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Downregulation of CD2‐associated protein impaired the physiological functions of podocytes
Author(s) -
Zhang Chun,
Jiang HuaJun,
Chang Ying,
Fang Zhan,
Sun XiFeng,
Liu JianShe,
Deng AnGuo,
Zhu ZhongHua
Publication year - 2009
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1016/j.cellbi.2009.02.017
Subject(s) - nephrin , podocyte , microbiology and biotechnology , downregulation and upregulation , transfection , phosphorylation , cortactin , actin cytoskeleton , cell cycle , cytoskeleton , biology , cell , chemistry , cell culture , gene , endocrinology , kidney , proteinuria , biochemistry , genetics
Emerging evidences show that CD2‐associated protein (CD2AP) is involved in podocyte injury and the pathogenesis of proteinuria. However, the exact molecular mechanism by which CD2AP exerts its biological function is elusive. We knocked down CD2AP gene by target siRNA in conditionally immortalized mouse podocytes, which showed lowered cell adhesion and spreading ability ( P < 0.05). At the same time, cell cycle was arrested in G2/M phase ( P < 0.05), and pathologic nuclear division could easily be seen in CD2AP siRNA‐transfected podocytes. The proliferation of podocytes were also inhibited significantly by CD2AP siRNA transfection ( P < 0.05). Further study revealed disordered distributions of F‐actin, as well as lowered nephrin expression and phosphorylation in podocytes. These data suggest that CD2AP may play a crucial role in maintaining the normal function of podocytes and lowered CD2AP causes podocyte injury by disrupting the cytoskeleton and disturbing the nephrin‐CD2AP signaling pathway.