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 2019 and some content may be unavailable. To unlock all content for 2019, please visit the archives.

Abstract: SA-PO425

Tunneling Nanotubes Shuttle Lysosomes with Low-Level α-Galactosidase A from Non-Fabry to Fabry Podocytes In Vitro

Session Information

Category: Genetic Diseases of the Kidneys

  • 1002 Genetic Diseases of the Kidneys: Non-Cystic

Authors

  • Dastvan, Frank, University of Washington, Seattle, Washington, United States
  • Najafian, Behzad, University of Washington, Seattle, Washington, United States
Background

Fabry disease is an X-linked disease; however, females can suffer from serious complications. Biopsy studies are suggestive of no efficient cross-correction between non-Fabry and Fabry podocytes. We aimed to examine if there is any level of cross-correction between these cells in-vitro.

Methods

A conditionally immortalized human podocyte cell line with complete knock out of GLA (GLA-ko) using CRISPR-Cas9 was developed. Wild type (WT) podocytes were co-cultured with GLA-ko cells for a week, after which, GLA-ko and WT cells were separated by FACS sorting based on GFP expression in GLA-ko cells. Purity of sorted cells was confirmed by genotyping. Sorted co-cultured (CC) WT and GLA-ko, no co-culture (no-CC) WT and GLA-ko cells and culture media were tested for GLA-mRNA (qPCR), α-Gal-A [western blot (WB) and immunofluorescence (IF)], and α-Gal-A activity.

Results

GLA-mRNA in CC-GLA-ko cells was 2.6 fold less than WT podocytes, but 2.7 fold greater than no-CC-GLA-ko podocytes. No GLA-mRNA was detected in culture media. By WB, while no α-Gal-A protein was detected in no-CC-GLA-ko cells, this was present in CC-GLA-ko cells, albeit being 6 fold less than in WT podocytes, confirmed by IF for α-Gal-A. There was very scant α-Gal-A in media from WT and co-cultured podocytes by WB (31 fold and 15 fold less than intracellular WT, respectively). While there was almost no α-Gal-A activity in no-CC-GLA-ko podocytes, this was present in CC-GLA-ko cells, albeit being 6 fold less than in WT podocytes. There was no detectable α-Gal-A mRNA or enzyme activity in the media. A survival assay showed similarly reduced cellular proliferation in both CC-GLA-ko and no-CC-GLA-ko podocytes compared to CC-WT or no-CC-WT podocytes. IF staining showed tunneling nanotubes (TNTs) containing lysosomes and α-Gal-A running between the cells.

Conclusion

Our data suggest that there is small transfer of GLA-mRNA and α-Gal-A protein from non-Fabry to Fabry podocytes through TNTs. This low level cross-correction led to small increase in α-Gal-A activity in Fabry podocytes but was not enough to improve survival of these cells. It will be important to demonstrate if this phenomenon exists in-vivo and between other cells. These studies may lead to novel treatment options for females with Fabry disease.

Funding

  • Commercial Support –