hsp70, hsp32, and grp78 are increased in thermally injured skin with and without antithrombin(Human) concentrate infusion

An acquired deficiency of antithrombin (AT), an anti-inflammatory protein, develops in patients with thermal injuries. Skin thermotolerance is regulat ed by heat shock protein (hsp) genes. hsp70, hsp32, hsp27, and glucose-regu lated protein78 (grp78) were studied in burned and unburned human skin to d etermine whether correction of the AT deficiency modulated the intensity of expression of these proteins. Fifty-four human skin samples were prepared by Western blot analysis: 11 unburned and 22 burned control skin samples an d 7 unburned and 14 burned skin samples from patients treated with AT(Human ), or AT(H). The intensity of hsp32 expression in burned AT(H)-treated skin (P < .001) and in burned control skin (P < .01) was significantly increase d compared with unburned control skin. The intensity of expression of hsp70 was statistically significant in burned AT(H)-treated skin compared with u nburned control skin (P < .02), as was that of grp78 (P < .01). Thermally i njured skin with or without AT(H) treatment had an increased expression of hsp70, hsp32, and grp78 compared with unburned control skin.