Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/199626
Type: Artigo de periódico
Title: Stretch-activated Calcium Channel Protein Trpc1 Is Correlated With The Different Degrees Of The Dystrophic Phenotype In Mdx Mice.
Author: Matsumura, Cíntia Yuri
Taniguti, Ana Paula Tiemi
Pertille, Adriana
Santo Neto, Humberto
Marques, Maria Julia
Abstract: In Duchenne muscular dystrophy (DMD) and in the mdx mouse model of DMD, the lack of dystrophin is related to enhanced calcium influx and muscle degeneration. Stretch-activated channels (SACs) might be directly involved in the pathology of DMD, and transient receptor potential cation channels have been proposed as likely candidates of SACs. We investigated the levels of transient receptor potential canonical channel 1 (TRPC1) and the effects of streptomycin, a SAC blocker, in muscles showing different degrees of the dystrophic phenotype. Mdx mice (18 days old, n = 16) received daily intraperitoneal injections of streptomycin (182 mg/kg body wt) for 18 days, followed by removal of the diaphragm, sternomastoid (STN), biceps brachii, and tibialis anterior muscles. Control mdx mice (n = 37) were injected with saline. Western blot analysis showed higher levels of TRPC1 in diaphragm muscle compared with STN and limb muscles. Streptomycin reduced creatine kinase and prevented exercise-induced increases of total calcium and Evans blue dye uptake in diaphragm and in STN muscles. It is suggested that different levels of the stretch-activated calcium channel protein TRPC1 may contribute to the different degrees of the dystrophic phenotype seen in mdx mice. Early treatment designed to regulate the activity of these channels may ameliorate the progression of dystrophy in the most affected muscle, the diaphragm.
Subject: Animals
Blotting, Western
Fluorescent Antibody Technique
Ion Channels
Male
Mice
Mice, Inbred Mdx
Muscle, Skeletal
Muscular Dystrophy, Duchenne
Phenotype
Protein Synthesis Inhibitors
Streptomycin
Trpc Cation Channels
Citation: American Journal Of Physiology. Cell Physiology. v. 301, n. 6, p. C1344-50, 2011-Dec.
Rights: fechado
Identifier DOI: 10.1152/ajpcell.00056.2011
Address: http://www.ncbi.nlm.nih.gov/pubmed/21900691
Date Issue: 2011
Appears in Collections:Unicamp - Artigos e Outros Documentos

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