Key result
Heat stress increases CAR expression ~63% in mouse skin keratinocytes.
Why the study?
Does heat stress increase the expression of CAR in mouse skin keratinocytes?
Does heat stress increase the expression of CAR in mouse skin keratinocytes?
Absolute Event Rate: 78.64% vs 48.36%
p-value: p=<0.05
Heat stress upregulates CAR expression in mouse skin keratinocytes, which may play a role in burn wound healing.
May link heat stress to keratinocyte responses in burns; hypothesis-generating for mechanisms and human relevance.
The aim of this study was to investigate the effects of heat stress on the expression of the coxsackievirus and adenovirus receptor (CAR) in mouse skin keratinocytes. Twenty BALB/c mice were randomly divided into two groups: the sham heat (control) and scald groups. Skin specimens were obtained 6 h after the treatments. Changes in the expression of CAR in skin keratinocyte samples were detected by immunohistochemistry, quantitative polymerase chain reaction and western blotting. In an in vitro assay, mouse skin keratinocytes were cultured and randomly divided into two groups: the normal control and heat stress groups. Six hours subsequently, the changes in CAR expression in the two groups were estimated by flow cytometry to determine the differences between the two groups. Heat stress significantly increased the expression of CAR in the mouse skin keratinocytes (P<0.05). The upregulation of CAR in mouse keratinocytes in burn wounds may be beneficial for restoring healing in organisms.
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Deng et al. (2013) studied Burn wounds (n=20). Heat stress vs. Sham heat / normal control was evaluated on CAR expression in keratinocytes (p=<0.05). Heat stress significantly increased the expression of the coxsackievirus and adenovirus receptor (CAR) in mouse skin keratinocytes from 48.36% to 78.64% (P<0.05).
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