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

Feng Hong; Keun ai Moon; Sam Soo Kim; Young Seol Kim; Young Kil Choi; Yun Soo Bae; Pann Ghill Suh; Sung Ho Ryu; Eui Ju Choi; Joohun Ha; Sung Soo Kim

doi:10.1006/bbrc.2001.4644

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

Feng Hong, Keun ai Moon, Sam Soo Kim, Young Seol Kim, Young Kil Choi, Yun Soo Bae, Pann Ghill Suh, Sung Ho Ryu, Eui Ju Choi, Joohun Ha, Sung Soo Kim

Research output: Contribution to journal › Article › peer-review

20 Citations (Scopus)

Abstract

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-γ1 (PLC-γ1). We investigated whether PLC-γ1 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-γ1 via both PI 3-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-γ1. In addition, PLC-γ1 activation was independent of Akt/protein kinase B (Akt/PKB). Importantly, PLC-γ1 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-γ1 and Akt/PKB, both of which are downstream mediators of PI 3-kinase.

Original language	English
Pages (from-to)	816-822
Number of pages	7
Journal	Biochemical and biophysical research communications
Volume	282
Issue number	3
DOIs	https://doi.org/10.1006/bbrc.2001.4644
Publication status	Published - 2001

Bibliographical note

Funding Information:
We are very grateful to Dr. Julian Downward at the Imperial Cancer Research Fund Laboratory, United Kingdom, and Dr. Masato Kasuga at Kobe University, Japan, for providing us with vectors encoding a constitutively active (p110*) and a dominant negative (Δp85) form of PI3-kinase. Dr. Feng Hong is a recipient of fellowship provided by Korea United Pharmaceutical Inc.

ASJC Scopus subject areas

Biophysics
Biochemistry
Molecular Biology
Cell Biology

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@article{ad5ec60bba9a40f4ad0db95c0ea44eb1,

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

abstract = "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-γ1 (PLC-γ1). We investigated whether PLC-γ1 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-γ1 via both PI 3-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-γ1. In addition, PLC-γ1 activation was independent of Akt/protein kinase B (Akt/PKB). Importantly, PLC-γ1 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-γ1 and Akt/PKB, both of which are downstream mediators of PI 3-kinase.",

author = "Feng Hong and Moon, {Keun ai} and Kim, {Sam Soo} and Kim, {Young Seol} and Choi, {Young Kil} and Bae, {Yun Soo} and Suh, {Pann Ghill} and Ryu, {Sung Ho} and Choi, {Eui Ju} and Joohun Ha and Kim, {Sung Soo}",

note = "Funding Information: We are very grateful to Dr. Julian Downward at the Imperial Cancer Research Fund Laboratory, United Kingdom, and Dr. Masato Kasuga at Kobe University, Japan, for providing us with vectors encoding a constitutively active (p110*) and a dominant negative (Δp85) form of PI3-kinase. Dr. Feng Hong is a recipient of fellowship provided by Korea United Pharmaceutical Inc.",

year = "2001",

doi = "10.1006/bbrc.2001.4644",

language = "English",

volume = "282",

pages = "816--822",

journal = "Biochemical and biophysical research communications",

issn = "0006-291X",

publisher = "Elsevier B.V.",

number = "3",

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TY - JOUR

T1 - Role of phospholipase C-γ1 in insulin-like growth factor I-induced muscle differentiation of H9c2 cardiac myoblasts

AU - Hong, Feng

AU - Moon, Keun ai

AU - Kim, Sam Soo

AU - Kim, Young Seol

AU - Choi, Young Kil

AU - Bae, Yun Soo

AU - Suh, Pann Ghill

AU - Ryu, Sung Ho

AU - Choi, Eui Ju

AU - Ha, Joohun

AU - Kim, Sung Soo

N1 - Funding Information: We are very grateful to Dr. Julian Downward at the Imperial Cancer Research Fund Laboratory, United Kingdom, and Dr. Masato Kasuga at Kobe University, Japan, for providing us with vectors encoding a constitutively active (p110*) and a dominant negative (Δp85) form of PI3-kinase. Dr. Feng Hong is a recipient of fellowship provided by Korea United Pharmaceutical Inc.

PY - 2001

Y1 - 2001

N2 - 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-γ1 (PLC-γ1). We investigated whether PLC-γ1 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-γ1 via both PI 3-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-γ1. In addition, PLC-γ1 activation was independent of Akt/protein kinase B (Akt/PKB). Importantly, PLC-γ1 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-γ1 and Akt/PKB, both of which are downstream mediators of PI 3-kinase.

AB - 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-γ1 (PLC-γ1). We investigated whether PLC-γ1 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-γ1 via both PI 3-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-γ1. In addition, PLC-γ1 activation was independent of Akt/protein kinase B (Akt/PKB). Importantly, PLC-γ1 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-γ1 and Akt/PKB, both of which are downstream mediators of PI 3-kinase.

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ER -

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

Abstract

Bibliographical note

ASJC Scopus subject areas

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