SalA Attenuates Hypoxia-Induced Endothelial Endoplasmic Reticulum Stress and Apoptosis via Down-Regulation of VLDL Receptor Expression | Zendy

Ping Xie | Zendy; Yingchun Duan | Zendy; Xianzhi Guo | Zendy; Lina Hu | Zendy; Minghua Yu | Zendy

Open Access

SalA Attenuates Hypoxia-Induced Endothelial Endoplasmic Reticulum Stress and Apoptosis via Down-Regulation of VLDL Receptor Expression

Author(s) -

Ping Xie,

Yingchun Duan,

Xianzhi Guo,

Lina Hu,

Minghua Yu

Publication year - 2015

Publication title -

cellular physiology and biochemistry

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.486

H-Index - 87

eISSN - 1421-9778

pISSN - 1015-8987

DOI - 10.1159/000369671

Subject(s) - apoptosis , unfolded protein response , umbilical vein , hypoxia (environmental) , microbiology and biotechnology , chemistry , endothelial stem cell , endoplasmic reticulum , biology , biochemistry , organic chemistry , oxygen , in vitro

Salvianolic acid A (SalA) has been shown to display robust protection against endothelial injury. VLDL receptor (VLDLr) is expressed at high levels in the endothelial cells. However its endothelial biological function has not been completely elucidated. Here, we investigated molecular effects of SalA on endothelial VLDLr expression, ER stress, and apoptosis under hypoxia condition.

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