Morita K, Wakui H, Komatsuda A, Ohtani H, Miura A B, Itoh H, Tashima Y
Third Department of Internal Medicine, Akita University School of Medicine, Japan.
Ren Fail. 1995 Jul;17(4):405-19. doi: 10.3109/08860229509037605.
We examined rat kidneys for serial expressions of two major heat-shock proteins (HSPs), HSP73 and HSP90, after 60 min of unilateral renal ischemia up to day 28. Immunohistochemical studies showed that HSP73 and HSP90 were rapidly induced in the cytoplasm of injured epithelial cells of the S3 segment of proximal tubules and were again induced in the cytoplasm of regenerative cells in this segment from day 3. In epithelial cells of the Henle's loops, HSP90 was also induced in the cytoplasm of both injured and regenerative cells, but HSP73 was not induced in this portion. Furthermore, a transient accumulation of HSP73 into the nucleus was observed in epithelial cells of papillary collecting ducts shortly after ischemia. Serial immunoblot analysis of isotonic buffer extractable fractions from ischemic kidneys revealed the induction of both HSP73 and HSP90 in the degenerative and regenerative phases: the maximal inductions in the two phases were at 3-6 and on days 5-7, respectively. These results demonstrate that HSP73 and HSP90 are induced in injured tubular epithelial cells with a regional heterogeneity during the degenerative and regenerative phases after renal ischemia and suggest that these HSPs are involved in the process of postischemic cellular recovery.
