본문 바로가기
HOME> 논문 > 논문 검색상세

논문 상세정보

Journal of cellular physiology v.233 no.10, 2018년, pp.6839 - 6850  

ROS‐Autophagy pathway mediates monocytes‐human umbilical vein endothelial cells adhesion induced by apelin‐13

Liu, Meiqing (Institute of Pharmacy and Pharmacology, University of South China, Hengyang, China ) ; Li, Hening (Institute of Pharmacy and Pharmacology, University of South China, Hengyang, China ) ; Zhou, Qun (Institute of Pharmacy and Pharmacology, University of South China, Hengyang, China ) ; Zhao, Hong (Institute of Pharmacy and Pharmacology, University of South China, Hengyang, China ) ; Lv, Deguan (Institute of Pharmacy and Pharmacology, University of South China, Hengyang, China ) ; Cao, Jiangang (Institute of Pharmacy and Pharmacology, University of South China, Hengyang, China ) ; Jiang, Jinyong (Institute of Pharmacy and Pharmacology, University of South China, Hengyang, China ) ; Tang, Mingzhu (Institute of Pharmacy and Pharmacology, University of South China, Hengyang, China ) ; Wu, Di (Institute of Pha ) ; Liu, Jiaqi ; Wu, Lele ; Hu, Haoliang ; He, Lu ; Huang, Shifang ; Chen, Zhe ; Li, Lanfang ; Chen, Linxi ;
  • 초록  

    Apelin is the endogenous ligand of APJ receptor. Both monocytes (MCs) and human umbilical vein endothelial cells (HUVECs) express apelin and APJ, which play important roles in the physiological processes of atherosclerosis. Our previous research indicated that apelin‐13 promoted MCs‐HUVECs adhesion. Here, we further explore the mechanism responsible for MCs‐HUVECs adhesion induced by apelin‐13. Apelin‐13 promoted reactive oxygen species (ROS) generation and NOX4 expression in HUVECs. Apelin‐13 inducedautophagy, increased proteins beclin1 and LC3‐II/I expression and induced autophagy flux in HUVECs, which was blocked by NAC, catalase and DPI. Autophagy flux induced by apelin‐13 was inhibited by NAC and catalase but not hydroxychloroquine (HCQ). NAC, catalase, and DPI prevented apelin‐13 induced ICAM‐1 expression in HUVECs. Rapamycin enhanced MCs–HUVECs adhesion that was reversed by NAC, catalase, and DPI. Down‐regulation of beclin1 and LC3 by siRNA blocked MCs‐HUVECs adhesion. Apelin‐13 induced atherosclerotic plaque and increased NOX4, LC3‐II/I expression in ApoE−/−(HFD) mouse model. Our results demonstrated that apelin‐13 induced MCs–HUVECs adhesion via a ROS‐autophagy pathway.


  • 주제어

    apelin‐13 .   autophagy .   cell adhesion .   NOX .   ROS.  

 활용도 분석

  • 상세보기

    amChart 영역
  • 원문보기

    amChart 영역

원문보기

무료다운로드
  • 원문이 없습니다.
유료다운로드

유료 다운로드의 경우 해당 사이트의 정책에 따라 신규 회원가입, 로그인, 유료 구매 등이 필요할 수 있습니다. 해당 사이트에서 발생하는 귀하의 모든 정보활동은 NDSL의 서비스 정책과 무관합니다.

원문복사신청을 하시면, 일부 해외 인쇄학술지의 경우 외국학술지지원센터(FRIC)에서
무료 원문복사 서비스를 제공합니다.

NDSL에서는 해당 원문을 복사서비스하고 있습니다. 위의 원문복사신청 또는 장바구니 담기를 통하여 원문복사서비스 이용이 가능합니다.

이 논문과 함께 출판된 논문 + 더보기