Effect of activating PKA signaling on dedifferentiation of podocytes in adriamycin-induced nephropathy mice / 上海交通大学学报(医学版)
Journal of Shanghai Jiaotong University(Medical Science)
; (12): 462-466, 2017.
Article
in Zh
| WPRIM
| ID: wpr-512547
Responsible library:
WPRO
ABSTRACT
Objective·To explore effects of pCPT-cAMP on proteinuria and dedifferentiation of podocytes in adriamycin (ADR)-induced nephropathy mice. Methods·Male BALB/c mice were divided into three groups. The control group did not make any intervention, and the other mice were administrated with ADR in a dose of 10 mg/kg by intravenous injection (ADR group). Some ADR-injected mice were treated with pCPT-cAMP [50 mg/(kg·d)] by intraperitoneal injection everyday (A+P group). Albumin urine was detected by Coomassie blue stain. Urine creatinine concentration was estimated by ELISA. The expression of WT-1 was detected by immunohistochemical staining. Immunofluorescence staining and Western blotting were used to evulate the dedifferentiation of podocytes. Results·Compared with the control group, the ratio of urinary albumin/creatinine in ADR nephropathy mice was significantly increased. WT-1 immunohistochemical staining showed that the number of podocytes was significantly decreased, while immunofluorescence double staining of podocyte-specific protein synaptopodin and podocalyxin remarkably reduced, and the expression of desmin was increased. pCPT-cAMP intervention decreased the ratio of albumin/creatinine in ADR mice, elevated the quantity of WT-1 positive cells and the expression of synaptopodin and podocalyxin, while desmin expression decreased. Conclusion·pCPT-cAMP activates the PKA signaling and protects ADR nephropathy mice by preventing the loss of podocytes and ameliorating the urine albumin/creatinine ratio, which may be mediated by pCPT-cAMP-prevented dedifferentiation of podocytes.
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Database:
WPRIM
Language:
Zh
Journal:
Journal of Shanghai Jiaotong University(Medical Science)
Year:
2017
Document type:
Article