Dihydropyridine receptor gene expression in skeletal muscle from mdx and control mice

Yann Péréon, Christine Dettbarn, Javier Navarro, Jacques Noireaud, Philip T. Palade

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

The expression of isoform-specific dihydropyrine receptor-calcium channel (DHPR) α 1-subunit genes was investigated in mdx and control mouse diaphragm (DIA) and tibialis anterior (TA). RNase protection assays were carried out with a rat DHPR cDNA probe specific for skeletal muscle and a mouse DHPR cDNA probe specific for cardiac muscle. The level of expression of the gene encoding the cardiac DHPR was very weak in TA muscle from both control and mdx mice. Compared to TA, DIA expressed mRNA for the cardiac isoform at significantly higher levels, but mdx and control mouse DIA levels were similar to one another. In contrast, mRNA expression levels for the DHPR skeletal muscle isoform were lower in control DIA than TA. However, there was a dramatic increase in the expression for the DHPR skeletal muscle isoform in mdx DIA compared with control DIA, reaching the TA expression level, whereas dystrophy did not affect TA expression. [3H]-PN200-110 binding was used to further assess DIA DHPR expression at the protein level. The density of binding sites for the probe was not significantly affected in DIA muscles of mdx vs. control mice, but it was reduced in older mdx and control mice. The increase in DHPR mRNA levels without a consequent increase in DHPR protein expression could be secondary to possible enhanced protein degradation which occurs in mdx DIA. The altered DHPR expression levels found here do not appear to be responsible for the severe deficits in contractile function of the mdx DIA.

Original languageEnglish (US)
Pages (from-to)201-207
Number of pages7
JournalBiochimica et Biophysica Acta - Molecular Basis of Disease
Volume1362
Issue number2-3
DOIs
StatePublished - Dec 31 1997

Fingerprint

Inbred mdx Mouse
L-Type Calcium Channels
Calcium Channels
Diaphragm
Skeletal Muscle
Gene Expression
Protein Isoforms
Complementary DNA
RNA Isoforms
Muscles
Messenger RNA
Ribonucleases
Proteolysis
Myocardium
Proteins
Binding Sites

Keywords

  • [H]-PN200-110 binding
  • Diaphragm
  • Dihydropyridine receptor
  • Excitation-contraction coupling
  • mdx
  • Muscular dystrophy
  • Skeletal muscle

ASJC Scopus subject areas

  • Molecular Biology
  • Molecular Medicine
  • Biophysics

Cite this

Dihydropyridine receptor gene expression in skeletal muscle from mdx and control mice. / Péréon, Yann; Dettbarn, Christine; Navarro, Javier; Noireaud, Jacques; Palade, Philip T.

In: Biochimica et Biophysica Acta - Molecular Basis of Disease, Vol. 1362, No. 2-3, 31.12.1997, p. 201-207.

Research output: Contribution to journalArticle

Péréon, Yann ; Dettbarn, Christine ; Navarro, Javier ; Noireaud, Jacques ; Palade, Philip T. / Dihydropyridine receptor gene expression in skeletal muscle from mdx and control mice. In: Biochimica et Biophysica Acta - Molecular Basis of Disease. 1997 ; Vol. 1362, No. 2-3. pp. 201-207.
@article{220f0da6ab3c44e289eb35169f3b344a,
title = "Dihydropyridine receptor gene expression in skeletal muscle from mdx and control mice",
abstract = "The expression of isoform-specific dihydropyrine receptor-calcium channel (DHPR) α 1-subunit genes was investigated in mdx and control mouse diaphragm (DIA) and tibialis anterior (TA). RNase protection assays were carried out with a rat DHPR cDNA probe specific for skeletal muscle and a mouse DHPR cDNA probe specific for cardiac muscle. The level of expression of the gene encoding the cardiac DHPR was very weak in TA muscle from both control and mdx mice. Compared to TA, DIA expressed mRNA for the cardiac isoform at significantly higher levels, but mdx and control mouse DIA levels were similar to one another. In contrast, mRNA expression levels for the DHPR skeletal muscle isoform were lower in control DIA than TA. However, there was a dramatic increase in the expression for the DHPR skeletal muscle isoform in mdx DIA compared with control DIA, reaching the TA expression level, whereas dystrophy did not affect TA expression. [3H]-PN200-110 binding was used to further assess DIA DHPR expression at the protein level. The density of binding sites for the probe was not significantly affected in DIA muscles of mdx vs. control mice, but it was reduced in older mdx and control mice. The increase in DHPR mRNA levels without a consequent increase in DHPR protein expression could be secondary to possible enhanced protein degradation which occurs in mdx DIA. The altered DHPR expression levels found here do not appear to be responsible for the severe deficits in contractile function of the mdx DIA.",
keywords = "[H]-PN200-110 binding, Diaphragm, Dihydropyridine receptor, Excitation-contraction coupling, mdx, Muscular dystrophy, Skeletal muscle",
author = "Yann P{\'e}r{\'e}on and Christine Dettbarn and Javier Navarro and Jacques Noireaud and Palade, {Philip T.}",
year = "1997",
month = "12",
day = "31",
doi = "10.1016/S0925-4439(97)00079-3",
language = "English (US)",
volume = "1362",
pages = "201--207",
journal = "Biochimica et Biophysica Acta - Molecular Basis of Disease",
issn = "0925-4439",
publisher = "Elsevier",
number = "2-3",

