Antimitogenic effect of green tea (-)-epigallocatechin gallate on 3T3-L1 preadipocytes depends on the ERK and Cdk2 pathways

Pei Fang Hung, Bo Tsung Wu, Hui Chian Chen, Yen Hang Chen, Chia Lin Chen, Ming Hua Wu, Hsien Chun Liu, Meng Jung Lee, Yung Hsi Kao

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122 Scopus citations

Abstract

Green tea catechins, especially (-)-epigallocatechin gallate (EGCG), have been proposed as a chemopreventative for obesity, diabetes, cancer, and cardiovascular diseases. However, relatively little is known about the mechanism of the action of EGCG on fat cell function. This study was designed to investigate the pathways of EGCG's modulation of the mitogenesis of 3T3-L1 preadipocytes. Preadipocyte proliferation as indicated by an increased number of cells and greater incorporation of bromodeoxyuridine (BrdU) was inhibited by EGCG in dose-, time-, and growth phase-dependent manners. Also, EGCG dose and time dependently decreased levels of phospho-ERK1/2, Cdk2, and cyclin D 1 proteins, reduced Cdk2 activity, and increased levels of G 0/G1 growth arrest, p21waf/cip, and p27 kip1, but not p18ink, proteins and their associations to Cdk2. However, neither MEK1, ERK1/2, p38 MAPK, phospho-p38, JNK, nor phospho-JNK was changed. Increased phospho-ERK1/2 content and Cdk2 activity, respectively, via the transfection of MEK1 and Cdk2 cDNA into preadipocytes prevented EGCG from reducing cell numbers. These data demonstrate the ERK- and Cdk2-dependent antimitogenic effects of EGCG. Moreover, EGCG was more effective than epicatechin, epicatechin gallate, and epigallocatechin in changing the mitogenic signals. The signal of EGCG in reducing growth of 3T3-L1 preadipocytes differed from that of 3T3 fibroblasts. Results of this study may relate to the mechanism by which EGCG modulates body weight.

Original languageEnglish
Pages (from-to)C1094-C1108
JournalAmerican Journal of Physiology - Cell Physiology
Volume288
Issue number5 57-5
DOIs
StatePublished - May 2005

Keywords

  • 3t3-L1 preadipocyte
  • Cyclin-dependent kinase
  • Mitogen-activated protein kinase

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