Heat stress-induced PPAR-β enhances HUVEC resistance to oxidant injury

Background: Mild heat stress provides protection to cells, which is known as thermal tolerance. Various kinds of heat shock proteins have been proven to play important roles in this process. Another antiapoptotic factor induced by mild heat stress, peroxisome proliferator activated receptor beta (PPAR-β), provides a protective effect to cells against subsequent oxidant injury.

Objective: To understand the expression of PPAR-β and other proteins in human umbilical vein endothelial cells (HUVECs) during mild heat stress. H₂O₂-induced apoptosis of cells with mild heat pretreatment were also investigated to elucidate cell resistance to oxidant injury.

Methods: HUVECs were chosen in the current study because vascular endothelial cells in burn wounds, especially in the zone of stasis, suffer sequentially from heat stimulus and oxidant injury.

Results: The cells were subjected to 43 ☐C for 25 minutes and allowed to recover for different times (from 1 to 72 hours). The PPAR-β expression was found to be upregulated in the later recovery stage. BCL-2 also showed a similar trend, but P53 showed otherwise. Heat pretreated HUVECs were exposed to 400 μmol/L of H₂O₂ for 12 hours, and apoptosis rate was assessed. H₂O₂-induced apoptosis was attenuated by heat pretreatment and by the PPAR-β agonist GW0742 (p < 0.01 and p < 0.05 versus control group); HUVECs transfected with PPAR-β shRNA seemed much more susceptible to oxidation damage (p < 0.05 versus the control group). Mild heat stress also upregulated the BCL-2 expression relative to PPAR-β.

Conclusion: Heat-induced PPAR-β may be partly responsible for this process, which may also be one of the possible explanations of the antiapoptotic function of PPAR-β, although the specific mechanism needs further examination.