}

TY - JOUR

T1 - Dihydropyridine receptor gene expression in skeletal muscle from mdx and control mice

AU - Péréon, Yann

AU - Dettbarn, Christine

AU - Navarro, Javier

AU - Noireaud, Jacques

AU - Palade, Philip T.

PY - 1997/12/31

Y1 - 1997/12/31

N2 - The expression of isoform-specific dihydropyrine receptor-calcium channel (DHPR) α 1-subunit genes was investigated in mdx and control mouse diaphragm (DIA) and tibialis anterior (TA). RNase protection assays were carried out with a rat DHPR cDNA probe specific for skeletal muscle and a mouse DHPR cDNA probe specific for cardiac muscle. The level of expression of the gene encoding the cardiac DHPR was very weak in TA muscle from both control and mdx mice. Compared to TA, DIA expressed mRNA for the cardiac isoform at significantly higher levels, but mdx and control mouse DIA levels were similar to one another. In contrast, mRNA expression levels for the DHPR skeletal muscle isoform were lower in control DIA than TA. However, there was a dramatic increase in the expression for the DHPR skeletal muscle isoform in mdx DIA compared with control DIA, reaching the TA expression level, whereas dystrophy did not affect TA expression. [3H]-PN200-110 binding was used to further assess DIA DHPR expression at the protein level. The density of binding sites for the probe was not significantly affected in DIA muscles of mdx vs. control mice, but it was reduced in older mdx and control mice. The increase in DHPR mRNA levels without a consequent increase in DHPR protein expression could be secondary to possible enhanced protein degradation which occurs in mdx DIA. The altered DHPR expression levels found here do not appear to be responsible for the severe deficits in contractile function of the mdx DIA.

AB - The expression of isoform-specific dihydropyrine receptor-calcium channel (DHPR) α 1-subunit genes was investigated in mdx and control mouse diaphragm (DIA) and tibialis anterior (TA). RNase protection assays were carried out with a rat DHPR cDNA probe specific for skeletal muscle and a mouse DHPR cDNA probe specific for cardiac muscle. The level of expression of the gene encoding the cardiac DHPR was very weak in TA muscle from both control and mdx mice. Compared to TA, DIA expressed mRNA for the cardiac isoform at significantly higher levels, but mdx and control mouse DIA levels were similar to one another. In contrast, mRNA expression levels for the DHPR skeletal muscle isoform were lower in control DIA than TA. However, there was a dramatic increase in the expression for the DHPR skeletal muscle isoform in mdx DIA compared with control DIA, reaching the TA expression level, whereas dystrophy did not affect TA expression. [3H]-PN200-110 binding was used to further assess DIA DHPR expression at the protein level. The density of binding sites for the probe was not significantly affected in DIA muscles of mdx vs. control mice, but it was reduced in older mdx and control mice. The increase in DHPR mRNA levels without a consequent increase in DHPR protein expression could be secondary to possible enhanced protein degradation which occurs in mdx DIA. The altered DHPR expression levels found here do not appear to be responsible for the severe deficits in contractile function of the mdx DIA.

KW - [H]-PN200-110 binding

KW - Diaphragm

KW - Dihydropyridine receptor

KW - Excitation-contraction coupling

KW - mdx

KW - Muscular dystrophy

KW - Skeletal muscle

UR - http://www.scopus.com/inward/record.url?scp=0031593173&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0031593173&partnerID=8YFLogxK

U2 - 10.1016/S0925-4439(97)00079-3

DO - 10.1016/S0925-4439(97)00079-3

M3 - Article

VL - 1362

SP - 201

EP - 207

JO - Biochimica et Biophysica Acta - Molecular Basis of Disease

JF - Biochimica et Biophysica Acta - Molecular Basis of Disease

SN - 0925-4439

IS - 2-3

ER -