Epigallocatechin Gallate Induces Upregulation of LDL Receptor via the 67 kDa Laminin Receptor-Independent Pathway in HepG2 Cells.

Epigallocatechin gallate (EGCG), an active polyphenol in green tea, exhibits various physiological effects, including activation of low-density lipoprotein receptors (LDLR). The previous studies have suggested that EGCG activates LDLR via extracellular signal-regulated kinase (ERK) pathway in HepG2 cells. However, the detailed molecular mechanism remains unclear. Recently, 67 kDa laminin receptor (67LR) is identified as a receptor for EGCG. Therefore, this study aims to determine whether 67LR is involved in the mechanism of LDLR activation by EGCG. EGCG induces upregulation of LDLR when 67LR is knocked down in HepG2 cells. Similar effect is observed after the cells are treated with 67LR monoclonal antibody. The loss of antiallergic effect following 67LR siRNA knockdown and 67LR antibody treatment confirms the results since the antiallergic effect of EGCG is known to be mediated by 67LR. EGCG activates LDLR expression via 67LR-independent pathway in HepG2 cells. © 2020 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.

Citation

Kumiko Zanka, Yuya Kawaguchi, Yudai Okada, Satoshi Nagaoka. Epigallocatechin Gallate Induces Upregulation of LDL Receptor via the 67 kDa Laminin Receptor-Independent Pathway in HepG2 Cells. Molecular nutrition & food research. 2020 Apr;64(7):e1901036

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PMID: 31978263

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