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고온 스트레스가 닭 근육 위성세포 내미토콘드리아 대사에 미치는 영향

Effects of Heat Stress on Mitochondrial Metabolism in Chicken Skeletal Muscle Satellite Cells

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This study investigated how culture temperature and cellular state influence the expression of mitochondrial-related genes in chicken muscle satellite cells (CMSCs) isolated from breast and leg muscles. CMSCs were cultured at either 37℃ or 41℃ under proliferative or differentiation conditions, and the expression of genes associated with mitochondrial function was assessed. In breast-derived CMSCs, proliferation at 41℃ induced marked upregulation of ATP5B, CYCS, PGC-1α, TFAM, NRF1, NRF2, DRP1, MFN1, MFN2, OPA1, PINK1, PRKN, and UCP3. During differentiation, however, several of these genes showed higher expression at 37℃. In leg-derived CMSCs, proliferation at 41℃ increased the expression of TFAM, NRF1, MFN2, PRKN, and UCP3. Conversely, differentiation at 37℃ elevated TFAM, MFN1, ATP5B, and UCP3 expression. These temperature-dependent patterns demonstrate that genes related to ATP synthesis, mitochondrial biogenesis, mitophagy, and thermogenesis exhibit muscle-type- and stage-specific regulatory profiles. The enhanced responses at 41℃ reflect the fact that this temperature represents a relative heat stress condition for cells cultured in vitro, leading to the activation of mitochondrial metabolic and homeostatic pathways. In summary, these findings show that mitochondrial gene regulation in CMSCs is shaped by muscle origin, culture temperature, and developmental stage. This study provides foundational insight into muscle-type-specific mitochondrial adaptation to heat exposure in chickens.

Abstract

This study investigated how culture temperature and cellular state influence the expression of mitochondrial-related genes in chicken muscle satellite cells (CMSCs) isolated from breast and leg muscles. CMSCs were cultured at either 37℃ or 41℃ under proliferative or differentiation conditions, and the expression of genes associated with mitochondrial function was assessed. In breast-derived CMSCs, proliferation at 41℃ induced marked upregulation of ATP5B, CYCS, PGC-1α, TFAM, NRF1, NRF2, DRP1, MFN1, MFN2, OPA1, PINK1, PRKN, and UCP3. During differentiation, however, several of these genes showed higher expression at 37℃. In leg-derived CMSCs, proliferation at 41℃ increased the expression of TFAM, NRF1, MFN2, PRKN, and UCP3. Conversely, differentiation at 37℃ elevated TFAM, MFN1, ATP5B, and UCP3 expression. These temperature-dependent patterns demonstrate that genes related to ATP synthesis, mitochondrial biogenesis, mitophagy, and thermogenesis exhibit muscle-type- and stage-specific regulatory profiles. The enhanced responses at 41℃ reflect the fact that this temperature represents a relative heat stress condition for cells cultured in vitro, leading to the activation of mitochondrial metabolic and homeostatic pathways. In summary, these findings show that mitochondrial gene regulation in CMSCs is shaped by muscle origin, culture temperature, and developmental stage. This study provides foundational insight into muscle-type-specific mitochondrial adaptation to heat exposure in chickens.

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