Regulation of connexin 43 gene expression by cyclical mechanical stretch in neonatal rat cardiomyocytes

Tzong Luen Wang, Yung Z. Tseng, Hang Chang

Research output: Contribution to journalArticle

50 Citations (Scopus)

Abstract

Myocardial cells respond to changes in the mechanical forces imposed on them with changes in myocardial tension in the short term and with structural remodeling in the long term. Since these responses involve intercellular communication, we have investigated regulation of the gap junction proteins, connexin 43 (C x 43), connexin 40 (C x 40) and connexin 37 (C x 37), by cyclical mechanical stretch. Results were compared with parallel experiments on c-fos and GAPDH. Twenty percent stretch of cultured rat cardiomyocytes caused a 3-fold increase in C x 43 mRNA levels by 2 h. c-fos mRNA levels increased after 30 min of stretch, whereas C x 40, C x 37, and GADPH mRNA did not change. Protein levels of C x 43 increased by 4 h and remained elevated for 16 h. New protein synthesis was not a requirement for the stretch-induced rise in C x 43 expression, since mRNA levels were unaffected by treatment with cycloheximide. In addition, mechanical stretch induced alkalization of cardiomyocytes that was antagonized by inhibiting Na-H exchanger (NHE). Gap junction potential (Gj) was concomitantly elevated. Chemical closure of Cx channels by insulin was followed by inhibition of NHE. In conclusion, cyclical mechanical stretch caused increased expression of the gap junction protein C x 43 in cardiomyocytes and also the Gj. The augmentation of C x 43 mRNA expression and its functional status were associated with activation of NHE. (C) 2000 Academic press.

Original languageEnglish
Pages (from-to)551-557
Number of pages7
JournalBiochemical and Biophysical Research Communications
Volume267
Issue number2
DOIs
Publication statusPublished - Jan 19 2000
Externally publishedYes

Fingerprint

Connexin 43
Cardiac Myocytes
Gene expression
Rats
Gene Expression
Sodium-Hydrogen Antiporter
Messenger RNA
Connexins
Gap Junctions
Cycloheximide
Proteins
Chemical activation
Insulin
Communication
Experiments

Keywords

  • Cell stretch
  • Connexin
  • Gap junctions
  • Myocardium

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology

Cite this

Regulation of connexin 43 gene expression by cyclical mechanical stretch in neonatal rat cardiomyocytes. / Wang, Tzong Luen; Tseng, Yung Z.; Chang, Hang.

In: Biochemical and Biophysical Research Communications, Vol. 267, No. 2, 19.01.2000, p. 551-557.

Research output: Contribution to journalArticle

@article{4e1a1ac519e64d4f99e7f3a560d6a54a,
title = "Regulation of connexin 43 gene expression by cyclical mechanical stretch in neonatal rat cardiomyocytes",
abstract = "Myocardial cells respond to changes in the mechanical forces imposed on them with changes in myocardial tension in the short term and with structural remodeling in the long term. Since these responses involve intercellular communication, we have investigated regulation of the gap junction proteins, connexin 43 (C x 43), connexin 40 (C x 40) and connexin 37 (C x 37), by cyclical mechanical stretch. Results were compared with parallel experiments on c-fos and GAPDH. Twenty percent stretch of cultured rat cardiomyocytes caused a 3-fold increase in C x 43 mRNA levels by 2 h. c-fos mRNA levels increased after 30 min of stretch, whereas C x 40, C x 37, and GADPH mRNA did not change. Protein levels of C x 43 increased by 4 h and remained elevated for 16 h. New protein synthesis was not a requirement for the stretch-induced rise in C x 43 expression, since mRNA levels were unaffected by treatment with cycloheximide. In addition, mechanical stretch induced alkalization of cardiomyocytes that was antagonized by inhibiting Na-H exchanger (NHE). Gap junction potential (Gj) was concomitantly elevated. Chemical closure of Cx channels by insulin was followed by inhibition of NHE. In conclusion, cyclical mechanical stretch caused increased expression of the gap junction protein C x 43 in cardiomyocytes and also the Gj. The augmentation of C x 43 mRNA expression and its functional status were associated with activation of NHE. (C) 2000 Academic press.",
keywords = "Cell stretch, Connexin, Gap junctions, Myocardium",
author = "Wang, {Tzong Luen} and Tseng, {Yung Z.} and Hang Chang",
year = "2000",
month = "1",
day = "19",
doi = "10.1006/bbrc.1999.1988",
language = "English",
volume = "267",
pages = "551--557",
journal = "Biochemical and Biophysical Research Communications",
issn = "0006-291X",
publisher = "Elsevier B.V.",
number = "2",

