Temporal variations of Hsp60 and HSF-1 in primary rat myocardial cells in vitro under heat stress

Abstract

ABSTRACT. The mechanisms involved in sudden animal death due to acute heart failure during heat stress are not well understood. We examined the relationship between heat stress-induced variations of protective Hsp60 and expression of its regulatory factor, HSF-1, in heat-stressed primary myocardial cells of neonatal rats in vitro through cardiac enzyme detection, immunoblotting, immunocytochemistry, and qPCR. Increases in cardiac damage-related enzyme levels demonstrated injury to myocardial cells after heat exposure at 42°C. Hsp60 expression levels fluctuated during heat stress; they decreased significantly after 20 min, then increased at 120 min and decreased again at 360 min after initiation of heat stress. The highest levels of Hsp60 were observed at 240 min, while the lowest were at 60 min. Damage to myocardial cells was characterized by increases in cardiac enzyme levels and low levels of Hsp60 due to functional disorder of myocardial cells at early stages of heat stress. However, the significant induction of hsp60 mRNA levels from the beginning up to 240 min of heat stress was not consistent with the classic regulatory mechanisms that link transcription and translation, suggesting that Hsp60 expression is delayed due to loss of Hsp60 during the early stages of heat stress. hsf-1 mRNA levels were significantly increased from 10 min of heat stress; however, HSF-1 protein levels did not simultaneously increase, indicating that HSF-1 is not the sole regulator of Hsp60 expression.

The interactive association between heat shock factor 1 and heat shock proteins in primary myocardial cells subjected to heat stress

“…Moreover, HSF1 may play different roles in its interaction with HSPs in different species or cell types. STRING analysis confirmed our previous finding that HSF1 is not the sole factor for HSP60 ( 36 ).…”

“…It has been suggested that HSP70 represses HSF1 during heat stress ( 12 ). Furthermore, a previous study indicated that HSF1 is not the sole factor for HSP60 in rats [Buriro et al ( 36 )]. Furthermore, data analysis confirmed that the expression levels of CRYAB were inconsistent with those of HSF1.…”

“…However, the HSF1 protein expression levels were not simultaneously increased as were the HSF1 mRNA levels during heat stress. These findings may be associated with the fact that a single HSF1 phosphorylation event has been shown to result in the rapid aggregation of HSF1 into a trimer that can bind to HSE and initiate the transcription process ( 36 – 39 ). The expression levels of HSP90 were also not consistent with its mRNA levels.…”

The association of Hsp90 expression induced by aspirin with anti-stress damage in chicken myocardial cells

“…Heart and liver diseases or damage are always accompanied by elevated blood levels of AST [ 36 ]. In vitro tests showed that the LDH content is a sensitive parameter of myocardial damage [ 6 ]. In the present study, heart damage was monitored in real-time during HS based on fluctuations in AST, CK and LDH.…”

Prokaryotic expression of chicken interferon‐γ fusion protein and its effect on expression of poultry heat shock protein 70 under heat stress

“…Previous studies on HSPs mainly focused on the regulation of function and expression, including transcription and translation levels (Buriro et al ; Morimoto ). The concentration of mRNA template was regulated for optimal sample amplification.…”