Role of phospholipase C-γ1 in insulin-like growth factor I-induced muscle differentiation of H9c2 cardiac myoblasts

被引:18
作者
Hong, F
Moon, KA
Kim, SS
Kim, YS
Choi, YK
Bae, YS
Suh, PG
Ryu, SH
Choi, EJ
Ha, J
Kim, SS
机构
[1] Kyung Hee Univ, Sch Med, Dept Mol Biol, Dongdaemoon Gu, Seoul 130701, South Korea
[2] Kyung Hee Univ, Sch Med, Dept Internal Med, Div Endocrinol,Dongdaemoon Gu, Seoul 130701, South Korea
[3] Kyung Hee Univ, Grad Sch Biotechnol, Seoul 130701, South Korea
[4] Pohang Univ Sci & Technol, Div Mol & Life Sci, Dept Signal Transduct, Pohang 790784, South Korea
[5] Ewha Womans Univ, Dept Biol Sci, Seoul 120750, South Korea
[6] Ewha Womans Univ, Ctr Cell Signaling Res, Seoul 120750, South Korea
关键词
D O I
10.1006/bbrc.2001.4644
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Insulin-like growth factor-I (IGF-I) regulates muscle differentiation through phosphatidylinositol 3-kinase (PI 3-kinase), Also it was recently reported that PI 3-kinase is involved in the activation of phospholipase C-gamma1 (PLC-gamma1), We investigated whether PLC-gamma1 therefore plays a role in IGF-I-induced muscle differentiation using H9c2 rat cardiac myoblasts as a model. IGF-I was able to activate PLC-gamma1 via both PI3-kinase-dependent and tyrosine phosphorylation-dependent mechanisms in this model. However, PI 3-kinase appeared to play a more important role than tyrosine phosphorylation in IGF-I activation of PLC-gamma1, In addition, PLC-gamma1. activation was independent of Akt/ protein kinase B (Akt/PKB), Importantly, PLC-gamma1 was involved in IGF-I-induced muscle differentiation in parallel with Akt/PKB, Taken together, these results suggest that IGF-I regulation of muscle differentiation is dependent on the activation of PLC-gamma1 and Akt/PKB, both of which are downstream mediators of PI 3-kinase. (C) 2001 Academic Press.
引用
收藏
页码:816 / 822
页数:7
相关论文
共 28 条
[1]   Activation of phospholipase C-γ by phosphatidylinositol 3,4,5-trisphosphate [J].
Bae, YS ;
Cantley, LG ;
Chen, CS ;
Kim, SR ;
Kwon, KS ;
Rhee, SG .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1998, 273 (08) :4465-4469
[2]   Phosphatidylinositol 3-kinase stimulates muscle differentiation by activating p38 mitogen-activated protein kinase [J].
Chun, YK ;
Kim, J ;
Kwon, S ;
Choi, SH ;
Hong, F ;
Moon, KA ;
Kim, JM ;
Choi, SL ;
Kim, BS ;
Ha, J ;
Kim, SS .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 2000, 276 (02) :502-507
[3]  
COCKCROFT S, 1992, BIOCHEM J, V288, P1
[4]  
Coffer PJ, 1998, BIOCHEM J, V335, P1
[5]   The mitogenic and myogenic actions of insulin-like growth factors utilize distinct signaling pathways [J].
Coolican, SA ;
Samuel, DS ;
Ewton, DZ ;
McWade, FJ ;
Florini, JR .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1997, 272 (10) :6653-6662
[6]   Stress-activated protein kinase-2 p38 and a rapamycin-sensitive pathway are required for C2C12 myogenesis [J].
Cuenda, A ;
Cohen, P .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1999, 274 (07) :4341-4346
[7]   Activation of phospholipase Cγ by PI 3-kinase-induced PH domain-mediated membrane targeting [J].
Falasca, M ;
Logan, SK ;
Lehto, VP ;
Baccante, G ;
Lemmon, MA ;
Schlessinger, J .
EMBO JOURNAL, 1998, 17 (02) :414-422
[8]   Growth hormone and the insulin-like growth factor system in myogenesis [J].
Florini, JR ;
Ewton, DZ ;
Coolican, SA .
ENDOCRINE REVIEWS, 1996, 17 (05) :481-517
[9]   HORMONES, GROWTH-FACTORS, AND MYOGENIC DIFFERENTIATION [J].
FLORINI, JR ;
EWTON, DZ ;
MAGRI, KA .
ANNUAL REVIEW OF PHYSIOLOGY, 1991, 53 :201-216
[10]   Myogenic signaling of phosphatidylinositol 3-kinase requires the serine-threonine kinase Akt protein kinase B [J].
Jiang, BH ;
Aoki, M ;
Zheng, JZ ;
Li, J ;
Vogt, PK .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1999, 96 (05) :2077-2081