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Enhancement and Co-Localization of Erk and Collagens in Human Myocardium with Congestive Heart Failure

Published online by Cambridge University Press:  02 July 2020

Y. Dong ,
R. Lin  and
C Wei
Y. Dong
Affiliation:
Cardiovascular Molecular Research, Department of Surgery, University of Maryland School of Medicine, Baltimore, MD, 21201
R. Lin
Affiliation:
Cardiovascular Molecular Research, Department of Surgery, University of Maryland School of Medicine, Baltimore, MD, 21201
C Wei
Affiliation:
Cardiovascular Molecular Research, Department of Surgery, University of Maryland School of Medicine, Baltimore, MD, 21201
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Abstract

Mechanical stimuli frequently trigger signals leading to increase gene expression, protein synthesis, or mitogenesis. Cardiac fibroblasts respond to changes in ventricular hemodynamic loading by increasing matrix production in models of pressure-overload hypertrophy and myocardial infarction. Recent studies have identified some of the intracellular signaling pathways that mediate the biological effects observed upon mechanical stimulation in vitro. These include mitogenactivated protein kinases (MAPKs) and protein kinase C (PKC) family. MAPKs include extracellular signal-regulated kinase (ERK), C-Jun NH2-terminal kinase (JNK), and p38 MAPK. ERK pathway is frequently stimulated in response to mitogen.

Previous studies demonstrated that mechanical stretch stimulated MAPK activities in normal adult rat cardiac fibroblasts. On the other hand, mechanical stretch also increases transcription and production of the matrix proteins collagen (type I and HI) and fibronectin in cardiac fibroblasts. MAPKs are activated by mechanical stretch during cardiac myocytes hypertrophy through both PKCdependent and independent pathways.

Type
Pathology
Information
Microscopy and Microanalysis , Volume 7 , Issue S2: Proceedings: Microscopy & Microanalysis 2001, Microscopy Society of America 59th Annual Meeting, Microbeam Analysis Society 35th Annual Meeting, Long Beach, California August 5-9, 2001 , August 2001 , pp. 648 - 649
Copyright
Copyright © Microscopy Society of America 2001

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References

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5.This research was supported in part by grants from the NIH (HL03174 & HL61299, C. Wei), AHAMD, NKF and University of Maryland School of Medicine.Google Scholar