Amy Sussman and colleagues at the University of Washington, Seattle have found that SPARC may contribute to kidney disease.
These findings are presented in the May 2009 issue of The American Journal of Pathology.
Chronic kidney disease is associated with significant injury and loss of podocytes, which are cells crucial for filtering the blood of toxins. SPARC, a counter-adhesive protein, is upregulated in podocytes upon injury.
To define the role of SPARC in kidney disease, Sussman et al examined immune-mediated kidney disease in mice deficient in SPARC as well as in normal mice. They found that hardening of the kidney was reduced in SPARC-null mice compared with normal controls, in part due to maintenance of podocytes. In addition, SPARC-deficient podocytes were more resistant to stress-induced detachment.
Sussman et al "have established a causal role for SPARC in the progression of glomerular disease following immune-mediated injury of the podocyte. [These] findings support a causal role for induction of the matricellular protein SPARC in mediating podocyte loss, thereby accelerating [kidney] injury."
Materials provided by American Journal of Pathology. Note: Content may be edited for style and length.
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