}

TY - JOUR

T1 - Regulation of connexin 43 gene expression by cyclical mechanical stretch in neonatal rat cardiomyocytes

AU - Wang, Tzong Luen

AU - Tseng, Yung Z.

AU - Chang, Hang

PY - 2000/1/19

Y1 - 2000/1/19

N2 - Myocardial cells respond to changes in the mechanical forces imposed on them with changes in myocardial tension in the short term and with structural remodeling in the long term. Since these responses involve intercellular communication, we have investigated regulation of the gap junction proteins, connexin 43 (C x 43), connexin 40 (C x 40) and connexin 37 (C x 37), by cyclical mechanical stretch. Results were compared with parallel experiments on c-fos and GAPDH. Twenty percent stretch of cultured rat cardiomyocytes caused a 3-fold increase in C x 43 mRNA levels by 2 h. c-fos mRNA levels increased after 30 min of stretch, whereas C x 40, C x 37, and GADPH mRNA did not change. Protein levels of C x 43 increased by 4 h and remained elevated for 16 h. New protein synthesis was not a requirement for the stretch-induced rise in C x 43 expression, since mRNA levels were unaffected by treatment with cycloheximide. In addition, mechanical stretch induced alkalization of cardiomyocytes that was antagonized by inhibiting Na-H exchanger (NHE). Gap junction potential (Gj) was concomitantly elevated. Chemical closure of Cx channels by insulin was followed by inhibition of NHE. In conclusion, cyclical mechanical stretch caused increased expression of the gap junction protein C x 43 in cardiomyocytes and also the Gj. The augmentation of C x 43 mRNA expression and its functional status were associated with activation of NHE. (C) 2000 Academic press.

AB - Myocardial cells respond to changes in the mechanical forces imposed on them with changes in myocardial tension in the short term and with structural remodeling in the long term. Since these responses involve intercellular communication, we have investigated regulation of the gap junction proteins, connexin 43 (C x 43), connexin 40 (C x 40) and connexin 37 (C x 37), by cyclical mechanical stretch. Results were compared with parallel experiments on c-fos and GAPDH. Twenty percent stretch of cultured rat cardiomyocytes caused a 3-fold increase in C x 43 mRNA levels by 2 h. c-fos mRNA levels increased after 30 min of stretch, whereas C x 40, C x 37, and GADPH mRNA did not change. Protein levels of C x 43 increased by 4 h and remained elevated for 16 h. New protein synthesis was not a requirement for the stretch-induced rise in C x 43 expression, since mRNA levels were unaffected by treatment with cycloheximide. In addition, mechanical stretch induced alkalization of cardiomyocytes that was antagonized by inhibiting Na-H exchanger (NHE). Gap junction potential (Gj) was concomitantly elevated. Chemical closure of Cx channels by insulin was followed by inhibition of NHE. In conclusion, cyclical mechanical stretch caused increased expression of the gap junction protein C x 43 in cardiomyocytes and also the Gj. The augmentation of C x 43 mRNA expression and its functional status were associated with activation of NHE. (C) 2000 Academic press.

KW - Cell stretch

KW - Connexin

KW - Gap junctions

KW - Myocardium

UR - http://www.scopus.com/inward/record.url?scp=0034685023&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0034685023&partnerID=8YFLogxK

U2 - 10.1006/bbrc.1999.1988

DO - 10.1006/bbrc.1999.1988

M3 - Article

C2 - 10631100

AN - SCOPUS:0034685023

VL - 267

SP - 551

EP - 557

JO - Biochemical and Biophysical Research Communications

JF - Biochemical and Biophysical Research Communications

SN - 0006-291X

IS - 2

ER -