NDLI: Tweak induces proliferation in renal tubular epithelium: a role in uninephrectomy induced renal hyperplasia

Content Provider	PubMed Central
Author	Sanz, Ana B. Dolores, Sanchez-niño Maria Izquierdo, Maria Concepcion Jakubowski, Aniela Justo, Pilar Blanco-colio, Luis M. Marta, Ruiz-ortega Egido, Jesús Ortiz, Alberto
Copyright Year	2009
Abstract	The tumour necrosis factor (TNF) family member TWEAK activates the Fn14 receptor and has pro-apoptotic, proliferative and pro-inflammatory actions that depend on the cell type and the microenvironment. We explored the proliferative actions of TWEAK on cultured tubular cells and in vivo on renal tubules. Additionally, we studied the role of TWEAK in compensatory proliferation following unilateral nephrectomy and in an inflammatory model of acute kidney injury (AKI) induced by a folic acid overdose. TWEAK increased the proliferation, cell number and cyclin D1 expression of cultured tubular cells, in vitro. Exposure to serum increased TWEAK and Fn14 expression and the proliferative response to TWEAK. TWEAK activated the mitogen-activated protein kinases ERK and p38, the phosphatidyl-inositol 3-kinase (PI3K)/Akt pathway and NF-κB. TWEAK-induced proliferation was prevented by inhibitors of these protein kinases and by the NF-κB inhibitor parthenolide. TWEAK-induced tubular cell proliferation as assessed by PCNA and cyclin D1 expression in the kidneys of adult healthy mice in vivo. By contrast, TWEAK knock-out mice displayed lower tubular cell proliferation in the remnant kidney following unilateral nephrectomy, a non-inflammatory model. This is consistent with TWEAK-induced proliferation on cultured tubular cells in the absence of inflammatory cytokines. Consistent with our previously published data, in the presence of inflammatory cytokines TWEAK promoted apoptosis, not proliferation, of cultured tubular cells. In this regard, TWEAK knock-out mice with AKI displayed less tubular apoptosis and proliferation, as well as improved renal function. In conclusion, TWEAK actions in tubular cells are context dependent. In a non-inflammatory milieu TWEAK induces proliferation of tubular epithelium. This may be relevant for compensatory renal hyperplasia following nephrectomy.
Related Links	http://dx.doi.org/10.1111/j.1582-4934.2009.00766.x
Ending Page	3342
Page Count	14
Starting Page	3329
File Format	PDF
ISSN	15821838
e-ISSN	15824934
Journal	Journal of Cellular and Molecular Medicine
Issue Number	9b
Volume Number	13
Language	English
Publisher	John Wiley & Sons, Ltd
Publisher Date	2009-05-01
Access Restriction	Open
Rights Holder	John Wiley & Sons, Ltd
Subject Keyword	Molecular Medicine Cell Biology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Cell Biology Molecular Medicine

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