A transcriptomics study of differentiated C2C12 myoblasts identified novel functional responses to 17-estradiol

被引：5

作者：

Ding, JingJing ^{[1
]}

Peng, ZhaoHong ^{[1
]}

Wu, Di ^{[1
]}

Miao, JiaNing ^{[1
]}

Liu, Bo ^{[1
]}

Wang, LiLi ^{[1
]}

机构：

[1] China Med Univ, Shengjing Hosp, Med Res Ctr, Shenyang 110004, Liaoning, Peoples R China

来源：

CELL BIOLOGY INTERNATIONAL | 2018年 / 42卷 / 08期

基金：

中国国家自然科学基金;

关键词：

17-estradiol; C2C12; myoblast; cell differentiation; SKELETAL-MUSCLE DIFFERENTIATION; CELL-CYCLE EXIT; MYOGENIC DIFFERENTIATION; SATELLITE CELLS; LIM PROTEIN-1; POTASSIUM CHANNELS; GROWING RATS; EXPRESSION; ESTROGEN; RECEPTOR;

D O I：

10.1002/cbin.10962

中图分类号：

Q2 [细胞生物学];

学科分类号：

071013 [干细胞生物学];

摘要：

Previous studies of the role of 17-estradiol (E2) in myoblast differentiation have produced conflicting data. Therefore, this work aimed to determine the role of E2 on myoblast differentiation and specific myofiber formation. Murine C2C12 myoblasts were cultured in proliferation medium or differentiation medium/10nM E2. The role of E2 on specific myosin heavy chain (MyHC) or estrogen receptor (ER) expression was examined using real-time quantitative RT-PCR (RT-qPCR). Transcriptome studies of E2 on myoblast differentiation were accomplished by microarray analyses. The expression levels of candidate genes from microarrays and four and a half LIM domains 1 (Fhl1) were detected with RT-qPCR. E2 in differentiation medium significantly up-regulated MyHC I expression, but exerted the opposite effects on MyHC II a, MyHC II b, and MyHC II d. Both ER- and ER- were decreased in differentiated C2C12, and E2 partially restored ER- expression. Sixty-two up-regulated and 116 down-regulated genes treated by E2 were identified, and RT-qPCR validation results showed seven cytoskeletal genes (Myh8, Cenpe, Jak3, Obscn, Ldb3, Mybpc2, Col4a3bp), three genes related to ion channels (Kcnq1, Lrrc26, P2rx3) and Fhl1 transcript 2 were associated with the effects of E2 on myoblast differentiation. These findings suggested E2 helped slow type MyH I fiber formation and impeded fast 2A, 2X/D, and 2B fiber formation.

引用

页码：965 / 974

页数：10

共 42 条

[1]

The FgfrL1 receptor is required for development of slow muscle fibers [J].