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Genetic ablation of calcium-independent phospholipase A 2 γ (iPLA 2 γ) in mice results in marked damage of mitochondria and enhanced autophagy in glomerular visceral epithelial cells (GECs) or podocytes. The present study addresses the role of iPLA 2 γ in glomerular injury. In adriamycin nephrosis, deletion of iPLA 2 γ exacerbated albuminuria and reduced podocyte number. Glomerular LC3-II increased and p62 decreased in adriamycin-treated iPLA 2 γ knockout (KO) mice, compared with treated control, in keeping with increased autophagy in KO. iPLA 2 γ KO GECs in culture also demonstrated increased autophagy, compared with control GECs. iPLA 2 γ KO GECs showed a reduced oxygen consumption rate and increased phosphorylation of AMP kinase (pAMPK), consistent with mitochondrial dysfunction. Adriamycin further stimulated pAMPK and autophagy. After co-transfection of GECs with mito-YFP (to label mitochondria) and RFP-LC3 (to label autophagosomes), or RFP-LAMP1 (to label lysosomes), there was greater colocalization of mito-YFP with RFP-LC3-II and with RFP-LAMP1 in iPLA 2 γ KO GECs, compared with WT, indicating enhanced mitophagy in KO. Adriamycin increased mitophagy in WT cells. Thus, iPLA 2 γ has a cytoprotective function in the normal glomerulus and in glomerulopathy, as deletion of iPLA 2 γ leads to mitochondrial damage and impaired energy homeostasis, as well as autophagy and mitophagy.

Genetic Ablation of Calcium-independent Phospholipase A2γ Exacerbates Glomerular Injury in Adriamycin Nephrosis in Mice