期刊
PHYSIOLOGICAL REPORTS
卷 6, 期 13, 页码 -出版社
WILEY
DOI: 10.14814/phy2.13785
关键词
CuZn-SOD; kidney; nephrin; oxidative stress; podocyte injury; preeclampsia
类别
资金
- Bristol, UK
- Louisiana State University Health Sciences Center - Shreveport, LA, USA
Recent findings of podocyte shedding/podocyturia highlight the central significance of podocyte injury in preeclampsia, a hypertensive disorder unique to human pregnancy. To test the hypothesis that oxidative stress contributes to kidney podocyte injury in preeclampsia, we specifically examined expression and distribution of antioxidant CuZn-SOD with nephrin and podoplanin in shed podocytes from women with preeclampsia. Human podocyte AB 8/13 cells served as control. We found that CuZn-SOD was localized at the front/outreach region of nephrin at the cell periphery (foot process areas) in control podocytes and expression of CuZn-SOD, nephrin, and podoplanin were all dislocated or lost in shed podocytes from preeclamptic patients. We further tested oxidative stress-induced nephrin shedding in podocytes, in which AB 8/13 podocytes were cultured under lowered oxygen condition (2%O-2) or treated with hypoxic mimicking agent cobalt chloride. Our results showed that reduced nephrin and podoplanin expression were associated with downregulation of CuZn-SOD expression in podocytes when cells were cultured under lowered oxygen or hypoxic conditions. Nephrin shed in urinary specimen from preeclamptic women was also determined by immunoprecipitation/immunoblotting. The molecular sizes of nephrin that corresponded to that were lost when cells were cultured under hypoxic conditions. We concluded that increased oxidative stress plays a significant role in inducing podocyte protein shedding in preeclampsia.
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