.1016/j.aninu.2022.06.001

Keywords

Myotonic dystrophy-related Cdc42-binding kinase alpha; Bovine mammary gland; Prolactin; Mechanistic target of rapamycin; Sterol regulatory element-binding protein-1; Cyclin D1

Funding

  1. Natural Science Foundation of China, China [31872383]
  2. Key Research and Development Program of the Ningxia Hui Autonomous Region, China [2021BEF02018]
  3. Scienti fic Research Project for Major Achievements of the Agricultural Science and Technology Innovation Program (ASTIP) of Chinese Academy of Agricultural Sciences, China [ASTIP-IAS07-1, CAAS-XTCX2016011-01]
  4. International Atomic Energy Agency Technical Co -Operation and Assistance Programme, China [CPR5025]

Ask authors/readers for more resources

This study investigated the role of MRCK alpha in milk protein and fat production in dairy cows and found a positive correlation between MRCK alpha expression and beta-casein levels in the mammary gland. Silencing MRCK alpha in bovine mammary epithelial cells led to a decrease in basal beta-casein and cell growth, while overexpression had the opposite effect. These findings suggest that MRCK alpha plays an important role in mammary tissue development.
Myotonic dystrophy-related Cdc42-binding kinase alpha (MRCK alpha) is an integral component of signaling pathways controlling vital cellular processes, including cytoskeletal reorganization, cell proliferation and cell survival. In this study, we investigated the physiological role of MRCK alpha in milk protein and fat production in dairy cows, which requires a dynamic and strict organization of the cytoskeletal network in bovine mammary epithelial cells (BMEC). Within a selection of 9 Holstein cows, we found that both mRNA and protein expression of MRCK alpha in the mammary gland were upregulated during lactation and correlated positively (r > 0.89) with the mRNA and protein levels of beta-casein. Similar positive correlations (r > 0.79) were found in a primary culture of BMEC stimulated with prolactin for 24 h. In these cells, silencing of MRCK alpha decreased basal beta-casein, sterol-regulatory element binding protein (SREBP)-1 and cyclin D1 protein level, phosphorylation of mTOR, triglyceride secretion, cell number and viability-while overexpression of MRCK alpha displayed the reversed effect. Notably, silencing of MRCK alpha completely prevented the stimulatory action of prolactin on the same parameters. These data demonstrate that MRCK alpha is a critical mediator of prolactin-induced lactogenesis via stimulation of the mTOR/SREBP1/cyclin D1 signaling pathway. (C) 2022 Chinese Association of Animal Science and Veterinary Medicine. Publishing services by Elsevier B.V. on behalf of KeAi Communications Co. Ltd.

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