RESUMEN
Renal allograft loss is most often a chronic process, irrespective of the mechanism at stake. In this prospective study, we studied the expression of epithelial to mesenchymal transition (EMT) markers vimentin and ß-catenin by immunohistochemistry in the surveillance biopsy and measured the mRNA encoding vimentin (VIM), CD45, GAPDH and uroplakin 1a (UPK) by quantitative PCR in urinary cells in 75 renal transplant patients. The aim is to establish a simple screening test for chronic renal allograft dysfunction. We found that the value of the mRNA of vimentin and CD45 relative to the uroplakin 1a (UPK) mRNA is correlated with the score in vimentin immunostaining in routine biopsies. These biomarkers could be used as a noninvasive tool to monitor the renal graft fibrogenesis. This test could be used for early detection of fibrotic diseases of the kidney transplant.
Asunto(s)
Biomarcadores/metabolismo , Transición Epitelial-Mesenquimal/genética , Rechazo de Injerto/diagnóstico , Trasplante de Riñón/efectos adversos , ARN Mensajero/orina , Adulto , Aloinjertos , Femenino , Rechazo de Injerto/metabolismo , Humanos , Inmunohistoquímica , Riñón/metabolismo , Riñón/patología , Antígenos Comunes de Leucocito/metabolismo , Masculino , Tamizaje Masivo/métodos , Persona de Mediana Edad , Estudios Prospectivos , Curva ROC , Reacción en Cadena en Tiempo Real de la Polimerasa , Uroplaquina Ia/metabolismo , Vimentina/metabolismo , beta Catenina/metabolismoRESUMEN
Epithelial-mesenchymal transition (EMT) is a process by which differentiated epithelial cells undergo a phenotypic conversion and acquire a mesenchymal phenotype, including elongated morphology, enhanced migratory and invasion capacity, and greatly increased production of extracellular matrix (ECM) components. This phenomenon plays a pivotal role in embryonic development, wound healing and tissue regeneration. It has also been involved in organ fibrosis. Some studies suggest that following injury, renal tubular epithelial cells undergo reprograming in mesenchymal cells, and thus constitute an important source of de novo myofibroblasts invading the renal interstitium and contributing to fibrosis. However, an increasing number of studies raise doubts about the existence of this process in vivo. The role of EMT in the development of renal fibrosis remains a matter of intense debate and may depend on the model studied. In this review, we describe the role of EMT in the development of fibrosis of renal graft, and then we propose approaches for detecting and treating renal fibrogenesis by targeting TEM.
