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Mild Heat Shock Promotes Hypertrophy in Cardiac, Skeletal and Smooth Muscle Cells
Author(s) -
Hall Todd,
Craig Robin,
Touchberry Chad,
Silswal Neerupma,
Elmore Christopher,
Baker Kendra,
Andresen Jon,
Wacker Michael,
Brotto Marco
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.1047.3
Subject(s) - muscle hypertrophy , heat shock protein , skeletal muscle , myocyte , microbiology and biotechnology , biology , heat shock , c2c12 , medicine , cell , endocrinology , gene , myogenesis , genetics
Heat‐Shock Proteins (HSPs) are involved in growth and development of uscles, however, the exact role that hyperthermia and HSPs play in muscle hypertrophy and muscle repair is unknown. Here, for the first time, we present our findings on the effects of heat shock (HS) in representative cell culture models of cardiac (HL‐1), skeletal (C2C12) and smooth (A7R5) muscle cells. We used fully differentiated cells, and exposed them to a mild heat shock protocol (43ºC for 20 min). Cells were returned after HS to their normal culture environment and 24 hrs after HS, we measured cell area. Surprisingly, we discovered that HS induced significant hypertrophy in all three types of muscle cells. To begin deciphering the molecular machinery involved with the hypertrophic response we used a real‐time PCR array that included specific genes involved in hypertrophy, cell signaling and transduction, and excitation‐contraction coupling. In C2C12, 6 hrs after HS, we found an increase in the expression of Hsp genes and downregulation of IP3R‐1, TLR2, MHC6, and Titin. This is the first report to show that HS promotes cardiac, skeletal, and smooth muscle hypertrophy that associates with changes in a small subset of genes.