Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2011
[Activation of Rho-kinase pathway is involved in angiotensin II-induced contraction of human airway smooth muscle cells].
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Li Ning, Meng Ying, Cheng Yuan-xiong, Niu Yi, Shen Bin, Li Xu, Lai Wen-yan
Аннотация
OBJECTIVE: To investigate of the regulatory effect of Rho-kinase pathway activation on angiotensin II (Ang II)-induced contraction of human airway smooth muscle cells (HASMCs) in vitro.
METHODS: Cultured primary HASMCs were divided into control group, AngII group, AngII + irbesartan group and AngII + Y-27632 group with corresponding treatment. AngII-induced contraction of HASMCs was evaluated using collagen gel lattices and observed morphologically using immunofluorescence assay. Western Blotting was significantly performed to examine the protein expression of Rho-kinase signal pathway.
RESULTS: AngII-induced HASMC contraction was inhibited by treatments with irbesartan and Y-27632 as shown by gel contraction assay (P<0.001). Y-27632 treatment produced a stronger inhibitory effect than irbesartan on the expression of phosphorylated moesin, a substrate of Rho kinase (P<0.05).
CONCLUSION: AngII induces the contraction of HASMCs partially as a result of activation of Rho-kinase pathway.
METHODS: Cultured primary HASMCs were divided into control group, AngII group, AngII + irbesartan group and AngII + Y-27632 group with corresponding treatment. AngII-induced contraction of HASMCs was evaluated using collagen gel lattices and observed morphologically using immunofluorescence assay. Western Blotting was significantly performed to examine the protein expression of Rho-kinase signal pathway.
RESULTS: AngII-induced HASMC contraction was inhibited by treatments with irbesartan and Y-27632 as shown by gel contraction assay (P<0.001). Y-27632 treatment produced a stronger inhibitory effect than irbesartan on the expression of phosphorylated moesin, a substrate of Rho kinase (P<0.05).
CONCLUSION: AngII induces the contraction of HASMCs partially as a result of activation of Rho-kinase pathway.