Effect of m-nisoldipine on the Ca2+/CaM/CaN signal pathway in 5-HT-induced proliferation of rat PASMCs.
- Author:
Xue-Yan CHEN
1
;
Huan-Long LIU
;
Zhen-Hua PAN
;
Qing-Feng MIAO
;
Yong-Jian ZHANG
Author Information
1. Department of Pharmacology, Hebei Medical University, Shijiazhuang 050017, China.
- Publication Type:Journal Article
- MeSH:
Animals;
Antihypertensive Agents;
pharmacology;
Calcineurin;
genetics;
metabolism;
Calcium;
metabolism;
Calcium Channel Blockers;
pharmacology;
Calmodulin;
genetics;
metabolism;
Cell Proliferation;
drug effects;
Cells, Cultured;
Male;
Myocytes, Smooth Muscle;
cytology;
metabolism;
Nisoldipine;
pharmacology;
Pulmonary Artery;
cytology;
RNA, Messenger;
metabolism;
Rats;
Rats, Wistar;
Serotonin;
pharmacology;
Signal Transduction
- From:
Acta Pharmaceutica Sinica
2010;45(1):49-54
- CountryChina
- Language:Chinese
-
Abstract:
This study is to explore the activation of the Ca2+/CaM/CaN signal pathway in 5-HT-induced proliferation of rat pulmonary artery smooth muscle cells (PASMCs) and the inhibitory effect of m-nisoldipine (m-Nis) on this pathway. PASMCs were cultured with the explant technique. The proliferation of PASMCs was evaluated by MTT assay. Confocal microscopy was used to measure the change of [Ca2+]i. The mRNA expression of CaM and CaN was evaluated by RT-PCR and the activity of CaN was measured according to the instruction of kits. The results of MTT assay suggested that 5-HT (1 micromol x L(-1)) significantly induced the proliferation of rat PASMCs (P < 0.01), which was inhibited obviously by m-Nis (P < 0.05 or P < 0.01). Similarly, m-Nis inhibited 5-HT-induced elevation of [Ca2+]i (P < 0.01). The mRNA expression of CaM, CaN and the activation of CaN were also inhibited by m-Nis at different degrees (P < 0.05 or P < 0.01). Thus, the results of this study suggested that Ca2+/CaM/CaN signal pathway played an important role in 5-HT-induced proliferation of rat PASMCs, the inhibition of m-Nis on proliferation of rat PASMCs may be related to the blockage of Ca2+/CaM/CaN signal pathway by inhibiting the elevation of [Ca2+]i.
