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[Parathyroid hormone 1-34 induce cardiac myocytes hypertrophy via extracellular regulated protein kinase 1/2 pathway]

Xiao-gang Liu1, Hui-xia An, Su-yan Liu

  • 1Department of Nephrology, Second Hospital, Harbin Medical University, Harbin 150086, China.

Zhonghua Xin Xue Guan Bing Za Zhi
|December 23, 2008
PubMed
Abstract

Insights

Rat parathyroid hormone (PTH) induces cardiac hypertrophy by activating ERK1/2. MEK1 inhibition with PD98059 effectively reduces this PTH-induced cardiac hypertrophy in vitro.

Area of Science:

  • Cardiovascular Biology
  • Molecular Cardiology
  • Cell Signaling

Background:

  • Cardiac hypertrophy is a significant risk factor for heart failure.
  • Parathyroid hormone (PTH) has been implicated in cardiovascular remodeling.
  • The mitogen-activated protein kinase (MAPK) pathway, including MEK1 and ERK1/2, plays a crucial role in cellular growth and differentiation.

Purpose of the Study:

  • To investigate the role of mitogen activated protein kinase kinase 1 (MAPKK, MEK1) and extracellular signal-regulated kinase 1/2 (ERK1/2) in cardiac hypertrophy induced by rat parathyroid hormone (rPTH1-34).

Main Methods:

  • Neonatal rat cardiomyocytes were treated with rPTH1-34 in the presence or absence of PD98059, a MEK1 inhibitor.
  • Measurements included cellular diameter, protein synthesis rate (3H-leucine incorporation), atrial natriuretic peptide (ANP) mRNA expression, and ERK1/2/p-ERK1/2 protein levels.

Main Results:

  • rPTH1-34 significantly increased cardiomyocyte size, protein synthesis, and ANP mRNA expression.
  • These hypertrophic effects were significantly attenuated by PD98059.
  • PD98059 inhibited the rPTH1-34-induced increase in phosphorylated ERK1/2 (p-ERK1/2) protein expression.

Conclusions:

  • MEK1 and ERK1/2 signaling are critical mediators of rPTH1-34-induced cardiac hypertrophy in vitro.
  • Inhibiting MEK1 with PD98059 effectively attenuates PTH-induced cardiac hypertrophy by suppressing ERK1/2 activation.

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