<i>APOL1</i> Kidney-Risk Variants Induce Mitochondrial Fission.
Lijun Ma, Hannah C. Ainsworth, James A. Snipes, Mariana Murea, Young A. Choi, Carl D. Langefeld, John S. Parks, Manish S. Bharadwaj, Jeff W. Chou, Ashok K. Hemal, Snežana Petrović, Ann L. Craddock, Dongmei Cheng, Gregory A. Hawkins, Lance D. Miller, Pamela J Hicks, Moin A. Saleem, Jasmin Divers, Anthony Molina, Barry I. Freedman
Abstract
INTRODUCTION: -nephropathy. METHODS: A global gene expression analysis was performed in human primary renal tubule cell lines derived from 50 African American individuals. Follow-up gene knock out, cell-based rescue, and microscopy experiments were performed. RESULTS: G0, G1, and G2 were created; G0 cells appeared to promote mitochondrial fusion, whereas G1 and G2 induced mitochondrial fission. The mitochondrial dynamic regulator Mdivi-1 significantly preserved cell viability and mitochondrial cristae structure and reversed mitochondrial fission induced by overexpression of G1 and G2. CONCLUSION: -nephropathy.