Amelioration of denervation-induced atrophy by clenbuterol is associated with increased PKC-alpha activity

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Abstract

Rat soleus muscle was denervated for 3 or 7 days, and total membrane protein kinase C (PKC) activity and translocation and immunocytochemical localization of PKC isoforms were examined. Dietary administration of clenbuterol concomitant with denervation ameliorated the atrophic response and was associated with increased membrane PKC activity at both 3 (140%) and 7 (190%) days. Of the five PKC isoforms (alpha, epsilon, theta, zeta, and mu) detected in soleus muscle by Western immunoblotting, clenbuterol treatment affected only the PKC-alpha and PKC-theta forms. PKC-alpha was translocated to the membrane fraction upon denervation, and the presence of clenbuterol increased membrane-bound PKC-alpha and active PKC-alpha as assayed by Ser(657) phosphorylation. PKC-theta protein was downregulated upon denervation, and treatment with clenbuterol further decreased both cytosolic and membrane levels. Immunolocalization of PKC-theta showed differences for regulatory and catalytic domains, with the latter showing fast-fiber type specificity. The results suggest potential roles of PKC-alpha and PKC-theta in the mechanism of action of clenbuterol in alleviating denervation-induced atrophy.

Original languageEnglish
Pages (from-to)188-196
Number of pages8
JournalAmerican Journal of Physiology: Endocrinology and Metabolism
Volume279
Issue number1
Publication statusPublished - Jul 2000

Keywords

  • skeletal muscle
  • beta-agonist
  • kinase activity
  • PROTEIN-KINASE-C
  • CHICK SKELETAL-MUSCLE
  • AGONIST CLENBUTEROL
  • NPKC-THETA
  • RAT MUSCLE
  • EXPRESSION
  • MEMBRANE
  • STIMULATION
  • INSULIN
  • GROWTH

Cite this

@article{aa92277c742f443da2c8fc4a0e90665f,
title = "Amelioration of denervation-induced atrophy by clenbuterol is associated with increased PKC-alpha activity",
abstract = "Rat soleus muscle was denervated for 3 or 7 days, and total membrane protein kinase C (PKC) activity and translocation and immunocytochemical localization of PKC isoforms were examined. Dietary administration of clenbuterol concomitant with denervation ameliorated the atrophic response and was associated with increased membrane PKC activity at both 3 (140{\%}) and 7 (190{\%}) days. Of the five PKC isoforms (alpha, epsilon, theta, zeta, and mu) detected in soleus muscle by Western immunoblotting, clenbuterol treatment affected only the PKC-alpha and PKC-theta forms. PKC-alpha was translocated to the membrane fraction upon denervation, and the presence of clenbuterol increased membrane-bound PKC-alpha and active PKC-alpha as assayed by Ser(657) phosphorylation. PKC-theta protein was downregulated upon denervation, and treatment with clenbuterol further decreased both cytosolic and membrane levels. Immunolocalization of PKC-theta showed differences for regulatory and catalytic domains, with the latter showing fast-fiber type specificity. The results suggest potential roles of PKC-alpha and PKC-theta in the mechanism of action of clenbuterol in alleviating denervation-induced atrophy.",
keywords = "skeletal muscle, beta-agonist, kinase activity, PROTEIN-KINASE-C, CHICK SKELETAL-MUSCLE, AGONIST CLENBUTEROL, NPKC-THETA, RAT MUSCLE, EXPRESSION, MEMBRANE, STIMULATION, INSULIN, GROWTH",
author = "Sneddon, {Alan Arthur} and Delday, {Margaret Inkster} and Charlotte Maltin",
year = "2000",
month = "7",
language = "English",
volume = "279",
pages = "188--196",
journal = "American Journal of Physiology: Endocrinology and Metabolism",
issn = "0193-1849",
publisher = "American Physiological Society",
number = "1",

}

TY - JOUR

T1 - Amelioration of denervation-induced atrophy by clenbuterol is associated with increased PKC-alpha activity

AU - Sneddon, Alan Arthur

AU - Delday, Margaret Inkster

AU - Maltin, Charlotte

PY - 2000/7

Y1 - 2000/7

N2 - Rat soleus muscle was denervated for 3 or 7 days, and total membrane protein kinase C (PKC) activity and translocation and immunocytochemical localization of PKC isoforms were examined. Dietary administration of clenbuterol concomitant with denervation ameliorated the atrophic response and was associated with increased membrane PKC activity at both 3 (140%) and 7 (190%) days. Of the five PKC isoforms (alpha, epsilon, theta, zeta, and mu) detected in soleus muscle by Western immunoblotting, clenbuterol treatment affected only the PKC-alpha and PKC-theta forms. PKC-alpha was translocated to the membrane fraction upon denervation, and the presence of clenbuterol increased membrane-bound PKC-alpha and active PKC-alpha as assayed by Ser(657) phosphorylation. PKC-theta protein was downregulated upon denervation, and treatment with clenbuterol further decreased both cytosolic and membrane levels. Immunolocalization of PKC-theta showed differences for regulatory and catalytic domains, with the latter showing fast-fiber type specificity. The results suggest potential roles of PKC-alpha and PKC-theta in the mechanism of action of clenbuterol in alleviating denervation-induced atrophy.

AB - Rat soleus muscle was denervated for 3 or 7 days, and total membrane protein kinase C (PKC) activity and translocation and immunocytochemical localization of PKC isoforms were examined. Dietary administration of clenbuterol concomitant with denervation ameliorated the atrophic response and was associated with increased membrane PKC activity at both 3 (140%) and 7 (190%) days. Of the five PKC isoforms (alpha, epsilon, theta, zeta, and mu) detected in soleus muscle by Western immunoblotting, clenbuterol treatment affected only the PKC-alpha and PKC-theta forms. PKC-alpha was translocated to the membrane fraction upon denervation, and the presence of clenbuterol increased membrane-bound PKC-alpha and active PKC-alpha as assayed by Ser(657) phosphorylation. PKC-theta protein was downregulated upon denervation, and treatment with clenbuterol further decreased both cytosolic and membrane levels. Immunolocalization of PKC-theta showed differences for regulatory and catalytic domains, with the latter showing fast-fiber type specificity. The results suggest potential roles of PKC-alpha and PKC-theta in the mechanism of action of clenbuterol in alleviating denervation-induced atrophy.

KW - skeletal muscle

KW - beta-agonist

KW - kinase activity

KW - PROTEIN-KINASE-C

KW - CHICK SKELETAL-MUSCLE

KW - AGONIST CLENBUTEROL

KW - NPKC-THETA

KW - RAT MUSCLE

KW - EXPRESSION

KW - MEMBRANE

KW - STIMULATION

KW - INSULIN

KW - GROWTH

M3 - Article

VL - 279

SP - 188

EP - 196

JO - American Journal of Physiology: Endocrinology and Metabolism

JF - American Journal of Physiology: Endocrinology and Metabolism

SN - 0193-1849

IS - 1

ER -