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

K Abe, Y Ozono, M Miyazaki, T Koji… - Nephrology Dialysis …, 2000 - academic.oup.com
K Abe, Y Ozono, M Miyazaki, T Koji, K Shioshita, A Furusu, S Tsukasaki, F Matsuya…
Nephrology Dialysis Transplantation, 2000academic.oup.com
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 …
Abstract
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 α-smooth muscle actin (α-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 α-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 α-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.
Oxford University Press