Open AccessSulfur Dioxide Inhibits Extracellular Signal-regulated Kinase Signaling to Attenuate Vascular Smooth Muscle Cell Proliferation in Angiotensin II-induced Hypertensive Mice
Author(s) -
Huijuan Wu,
Yaqian Huang,
Qinghua Chen,
Xiaoyu Tian,
Jia Liu,
Chaoshu Tang,
Hongfang Jin,
Junbao Du
Publication year - 2016
Publication title -
chinese medical journal/chinese medical journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.537
H-Index - 63
eISSN - 2542-5641
pISSN - 0366-6999
DOI - 10.4103/0366-6999.189927
Subject(s) - angiotensin ii , vascular smooth muscle , mapk/erk pathway , cell growth , endocrinology , chemistry , proliferating cell nuclear antigen , kinase , medicine , extracellular , renin–angiotensin system , pharmacology , biology , biochemistry , receptor , blood pressure , smooth muscle
Clarifying the mechanisms underlying vascular smooth muscle cell (VSMC) proliferation is important for the prevention and treatment of vascular remodeling and the reverse of hyperplastic lesions. Previous research has shown that the gaseous signaling molecule sulfur dioxide (SO2) inhibits VSMC proliferation, but the mechanism for the inhibition of the angiotensin II (AngII)-induced VSMC proliferation by SO2has not been fully elucidated. This study was designed to investigate if SO2inhibited VSMC proliferation in mice with hypertension induced by AngII.