| First Author | Vasilopoulou E | Year | 2016 |
| Journal | Kidney Int | Volume | 90 |
| Issue | 5 | Pages | 1056-1070 |
| PubMed ID | 27575556 | Mgi Jnum | J:309992 |
| Mgi Id | MGI:6759095 | Doi | 10.1016/j.kint.2016.06.032 |
| Citation | Vasilopoulou E, et al. (2016) Loss of endogenous thymosin beta4 accelerates glomerular disease. Kidney Int 90(5):1056-1070 |
| abstractText | Glomerular disease is characterized by morphologic changes in podocyte cells accompanied by inflammation and fibrosis. Thymosin beta4 regulates cell morphology, inflammation, and fibrosis in several organs and administration of exogenous thymosin beta4 improves animal models of unilateral ureteral obstruction and diabetic nephropathy. However, the role of endogenous thymosin beta4 in the kidney is unknown. We demonstrate that thymosin beta4 is expressed prominently in podocytes of developing and adult mouse glomeruli. Global loss of thymosin beta4 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 beta4 in nephrotoxic nephritis led to the redistribution of podocytes from the glomerular tuft toward the Bowman capsule suggesting a role for thymosin beta4 in the migration of these cells. Thymosin beta4 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 beta4 is a modifier of glomerular injury, likely having a protective role acting as a brake to slow disease progression. |
