[Transdifferentiation of tubular epithelial cells in tubulointerstitial fibrosis].
OBJECTIVE
To observe the transdifferentiation of renal tubular epithelial cells in tubulointerstitial fibrosis.


METHODS
The renal tubulointerstitial fibrosis model in Wistar rats was established by unilateral renal vein ligature. The rats were kept 25 days after renal vein ligature. The kidneys were dissected every 5 days by killing 5 rats. The morphological changes of the kidney were observed by light microscopy, electron microscopy, polarizing microscopy and immunohistochemistry method.


RESULTS
The histological changes showed tubular atrophy and disappearance, widening of intertubular spaces with increased lymphocytes and mononuclear cells infiltration and fibrosis. The CK marker in injured and atrophic epithelial cells gradually weakened, but the alpha-SMA, vimentin, TGF-beta(1), collagen I and III showed gradually stronger positivity for immunohistochemistry. Some interstitial cells became positive for CK. Electron microscopy revealed decreased mitochondria, increased endoplasmic reticulum and microfilament of the tubular epithelial cells which merged into the interstitium. During the early stage of tubulointerstitial fibrosis, there was proliferation of type III collagen and then followed by type I collagen at later stage when observing the Sirius Red stained sections under the polarizing microscope.


CONCLUSIONS
Tubular epithelial cells can transdifferentiate to fibroblasts during the process of tubulointerstitial fibrosis.
D000199:Actins / Q000032:analysis; D000818:Animals; D002454:Cell Differentiation; D003094:Collagen / Q000032:analysis; D004847:Epithelial Cells / Q000166:cytology; D005355:Fibrosis; D007150:Immunohistochemistry; D007633:Keratins / Q000032:analysis; D007684:Kidney Tubules / Q000737:chemistry / Q000473:pathology* / Q000648:ultrastructure; D008297:Male; D051381:Rats; D017208:Rats, Wistar
D000199:Actins; D007633:Keratins; D003094:Collagen