Objective: To explore the effects of adiponectin (APN) on high glucose-induced endoplasmic reticulum stress (ERS)-mediated apoptosis and cytoskeleton.
Methods: The conditionally immortal human glomerular podocytes were divided into normal glucose, mannitol, high glucose and high glucose with adiponectin groups. Flow cytometry was employed to assess cell apoptosis.Real-time polymerase chain reaction (PCR) and Western blot were used to detect the expressions of such ERS molecules as GRP78, CHOP and caspase 12 and desmin and TRPC6. Immunofluorescent staining was used to detect the changes in the skeleton of podocyte.
Results: (1) The apoptosis rate in high glucose group is significantly higher than the other groups (26.15% ± 1.38% vs 2.39% ± 0.58%, 4.84% ± 0.87%, 16.71% ± 1.15%, all P < 0.05). Compared with control group, the mRNA and protein expressions of GRP78, CHOP and caspase 12 were all up-regulated significantly in high glucose group (P < 0.05). The high glucose with adiponectin group could reduce the podocyte apoptosis by 10% and down-regulated the mRNA and protein expressions of GRP78, CHOP and caspase 12 versus high glucose group (all P < 0.05). (2) High glucose-induced podocyte caused the up-regulated expressions of TRPC6 and desmin (all P < 0.05) and it was inhibited by adiponectin (all P < 0.05). Additionally, immunofluorescent assay of high glucose-induced podocyte cytoskeleton showed disorderly F-actin and absent tensile fiber. Adiponectin prevented the F-actin cytoskeleton disruption under high glucose.
Conclusion: Adiponectin plays a protective role in high glucose-induced podocyte through reducing endoplasmic reticulum stress-induced apoptosis and blunting the injury of cytoskeleton.