Procyanidin B2-induced LKB1-AMPK activation mitigates vascular smooth muscle cell proliferation through inhibition of mTOR signaling

• 발행기관: 대한생리학회-대한약리학회
• 저자명: Hee Young Park Seul Gi Kim Gyeong Ju Bae Jin Young Sung Hyoung Chul Choi
• 간행물 정보: 『The Korean Journal of Physiology & Pharmacology』제29권 제5호, 659~667쪽, 전체 9쪽
• 주제분류: 의약학 > 의학일반
• 파일형태: PDF
• 발행일자: 2025.09.01

국문 초록

Vascular smooth muscle cell (VSMC) proliferation contributes to intimal thickening in atherosclerosis and restenosis diseases. As a proanthocyanidin type B, procyanidin B2 (PB2) is abundantly found in cocoa, apples, and grapes and is reported to have vascular protective effects. However, the mechanisms by which PB2 inhibits proliferation of VSMCs are not clearly understood. Therefore, the purpose of this study was to investigate the underlying mechanism of PB2-induced inhibition of cell proliferation in VSMCs. We found that PB2 dose- and time-dependently increased phosphorylation of liver kinase B1 (LKB1) and AMP-activated protein kinase (AMPK) in VSMCs. AMPK is a serine-threonine kinase and serves as a key sensor of cellular energy. PB2 induced LKB1 translocation from nucleus to cytosol which led to AMPK activation. In addition, PB2-induced AMPK activation decreased cell proliferation and cell cycle progression by inhibiting mammalian target of rapamycin signaling pathway. Transfection with LKB1 or AMPK siRNA and transduction of dominant-negative isoforms of the α1 and α2 subunits of AMPK eliminated anti-proliferative effects of PB2. These results demonstrate that PB2 might be a preventive agent for cardiovascular disorders such as atherosclerosis and hypertension.

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키워드

AMP-activated protein kinase Liver kinase B1 Mammalian target of rapamycin Procyanidin B2 Vascular smooth muscle cell