Abstract:

Ｏｂｊｅｃｔｉｖｅ：To investigate the role of growth arrest and DNA damageinducible  protein 45β (GADD45B) in podocytes injury of zebrafish.
Ｍｅｔｈｏｄｏｌｏｇｙ：（1）Immunohistochemistry and QPCR were used to detect the expression of GADD45B in glomeruli of patients with focal segmental glomerulosclerosis (FSGS).（2）Correlation analysis was used to analyze the relationship between the expression level of GADD45B mRNA and the clinical related indexes of patients with FSGS.（3）RTPCR detected the expression of GADD45Ba/bb in the glomeruli of zebrafish.（4）Transgenic zebrafish was screened by fluorescence microscopy,and in situ hybridization identification of transgenic zebrafish GADD45Ba/bb was expressed on the glomeruli.（5）Metronidazole (MTZ) induced podocytes damage in transgenic zebrafish.(6) ELISA was used to detect proteinuria,and apoptosis was detected by caspase staining.
Ｒｅｓｕｌｔｓ：GADD45B mRNA and protein levels were upregulated in the glomeruli of  patients with FSGS and the expression level was negatively correlated with renal function of the patients.In an in vivo zebrafish model of inducible podocyte injury that we previously established,we found that podocytespecific overexpression of zebrafish orthologs of GADD45B exacerbated edema,proteinuria and foot effacement,while inhibition of GADD45B expression by morpholino oligo in zebrafish larvae ameliorated podocyte injury.
Ｃｏｎｃｌｕｓｉｏｎ：
Taken together,our findings demonstrated that GADD45B is an important mediator of podocyte apoptosis upon injury and may be a therapeutic target for the management of podocyte injury in glomerular diseases.

Key words: Growth Arrest and DNA-damage-inducible, beta, focal segmental glomerulosclerosis, zebrafish