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BioMed Research International
Volume 2013, Article ID 135608, 8 pages
Research Article

Angiopoietin-Like 3 Induces Podocyte F-Actin Rearrangement through Integrin /FAK/PI3K Pathway-Mediated Rac1 Activation

1Department of Nephrology and Rheumatism, Children’s Hospital of Fudan University, Shanghai 201102, China
2Department of Pediatrics, Affiliated Hospital of Medical College, Qingdao University, Shandong 266003, China
3Department of Biochemistry and Molecular Biology, Shanghai Medical College, Fudan University, Shanghai 200032, China

Received 4 July 2013; Revised 18 September 2013; Accepted 26 September 2013

Academic Editor: Steven N. Hochwald

Copyright © 2013 Yi Lin et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Glomerular podocytes are highly differentiated cells whose foot processes, which are mainly maintained by the architecture of actin filaments, have a unique morphology. A rearrangement of F-actin in podocytes causes changes in their motility that involve foot process effacement and proteinuria in glomerular diseases. Members of the Rho family small GTPases, especially RhoA, Rac1, and Cdc42, are key molecules in the regulation of actin cytoskeleton rearrangement. Our previous study showed that angiopoietin-like 3 (Angptl3) can increase the motility of podocytes in vitro. In this study, we found that recombinant Angptl3 treatment, together with the activation of Rac1, could cause F-actin rearrangement in podocytes. We also found that these effects could be blocked by an integrin inhibitor, implicating integrin as the Angptl3 receptor in its effects on actin cytoskeleton rearrangement. In addition, we studied the molecular pathway for this process. Our results showed that in podocytes, Angptl3 could induce actin filament rearrangement, mainly in lamellipodia formation, and that this process was mediated by integrin -mediated FAK and PI3K phosphorylation and Rac1 activation. Our results might provide a new explanation for the effect of Angptl3 on increasing podocyte motility.