[Effects of adiponectin on endoplasmic reticulum stress-mediated apoptosis and cell cytoskeleton and its mechanism of podocytes cultured in high glucose].
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.


CONCLUSIONS
Adiponectin plays a protective role in high glucose-induced podocyte through reducing endoplasmic reticulum stress-induced apoptosis and blunting the injury of cytoskeleton.
Department of Microbiology & Immunology, Shanxi Medical University, Taiyuan 030001, China.
Yanhong
Y
Wang
Jihua
J
Tian
Haixiu
H
Guo
Yang
Y
Mi
Jiaming
J
Li
Department of Nephrology, Shanxi Provincial People's Hospital, Shanxi Kidney Disease Institute, Taiyuan 030012, China. Email: rongshanli13@163.com.
Rongshan
R
Li
D052242:Adiponectin / Q000378:metabolism / Q000494:pharmacology*; D017209:Apoptosis; D053454:Caspase 12 / Q000378:metabolism; D002478:Cells, Cultured; D003599:Cytoskeleton / Q000187:drug effects*; D000091342:Endoplasmic Reticulum Chaperone BiP; D059865:Endoplasmic Reticulum Stress; D005947:Glucose / Q000378:metabolism / Q000494:pharmacology*; D006360:Heat-Shock Proteins / Q000378:metabolism; D006801:Humans; D050199:Podocytes / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D051742:Transcription Factor CHOP / Q000378:metabolism
D052242:Adiponectin; C497249:DDIT3 protein, human; D000091342:Endoplasmic Reticulum Chaperone BiP; C000717247:HSPA5 protein, human; D006360:Heat-Shock Proteins; D051742:Transcription Factor CHOP; C506444:CASP12 protein, human; D053454:Caspase 12; D005947:Glucose