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Nephrol Dial Transplant (2000) 15: 529-535
© 2000 European Renal Association-European Dialysis and Transplant Association

Interstitial expression of heat shock protein 47 and {alpha}-smooth muscle actin in renal allograft failure

Katsushige Abe, Yoshiyuki Ozono, Masanobu Miyazaki, Takehiko Koji1, Kei Shioshita, Akira Furusu, Shoko Tsukasaki, Fukuzo Matsuya2, Nobuko Hosokawa3, Takashi Harada4, Takashi Taguchi5, Kazuhiro Nagata3 and Shigeru Kohno

Second Department of Internal Medicine, 1 Department of Histology and Cell Biology, 2 Department of Urology, 4 Division of Renal Care Unit and 5 Second Department of Pathology, Nagasaki University School of Medicine, Sakamoto, Nagasaki and 3 Department of Cell Biology, Chest Disease Research Institute, Kyoto University, Kyoto, Japan

Correspondence and offprint requests to: Masanobu Miyazaki, MD, Second Department of Internal Medicine, Nagasaki University School of Medicine, 1–7-1 Sakamoto, Nagasaki 852–8501, Japan.

Background. Tubulointerstitial inflammation and fibrosis are the main pathological features of chronic renal allograft rejection, which is characterized by accumulation of extracellular matrix protein. Heat shock protein 47 (HSP47), known as a collagen-specific stress protein, is thought to be a molecular chaperone during the processing and/or secretion of procollagen. HSP47 is thought to be involved in the progression of fibrosis, but its expression in chronic renal allograft rejection is still unknown.

Methods. We examined the expression of HSP47 together with that of {alpha}-smooth muscle actin ({alpha}-SMA), a marker of myofibroblasts, and CD68, a marker of macrophages, by immunohistochemistry in allograft kidney tissues. Uninvolved portions of surgically removed kidneys with tumours served as control tissue.

Results. Expression of HSP47 was detected in the interstitium of fibrotic regions of allograft kidneys. Cells positive for HSP47 were also stained for {alpha}-SMA and type I collagen, and the expression of HSP47 correlated with the degree of interstitial fibrosis. Furthermore, the expression of HSP47 correlated with the number of infiltrating macrophages. In contrast, HSP47 and {alpha}-SMA were not expressed in the control tissues, sections of 1 h post-transplantation biopsy specimens and acute allograft rejection without fibrosis.

Conclusion. Our results suggest that HSP47 may contribute to the progression of interstitial fibrosis in allograft renal tissues.

Keywords: HSP47; myofibroblasts; transplantation kidney; fibrosis


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