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논문분류	춘계학술대회 초록집
제목	Mitochondrial Dysfunction in Podocyte Induces Proteinuria via Decrease of Alpha Actinin-4 and Synaptopodin
저자	Dae Eun Choi, Jin Young Jeong, Ki Ryang Na, Kang Wook Lee, Young Tai Shin
출판정보	2013; 2013(1):
키워드	Podocyte, Actin, Mitochondria
초록	Introduction: We reported that Crif1 deletion induce severe mitochondrial destruction in mice podocyte. There results induce massive albuminuria and effacement of foot process in mice. Actin cytoskeleton architecture and dynamics in podocyte are important constituents of the glomerular filtration barrier. There have been few studies about relation of mitochondria and actin cytoskeleton in podocytes of glomerulus. We evaluated the changes of actin cytoskeletal proteins and artchitecture in mitochondrial injured podocyte. Methods: We used immortalized mouse podocyte cell line. Crif1 silencing(si)RNA treatment was used for inducing mitochondrial injury. We divided 3 groups; control podocytes, scrumble(sc) RNA treated podocytes, Crif1 siRNA treated podocytes. We checked the expression of mitochondrial respiratory complex I-V, WT-1, and Crif1 for mitochondrial dysfunction in immortalized podocyte. We evaluated the expression of alpha actinin 4, synaptopodin, nephrin, ZO-1, and colfillin using western blot. Using confocal microscopy, we examined actin cytoskeleton architecture and mitochondria of podocyte. For evaluation of cell migration, we performed scratch assay. Results: Crif1 siRNA treatment reduced the expressions of mitochondrial respiratory complex IV and O2 consumption in cultured podocytes. Alpha actinin-4 and synaptopodin were decreased in Crif1 siRNA treated podocyte compared to control and Crif1 scRNA treated podocytes. There were no differences in nephrin and ZO-1. Crif1 siRNA treated podocyte showed an enhanced formation of dot-like alpha actinin-4 and an increase of fragment mitochondria in confocal microscopy compared to scRNA treated podocyte. Podocyte migration was increased in Crif1 siRNA treated podocyte. Conclusion: With the above results, it is speculated that mitochondrial dysfunction induced by crif1 inhibition reduces alpha actinin-4 and synaptopodin in podocyte.
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