By M. Sahay
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Extra resources for Chronic Kidney Disease and Renal Transplantation
2010). , 2010). Recently, Ardura et al. (2010) expanded these studies and show that PTHrP is capable of inducing a variety of phenotypic changes related to EMT in tubuloephithelial cells. Hence, this peptide induced snail overexpression and its nuclear translocation, associated with the loss of ZO-1 and E-cadherin, key proteins in the maintenance of basolateral polarity and intercellular junction in renal tubuloepithelial cells. PTHrP also induced the phenotypic conversion to a fibroblast-like morphology, related to α-SMA and ILK upregulation.
2008) without evidence of kidney damage in the absence of renal insult. In any case, these data strongly suggest that PTHrP might participate in the upregulation of glomerular TGF-β1 and p27Kip1. Collectively, these results indicate that the renal PTHrP/PTH1R system is upregulated in streptozotozin-induced diabetes in mice, and appears to be involved with renal hypertrophy and adversely affects the outcome of DN. PTHrP also participates in the hypertrophic signalling triggered by HG on podocytes.
1992; Rees, 2006). Both infiltrating leukocytes and damaged tubuloepithelial cells activate and induce proliferation of resident fibroblasts in the tubulointerstitial compartment. A severe and prolonged injury will determine a sustained activation of proinflammatory pathways, associated with overexpression of profibrogenic cytokines by tubulointerstitial cells leading to fibrogenesis and renal function loss (Strutz & Neilson, 2003). Early studies suggested that PTHrP might act as an important mediator of proinflammatory cytokines, namely tumour necrosis factor and interleukin-6, in multi-organ inflammation and rheumatoid arthritis (Funk, 2001).