Send to

Choose Destination
PLoS One. 2017 Dec 6;12(12):e0189156. doi: 10.1371/journal.pone.0189156. eCollection 2017.

Down-regulation of the klf5-c-Myc interaction due to klf5 phosphorylation mediates resveratrol repressing the caveolin-1 transcription through the PI3K/PKD1/Akt pathway.

Author information

Department of Clinical Nutrition, Kecheng People's Hospital, Quzhou, Zhejiang Province, China.
Department of Preventive Medicine, Wenzhou Medical University, Wenzhou, Zhejiang Province, China.
School of Basic Medical Sciences, Shandong Medical College, Linyi, Shandong Province, China.
School of Economics, Huazhong University of Science and Technology, Wuhan, Hubei Province, China.


Resveratrol (RSV), a natural polyphenol, has been reported to produce effect on genes transcription in lipid metabolism. In this study, we aim to explore the novel mechanisms of RSV on the regulation of caveolin-1 (Cav-1) transcription. Via body weight, blood glucose, serum lipid, and liver pathology detection, we found that RSV decreased body weight, blood glucose and lipid accumulation in rats fed high-fat diet. Based on co-immunoprecipitation (Co-IP) and western blotting assay, we found that RSV up-regulated klf5 phosphorylation and decreased the interaction of klf5 with c-Myc, which were accompanied by down-regulation of Cav-1 expression in livers of rats fed with high-fat diet. Moreover, in HEK293 cells, we observed RSV enhanced klf5 phosphorylation and separated the interaction of klf5 with c-Myc through inhibiting the activation of PI3K/PKD1/Akt pathway, which maybe promoted c-Myc binding to the promoter to inhibit Cav-1 expression. The results of the present study demonstrated that RSV activated klf5 phosphorylation by inhibiting PI3K/PKD1/Akt pathway, and then attenuated the interaction of klf5 with c-Myc, subsequently probably promoted the c-Myc binding to the promoter to repress Cav-1 expression.

[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Public Library of Science Icon for PubMed Central
Loading ...
Support Center