ASN's Mission

To create a world without kidney diseases, the ASN Alliance for Kidney Health elevates care by educating and informing, driving breakthroughs and innovation, and advocating for policies that create transformative changes in kidney medicine throughout the world.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005

email@asn-online.org

202-640-4660

The Latest on X

Kidney Week

Please note that you are viewing an archived section from 2022 and some content may be unavailable. To unlock all content for 2022, please visit the archives.

Abstract: FR-PO718

Geranylgeranylation of Small GTPase Is Critical to Preserving the Glomerular Filtration Barrier Integrity

Session Information

Category: Glomerular Diseases

  • 1304 Glomerular Diseases: Podocyte Biology

Authors

  • Boi, Roberto, University of Gothenburg, Institute of Neurosciences and Physiology, Gothenburg, Sweden
  • Bergwall, Lovisa, University of Gothenburg, Institute of Neurosciences and Physiology, Gothenburg, Sweden
  • Ebefors, Kerstin, University of Gothenburg, Institute of Neurosciences and Physiology, Gothenburg, Sweden
  • Nystrom, Jenny C., University of Gothenburg, Institute of Neurosciences and Physiology, Gothenburg, Sweden
  • Buvall, Lisa, University of Gothenburg, Institute of Neurosciences and Physiology, Gothenburg, Sweden
Background

Actin cytoskeleton maintenance in podocytes is carefully and yet dynamically regulated by RhoGTPases Rac1, Cdc42, and RhoA and other small GTPases such as Rap1. These GTPases are commonly post-translational modified by geranylgeranyltransferase type-I (GGTase-I) or farnesyltransferase (FTase), which covalently transfer respectively a geranylgeranyl or a farnesyl to their target GTPases. These modifications are known as prenylation and are known to have a regulatory activity on small GTPases. Our hypothesis is that prenylation plays an important role in the regulation of normal glomerular permselectivity and that dysregulation leads to proteinuria and progression of glomerular disease.

Methods

The glomerular expression of GGTase-I was localized using immunofluorescence. Podocyte-specific GGTase-I and FTase knockout mice were generated. Albuminuria and foot process effacement (TEM) were used to investigate filtration barrier function. Depletion of GGTase-I was studied also in vitro using an inhibitor or with knockdown of gene expression. Immunofluorescence was used to analyze modifications of the actin cytoskeleton and β1 integrin localization.

Results

GGTase-I was found to be expressed mainly by the podocytes in the human glomerulus. In vivo experiments in mice showed that GGTase-I knockout caused early-onset progressive albuminuria, accompanied by foot process effacement, while littermate controls and FTase knockout mice did not. In vitro, GGTase-I knockdown or inhibition markedly increased RhoA, Rac1, Cdc42, and Rap1 activation. This caused actin cytoskeleton disruption and altered β1 integrin distribution.

Conclusion

In podocytes, geranylgeranylation was shown to be important in maintaining the balance of RhoGTPases and Rap1 and to be crucial for maintaining glomerular integrity and function.

Funding

  • Government Support – Non-U.S.