Anti‐apoptosis endothelial cell‐secreted microRNA‐195‐5p promotes pulmonary arterial smooth muscle cell proliferation and migration in pulmonary arterial hypertension

2017 ◽  
Vol 119 (2) ◽  
pp. 2144-2155 ◽  
Author(s):  
Zhen Zeng ◽  
Jun Yao ◽  
Yinchuan Li ◽  
Ying Xue ◽  
Yinghua Zou ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Smooth Muscle ◽  
Endothelial Cell ◽  
Pulmonary Arterial Hypertension ◽  
Arterial Smooth Muscle Cell ◽  
Cell Proliferation And Migration ◽  
Pulmonary Arterial ◽  
Pulmonary Arterial Smooth Muscle ◽  
And Migration ◽  
Proliferation And Migration

scholarly journals Dissecting histone deacetylase role in pulmonary arterial smooth muscle cell proliferation and migration

2014 ◽  
Vol 91 (2) ◽  
pp. 181-190 ◽  
Author(s):  
Margherita Galletti ◽  
Silvia Cantoni ◽  
Filippo Zambelli ◽  
Sabrina Valente ◽  
Massimiliano Palazzini ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Histone Deacetylase ◽  
Arterial Smooth Muscle Cell ◽  
Cell Proliferation And Migration ◽  
Pulmonary Arterial ◽  
Pulmonary Arterial Smooth Muscle ◽  
And Migration ◽  
Proliferation And Migration

scholarly journals Calcineurin/NFAT Signaling Modulates Pulmonary Artery Smooth Muscle Cell Proliferation, Migration and Apoptosis in Monocrotaline-Induced Pulmonary Arterial Hypertension Rats

2018 ◽  
Vol 49 (1) ◽  
pp. 172-189 ◽  
Author(s):  
Rui-Lan He ◽  
Zhi-Juan Wu ◽  
Xiao-Ru Liu ◽  
Long-Xin Gui ◽  
Rui-Xing Wang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Smooth Muscle ◽  
Pulmonary Arterial Hypertension ◽  
Pulmonary Artery ◽  
Apoptosis Resistance ◽  
Pulmonary Arterial ◽  
Pulmonary Artery Smooth Muscle ◽  
And Migration ◽  
Excessive Proliferation ◽  
Proliferation And Migration

Background/Aims: Pulmonary arterial hypertension (PAH) is a severe and debilitating disease characterized by remodeling of the pulmonary vessels, which is driven by excessive proliferation and migration and apoptosis resistance in pulmonary artery smooth muscle cells (PASMCs). The calcineurin (CaN)/nuclear factor of activated T-cells (NFAT) signaling pathway is the most important downstream signaling pathway of store-operated Ca2+ entry (SOCE), which is increased in PAH. CaN/NFAT has been reported to contribute to abnormal proliferation in chronic hypoxia (CH)-induced PAH. However, the effect of CaN/NFAT signaling on PASMC proliferation, migration and apoptosis in monocrotaline (MCT)-induced PAH remains unclear. Methods: PAH rats were established by a single intraperitoneal injection of MCT for 21 days. PASMCs were isolated and cultured in normal and MCT-induced PAH Sprague-Dawley rat. PASMCs were treated with CsA targeting CaN and siRNA targeting NFATc2-4 gene respectively by liposome. We investigated the expression of calcineurin/NFAT signaling by immunofluorescence, qRT-PCR and Western blotting methods. Cell proliferation was monitored using MTS reagent or by assessing proliferating cell nuclear antigen (PCNA) expression. Cell apoptosis was evaluated with an Annexin V - FITC/propidium iodide (PI) apoptosis kit by flow cytometry. PASMC migration was assessed with a Transwell chamber. Results: MCT successfully induced PAH and pulmonary vascular remodeling in rats. CaN phosphatase activity and nuclear translocation of NFATc2-4 were increased in PASMCs derived from MCT-treated rats. In addition, CaNBβ/NFATc2-4 expression was amplified at the mRNA and protein levels. PASMC proliferation and migration were markedly inhibited in a dosedependent manner by cyclosporin A (CsA). Furthermore, siRNA targeting NFATc2 and NFATc4 attenuated the excessive proliferation and migration and apoptosis resistance in PASMCs derived from both CON and MCT-treated rats, while NFATc3 knockdown specifically affected MCT-PASMCs. Conclusion: Our results demonstrate that CaN/NFAT signaling is activated and involved in the modulation of PASMC proliferation, migration and apoptosis in MCT-induced PAH.

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