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FABP5 is a critical regulator of methionine‐ and estrogen‐induced SREBP‐1c gene expression in bovine mammary epithelial cells
Author(s) -
Li Ping,
Yu Mengmeng,
Zhou Chengjian,
Qi Hao,
Wen Xuepeng,
Hou Xiaoming,
Li Meng,
Gao Xuejun
Publication year - 2019
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.26762
Subject(s) - fatty acid binding protein , sterol regulatory element binding protein , gene expression , methionine , biology , gene , endocrinology , regulation of gene expression , mammary gland , regulator , medicine , estrogen , biochemistry , amino acid , genetics , cancer , breast cancer
The intracellular fatty acid‐binding proteins (FABPs) are a well‐conserved family that function as lipid chaperones. Ongoing studies are focused on identification of the mechanistic complexity and vast biological diversity of different isoforms of FABPs. However, the molecular mechanism of FABP5 in the regulation of milk fat synthesis in the mammary gland of dairy cows is still largely unknown. Here, we report that FABP5 acts as a critical regulator of terol response element‐binding protein‐1c (SREBP‐1c) gene expression induced by methionine (Met) and estrogen (E2) in bovine mammary epithelial cells (BMECs). We observed that the expression of FABP5 was markedly higher in dairy cow mammary tissue during the lactating period than the puberty period and the dry period. FABP5 is located in the cytoplasm, and Met and E2 significantly increase the protein levels of FABP5 in BMECs. Using gene function study approaches, we revealed that FABP5 positively regulates SREBP‐1c gene expression and promotes milk fat synthesis. We confirmed that FABP5 is required for Met‐ and E2‐induced SREBP‐1c gene expression and milk fat synthesis. We further uncovered that fatty acids are needed for FABP5‐mediated SREBP‐1c gene expression. Thus, our study demonstrates that FABP5 is a critical regulator of Met‐ and E2‐induced SREBP‐1c gene expression leading to milk fat synthesis.