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INTRACELLULAR SIGNAL-TRANSDUCTION PATHWAYS IN CULTURED SKELETAL MUSCLE CELLS IN RESPONSE TO HEAT AND MECHANICAL STRESSES DURING HYPERTROPHY.  K. Goto¹, T. Kobayashi¹, K. Uehara¹, M. Honda¹, T. Sugiura², S. Yamada³, T. Akema¹, and T. Yoshioka^1,4. ¹Dept of Physiol, St. Marianna Univ Sch of Med, Kawasaki; ²Faculty of Edu, Yamaguchi Univ, Yamaguchi; ³Dept of Life Sci, Graduate Sch of Arts and Sci, Univ of Tokyo, Tokyo; ⁴Aomori Univ of Health and Welfare, Aomori, Japan

   Mechanical stretching could induce muscular hypertrophy.  It has been reported that heat stress facilitates satellite cell proliferation and differentiation in chicks. However, the mechanism responsible for the effects of heat stress on muscular hypertrophy remains unclear.  To elucidate this issue, we investigated the extent to which heat and mechanical stresses induced the mitogen-activated protein kinase (MAPK) cascades, a series of signal-transduction pathways, in skeletal muscle cells. Cultured mouse skeletal muscle cells (C2C12) were plated on collagenized Silastic membranes and incubated at 41° for 60 minutes. Following the incubation, the cells were subjected to a continuous cycle of two-second stretching followed by four-second releasing for three days at 37°. The cellular protein concentrations in the homogenates of the cultured skeletal muscle cells increased under heat shock and/or mechanical stretching. Extracellular regulated kinase (ERK)1/2, p38MAPK, c-Jun NH2-terminal kinase (JNK)/stress-activated protein kinase (SAPK) were activated by heat and/or mechanical stresses. Protein kinase B (PKB) α/Akt1 transiently decreased following heat stress. Our results suggest that mechanical and heat stresses may promote gene expression and differentiation via separate signal-transduction pathways. Heat stress may be a useful tool for a countermeasure for muscoskeletal deconditioning.

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