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Lookup NU author(s): Dr Kathryn White
This work is licensed under a Creative Commons Attribution 4.0 International License (CC BY 4.0).
Glomerular disease is characterized by morphologic changes in podocyte cells accompanied by inflammation and fibrosis. Thymosin beta(4) regulates cell morphology, inflammation, and fibrosis in several organs and administration of exogenous thymosin beta(4) improves animal models of unilateral ureteral obstruction and diabetic nephropathy. However, the role of endogenous thymosin beta(4) in the kidney is unknown. We demonstrate that thymosin beta(4) is expressed prominently in podocytes of developing and adult mouse glomeruli. Global loss of thymosin beta(4) did not affect healthy glomeruli, but accelerated the severity of immune-mediated nephrotoxic nephritis with worse renal function, periglomerular inflammation, and fibrosis. Lack of thymosin beta(4) in nephrotoxic nephritis led to the redistribution of podocytes from the glomerular tuft toward the Bowman capsule suggesting a role for thymosin beta(4) in the migration of these cells. Thymosin beta(4) knockdown in cultured podocytes also increased migration in a wound-healing assay, accompanied by F-actin rearrangement and increased RhoA activity. We propose that endogenous thymosin beta(4) is a modifier of glomerular injury, likely having a protective role acting as a brake to slow disease progression.
Author(s): Vasilopoulou E, Kolatsi-Joannou M, Lindenmeyer MT, White KE, Robson MG, Cohen CD, Sebire NJ, Riley PR, Winyard PJ, Long DA
Publication type: Article
Publication status: Published
Journal: Kidney International
Year: 2016
Volume: 90
Issue: 5
Pages: 1056-1070
Print publication date: 01/11/2016
Online publication date: 26/08/2016
Acceptance date: 23/06/2016
Date deposited: 17/01/2017
ISSN (print): 0085-2538
ISSN (electronic): 1523-1755
Publisher: Elsevier
URL: http://dx.doi.org/10.1016/j.kint.2016.06.032
DOI: 10.1016/j.kint.2016.06.032
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