Abstract: Ｏｂｊｅｃｔｉｖｅ：To explore the possible molecular mechanisms involved in podocyte injury protection caused by growth associated protein43(GAP43).
Ｍｅｔｈｏｄｏｌｏｇｙ：(1)Expression of GAP43 in podocytes of patients with different glomerular diseases were observed by immunofluorescence staining and laser confocal microscopy. (2)Immortalized mouse podocytes was stimulated with lipopolysaccharide (LPS),expression of GAP43mRNA and protein were detected by Western blot,quantitative RTPCR and immunofluorescence staining.(3)Immortalized mouse podocytes were overexpressed GAP43 and were treated with LPS for 72h before harvest.Western blot,quantitative RTPCR and immunofluorescence staining were used to evaluate the expression of GAP43,nephrin,calcineurin and nuclear factor of activated T cells c1 (NFATc1).Using woundhealing assay,the migration in podocyte with overexpression GAP43 were analyzed.
Ｒｅｓｕｌｔｓ：GAP43 was decreased in LPStreated podocytes in vitro.Increased nephrin,decreased calcineurin and nuclear NFATc1 was observed in LPS treated podocyte with overexpression of GAP43; the migration ability was reduced after GAP43 overexpressing.
Ｃｏｎｃｌｕｓｉｏｎ：Our findings demonstrated that GAP43 ameliorates podocyte injury by suppressing calcineurin/NFATc1 signaling,which may present a promising target for therapeutic intervention.

Key words: growth associated protein-43, podocyte, apoptosis, nuclear factor of activated T cells cytoplasmic 1