Short-term heat stress results in increased apoptotic signaling and autophagy in oxidative skeletal muscle in Sus scrofa. (February 2018)

• Record Type: Journal Article
• Authors: Ganesan, Shanthi; Pearce, Sarah C.; Gabler, Nicholas K.; Baumgard, Lance H.; Rhoads, Robert P.; Selsby, Joshua T.
• Is Part Of: Journal of thermal biology. Volume 72(2018)
• Page Start: 73
• Page End: 80
• Publication Date: 2018-02
• Subjects: Apoptosis -- Hyperthermia -- Mitophagy -- Pig -- Mitochondria; Thermobiology -- Periodicals; Temperature -- Periodicals; Biology -- Periodicals; Thermobiologie -- Périodiques; Thermobiology; Periodicals; 571.46
• DOI: 10.1016/j.jtherbio.2018.01.003
• Languages: English
• ISSNs: 0306-4565

Abstract

Abstract: Prolonged environment-induced hyperthermia causes morbidities and mortality in humans and animals and appears to cause organ-specific injury and dysfunction. We have previously determined autophagic dysfunction and apoptotic signaling in oxidative skeletal muscle following prolonged hyperthermia. The aim of this investigation was to extend our knowledge regarding the early chronology of heat stress-mediated apoptotic and autophagic signaling in oxidative skeletal muscle. We hypothesized that 2, 4, and 6 h of hyperthermia would increase apoptosis and autophagy in oxidative skeletal muscle compared to thermoneutral (TN) conditions. Pigs were assigned to four groups (n = 8/group) and exposed to environmental heat stress (37 °C) for 0, 2, 4, or 6 h. Immediately following environmental exposure animals were euthanized and the red portion of the semitendinosus was collected. Markers of apoptotic signaling were increased following 2 h of heating but returned to baseline thereafter, while caspase 3 activity remained elevated 2–3 fold (p < .05) throughout the hyperthermic period. Heat stress increased (p < .05) markers of autophagic activation, and nucleation as well as autophagosome formation and degradation linearly throughout the heating intervention. In addition, 6 h of hyperthermia increased (p < .05) markers of mitophagy. These data suggest that apoptotic signaling precedes increased autophagy during acute heat stress in oxidative skeletal muscle. Highlights: Two hours of heat stress caused a transient increase in apoptotic signaling. Two through six hours of hyperthermia stimulated a robust increase in autophagy. Short-term heat stress appears mechanistically distinct from long-term heat stress.