Adiponectin inhibits foaming of vascular smooth muscle cells through PKC/RACK1 pathway

Objective To investigate the effect of adiponectin(APN) on the foaming process of vascular smooth muscle cells (VSMCs) through protein kinase C (PKC) / receptor for activated C kinase1 (RACK1) pathway and the relevant mechanism. Methods VSMCs were cultured in vitro and divided into blank control group, oxidized low-density lipoprotein (ox-LDL) treatment group, and ox-LDL+ APN treatment group.The blank control cells were cultured normally, and the other two groups were treated with ox-LDL (50 μg/mL) to establish foam models.After APN administration, oil red O staining and cholesterol content determination were used to analyze cell foaming conditions.Western-blotting and reverse transcription-polymerase chain reaction (RT-PCR) were utilized to detect the protein levels and gene expression of PKC and RACK1. Results Compared with control, the cell nucleus of the ox-LDL model group had a prominent nucleus, a large number of red lipid droplets accumulation in the cytoplasm, and foam cell formation.And at the same time, cellular cholesterol levels were significantly increased from (21.34±4.35) μmol/L to (109.97±11.60) μmol/L(t=41.27, P<0.05). The protein levels and gene expression of PKC/RACK1 increased significantly(t values were 11.64, 14.58 and 27.90, 24.38 respectively, all P values <0.05). After the APN intervention, the intracellular red lipid droplets and the number of foam cells were significantly reduced.The cholesterol content decreased to (54.27±6.89) μmol/L(P<0.05), and the protein levels and gene expression of PKC/RACK1 were significantly suppressed(t values were 7.57, 8.91 and 13.27, 10.99 respectively, all P values <0.05). Conclusion APN could significantly inhibit the foaming of VSMCs, which might be related to the regulation of PKC/RACK1 pathway. Key words: Adiponectin; Cell foaming; Protein kinase C/receptor for activated C kinase1