Activation of MEK-ERK by heregulin-β1 promotes the development of cardiomyocytes derived from ES cells

Hoe Suk Kim; Jin Won Cho; Kyoko Hidaka; Takayuki Morisaki

doi:10.1016/j.bbrc.2007.07.045

Activation of MEK-ERK by heregulin-β1 promotes the development of cardiomyocytes derived from ES cells

Hoe Suk Kim, Jin Won Cho, Kyoko Hidaka, Takayuki Morisaki

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Abstract

We have previously shown that heregulin-beta1 (HRG-β1) was involved in the development and survival of cardiomyocytes derived from embryonic stem (ES) cells. This study was conducted to investigate the intracellular signal mechanisms by which HRG-β1 stimulates cardiogenesis in ES cells. The treatment with ErbB receptor inhibitor decreased the population of cardiomyocytes and transcripts levels of cardiac genes (Nkx2.5, β-MHC, cTnI, and MLC2a). The phosphorylation of ERK and development of cardiomyocytes by treatment with HRG-β1 was suppressed upon treatment with MEK1 inhibitor. Furthermore, cardiomyocytes and level of MHC protein were significantly increased by overexpression of wild type MEK1 or constitutive active MEK1, but not dominant negative MEK1. These results suggest that HRG-β1 promotes the development of cardiomyocytes predominantly by activation of MEK-ERK.

Original language	English
Pages (from-to)	732-738
Number of pages	7
Journal	Biochemical and Biophysical Research Communications
Volume	361
Issue number	3
DOIs	https://doi.org/10.1016/j.bbrc.2007.07.045
Publication status	Published - 2007 Sept 28

Bibliographical note

Funding Information:
This work was supported by the Korea Research Foundation Grant funded by the Korean Government (MOEHRD)(KRF-2005-003-E00008, in part KRF-2006-311-C00399 and KRF-2004-005-C00112), in part by SRC program of MOST/KOSEF #R112000078020010(PNRC) and by Brain Korea 21(BK21) program. H.S. Kim was fellowship awardee by BK21 program.

All Science Journal Classification (ASJC) codes

Biophysics
Biochemistry
Molecular Biology
Cell Biology

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10.1016/j.bbrc.2007.07.045

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title = "Activation of MEK-ERK by heregulin-β1 promotes the development of cardiomyocytes derived from ES cells",

abstract = "We have previously shown that heregulin-beta1 (HRG-β1) was involved in the development and survival of cardiomyocytes derived from embryonic stem (ES) cells. This study was conducted to investigate the intracellular signal mechanisms by which HRG-β1 stimulates cardiogenesis in ES cells. The treatment with ErbB receptor inhibitor decreased the population of cardiomyocytes and transcripts levels of cardiac genes (Nkx2.5, β-MHC, cTnI, and MLC2a). The phosphorylation of ERK and development of cardiomyocytes by treatment with HRG-β1 was suppressed upon treatment with MEK1 inhibitor. Furthermore, cardiomyocytes and level of MHC protein were significantly increased by overexpression of wild type MEK1 or constitutive active MEK1, but not dominant negative MEK1. These results suggest that HRG-β1 promotes the development of cardiomyocytes predominantly by activation of MEK-ERK.",

author = "Kim, {Hoe Suk} and Cho, {Jin Won} and Kyoko Hidaka and Takayuki Morisaki",

note = "Funding Information: This work was supported by the Korea Research Foundation Grant funded by the Korean Government (MOEHRD)(KRF-2005-003-E00008, in part KRF-2006-311-C00399 and KRF-2004-005-C00112), in part by SRC program of MOST/KOSEF #R112000078020010(PNRC) and by Brain Korea 21(BK21) program. H.S. Kim was fellowship awardee by BK21 program.",

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N2 - We have previously shown that heregulin-beta1 (HRG-β1) was involved in the development and survival of cardiomyocytes derived from embryonic stem (ES) cells. This study was conducted to investigate the intracellular signal mechanisms by which HRG-β1 stimulates cardiogenesis in ES cells. The treatment with ErbB receptor inhibitor decreased the population of cardiomyocytes and transcripts levels of cardiac genes (Nkx2.5, β-MHC, cTnI, and MLC2a). The phosphorylation of ERK and development of cardiomyocytes by treatment with HRG-β1 was suppressed upon treatment with MEK1 inhibitor. Furthermore, cardiomyocytes and level of MHC protein were significantly increased by overexpression of wild type MEK1 or constitutive active MEK1, but not dominant negative MEK1. These results suggest that HRG-β1 promotes the development of cardiomyocytes predominantly by activation of MEK-ERK.

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Activation of MEK-ERK by heregulin-β1 promotes the development of cardiomyocytes derived from ES cells

Abstract

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