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Diacylglycerol kinase η regulates C2C12 myoblast proliferation through the mTOR signaling pathway.

Abstract：

:Diacylglycerol kinase (DGK) phosphorylates diacylglycerol to produce phosphatidic acid (PA). The η isozyme of DGK is abundantly expressed in C2C12 myoblasts. However, the role of DGKη in skeletal muscle cells remains unknown. In the present study, we showed that DGKη was downregulated at an early stage of myogenic differentiation. The knockdown of DGKη by siRNAs significantly inhibited C2C12 myoblast proliferation but did not inhibit differentiation. Moreover, the suppression of DGKη expression decreased the expression levels of mammalian target of rapamycin (mTOR), which is a key regulator of cell proliferation, and fatty acid synthase (FASN), which catalyzes the de novo synthesis of fatty acids for cell proliferation and is transcriptionally regulated via mTOR signaling. Furthermore, the knockdown of mTOR or raptor, which is a component of mTOR complex 1 (mTORC1), decreased the amount of FASN. These results indicate that DGKη regulates myoblast proliferation through the mTOR (mTORC1)-FASN pathway. Interestingly, the knockdown of mTOR reduced the expression levels of DGKη, implying mutual regulation between DGKη and mTOR. In DGKη-knockdown myoblasts, C30-C36-PA species, mTOR activators, were decreased, suggesting that the modulation of mTOR activity through these PA species also plays an important role in myoblast proliferation.

journal_name

Biochimie

journal_title

Biochimie

authors

Sakai H,Murakami C,Usuki T,Lu Q,Matsumoto KI,Urano T,Sakane F

doi

10.1016/j.biochi.2020.07.018

subject

Has Abstract

pub_date

2020-10-01 00:00:00

pages

13-24

eissn

0300-9084

issn

1638-6183

pii

S0300-9084(20)30172-3

journal_volume

177

pub_type

杂志文章

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