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

RuiLan He | Zendy; ZhiJuan Wu | Zendy; Xiaoru Liu | Zendy; LongXin Gui | Zendy; Ruixing Wang | Zendy; MoJun Lin | Zendy

Open Access

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

Author(s) -

RuiLan He,

ZhiJuan Wu,

Xiaoru Liu,

LongXin Gui,

Ruixing Wang,

MoJun Lin

Publication year - 2018

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 - 10.1159/000492852

Subject(s) - nfat , calcineurin , apoptosis , propidium iodide , cell growth , cancer research , signal transduction , proliferating cell nuclear antigen , chemistry , biology , microbiology and biotechnology , endocrinology , medicine , programmed cell death , biochemistry , transplantation

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.

The content you want is available to Zendy users.

Already have an account? Click here to sign in.

Having issues? You can contact us here

Accelerating Research