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Epithelial to mesenchymal transition during late deterioration of human kidney transplants: the role of tubular cells in fibrogenesis.
Am J Transplant. 2005 Jun; 5(6):1367-74.AJ

Abstract

The hallmark of failing renal transplants is tubular atrophy and interstitial fibrosis (TA/IF). Injury to tubular epithelial cells (TEC) could contribute to fibrogenesis via epithelial-mesenchymal transition (EMT). We examined the features of EMT in renal transplants that developed TA/IF. Biopsies from 10 allograft kidneys with impaired function and TA/IF and 10 biopsies from transplants with stable function were compared to their implantation biopsies. Relative to implantation biopsies, TEC in TA/IF kidneys showed loss of epithelial markers (E-cadherin, cytokeratin) with altered distribution. Some TEC also showed new cytoplasmic expression of mesenchymal markers vimentin, S100A4, and alpha smooth muscle actin (alpha-SMA) and collagen synthesis marker heat shock protein (HSP-47), both in deteriorating and atrophic tubules. Double immunostaining showed coexpression of cytokeratin and vimentin, S100A4 and HSP-47, indicating intermediate stages of EMT in TA/IF. These changes were absent or much less in transplants with stable function. EMT features in the TA/IF group correlated with serum creatinine (vimentin, S100A4, HSP-47), history of T-cell-mediated rejection (cytokeratin, S100A4) and proteinuria (cytokeratin). These findings support a model in which the TEC damage induces loss of epithelial features and expression of fibroblast features, as a common pathway of deterioration by either immunologic or nonimmunologic processes.

Authors+Show Affiliations

Medicine, Division of Nephrology and Transplantation Immunology, University of Alberta, Edmonton, Canada.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

15888043

Citation

Vongwiwatana, Attapong, et al. "Epithelial to Mesenchymal Transition During Late Deterioration of Human Kidney Transplants: the Role of Tubular Cells in Fibrogenesis." American Journal of Transplantation : Official Journal of the American Society of Transplantation and the American Society of Transplant Surgeons, vol. 5, no. 6, 2005, pp. 1367-74.
Vongwiwatana A, Tasanarong A, Rayner DC, et al. Epithelial to mesenchymal transition during late deterioration of human kidney transplants: the role of tubular cells in fibrogenesis. Am J Transplant. 2005;5(6):1367-74.
Vongwiwatana, A., Tasanarong, A., Rayner, D. C., Melk, A., & Halloran, P. F. (2005). Epithelial to mesenchymal transition during late deterioration of human kidney transplants: the role of tubular cells in fibrogenesis. American Journal of Transplantation : Official Journal of the American Society of Transplantation and the American Society of Transplant Surgeons, 5(6), 1367-74.
Vongwiwatana A, et al. Epithelial to Mesenchymal Transition During Late Deterioration of Human Kidney Transplants: the Role of Tubular Cells in Fibrogenesis. Am J Transplant. 2005;5(6):1367-74. PubMed PMID: 15888043.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Epithelial to mesenchymal transition during late deterioration of human kidney transplants: the role of tubular cells in fibrogenesis. AU - Vongwiwatana,Attapong, AU - Tasanarong,Adis, AU - Rayner,David C, AU - Melk,Anette, AU - Halloran,Philip F, PY - 2005/5/13/pubmed PY - 2005/9/2/medline PY - 2005/5/13/entrez SP - 1367 EP - 74 JF - American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons JO - Am J Transplant VL - 5 IS - 6 N2 - The hallmark of failing renal transplants is tubular atrophy and interstitial fibrosis (TA/IF). Injury to tubular epithelial cells (TEC) could contribute to fibrogenesis via epithelial-mesenchymal transition (EMT). We examined the features of EMT in renal transplants that developed TA/IF. Biopsies from 10 allograft kidneys with impaired function and TA/IF and 10 biopsies from transplants with stable function were compared to their implantation biopsies. Relative to implantation biopsies, TEC in TA/IF kidneys showed loss of epithelial markers (E-cadherin, cytokeratin) with altered distribution. Some TEC also showed new cytoplasmic expression of mesenchymal markers vimentin, S100A4, and alpha smooth muscle actin (alpha-SMA) and collagen synthesis marker heat shock protein (HSP-47), both in deteriorating and atrophic tubules. Double immunostaining showed coexpression of cytokeratin and vimentin, S100A4 and HSP-47, indicating intermediate stages of EMT in TA/IF. These changes were absent or much less in transplants with stable function. EMT features in the TA/IF group correlated with serum creatinine (vimentin, S100A4, HSP-47), history of T-cell-mediated rejection (cytokeratin, S100A4) and proteinuria (cytokeratin). These findings support a model in which the TEC damage induces loss of epithelial features and expression of fibroblast features, as a common pathway of deterioration by either immunologic or nonimmunologic processes. SN - 1600-6135 UR - https://www.unboundmedicine.com/medline/citation/15888043/Epithelial_to_mesenchymal_transition_during_late_deterioration_of_human_kidney_transplants:_the_role_of_tubular_cells_in_fibrogenesis_ L2 - https://onlinelibrary.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=1600-6135&date=2005&volume=5&issue=6&spage=1367 DB - PRIME DP - Unbound Medicine ER -