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Epigallocatechin Gallate Induces Upregulation of LDL Receptor via the 67 kDa Laminin Receptor‐Independent Pathway in HepG2 Cells
Author(s) -
Zanka Kumiko,
Kawaguchi Yuya,
Okada Yudai,
Nagaoka Satoshi
Publication year - 2020
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.201901036
Subject(s) - ldl receptor , downregulation and upregulation , receptor , mapk/erk pathway , microbiology and biotechnology , gene knockdown , signal transduction , biology , chemistry , cell culture , biochemistry , lipoprotein , cholesterol , gene , genetics
Scope 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. Methods and results 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. Conclusion EGCG activates LDLR expression via 67LR‐independent pathway in HepG2 cells.