Hyperthermia to normal human skin in vivo upregulates heat shock proteins 27, 60, 72i and 90

Abstract

This study was performed to test the hypothesis that expression of heat shock proteins (HSPs) exhibits a spatially selective response within intact human skin following in vivo exposure to thermal stress. This response is believed to protect cells and tissues from further damage. Using Western blotting and immunohistochemistry, we studied the expression of a range of HSPs in normal human skin of 5 subjects prior to and following heating in vivo. The skin was heated to 41 +/- 0.5 degrees C for 1 h and biopsies were taken at 4, 8 and 24 h and from control, untreated skin. HSPs 27, 60, 72i, 90, 110 and heat shock constitutive (HSC)70 were expressed in normal skin, but the extent and distribution of these HSPs showed considerable variation. HSP27, 60 and 72i were found predominantly in the epidermis, whereas HSC70 showed weak epidermal staining but strong dermal expression. Heating the skin in vivo resulted in an increased skin content of HSP27, 60, 72i and 90, with maximal increase at 24 h following hyperthermia, while the skin content of HSC70 and HSP110 were unchanged. Significant increases in the content of HSP72i and HSP90 had occurred by 4 h following hyperthermia, with a mean +/-SEM of 206 +/- 50% and 197 +/- 38% of the control, untreated values, respectively (p<0.05). These findings indicate the complexity of HSP dynamics in human skin, and suggest that heating within the experimental range may protect the skin from further stresses for at least 24 h.

Antioxidants and the Response of Skin to Oxidative Stress: Vitamin E as a Key Indicator

“…Increased expression of HSP27 has been demonstrated following heating of both keratinocyte cell lines and organ-cultured human skin [44,45]. Other studies have indicated that HSP70 predominates in the dermis compared with the epidermis, whereas HSP27 is predominantly present in the epidermis [46]. These differences in location between HSP27 and HSP70 might explain the different time course of induction of these stress proteins upon skin O 3 .…”

Lack of protection of prior heat shock against UV-induced oxidative stress in human skin fibroblasts

“…6 Thermal exposure of human skin has been reported to up-regulate HSP27, HSP60, HSP72i and HSP90. 13 Induction of HSPs by hyperthermia has been reported to protect cells against damaging processes that appear to involve oxidative stress, such as ischaemia-reperfusion injury 14 and hence we wished to determine whether stress proteins could influence the oxidative stress that results in skin cells exposed to UV radiation. Our hypothesis was that prior exposure of cultured skin fibroblasts to hyperthermia would induce synthesis of HSPs that would protect the cells against UV-induced oxidative stress.…”

Expression of the heat shock protein-27 in the adult human scalp skin and hair follicle: Hair cycle–dependent changes

“…3 Several studies revealed the expression of these proteins in human skin: HSP72 in both epidermis and dermis, and HSPs 27, 60, 90, and 110 in the epidermis. [3][4][5] In contrast to other body tissues, which express HSPs under stress conditions, normal human keratinocytes express HSPs under both normal and stress conditions. 1 HSPs are involved in a variety of disease processes such as autoimmune diseases and malignant conditions.…”