Plasminogen activator Inhibitor-2 inhibits pulmonary arterial smooth muscle cell proliferation in pulmonary arterial hypertension via PI3K/Akt and ERK signaling
Journal Article
·
· Experimental Cell Research
- Department of Pulmonary and Critical Care Medicine, Center of Respiratory Medicine, China-Japan Friendship Hospital, Beijing (China)
- Department of Pulmonary and Critical Care Medicine, Beijing Hospital, National Center of Gerontology, Institute of Geriatric Medicine, Chinese Academy of Medical Sciences, Beijing (China)
- State Key Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, Department of Pathophysiology, Peking Union Medical College, Beijing (China)
- Cardiovascular Research Institute, Baylor College of Medicine, Houston, TX (United States)
Highlights: • Serum PAI-2 is decreased in patients with pulmonary arterial hypertension. • Serum PAI-2 is associated with disease severity in pulmonary arterial hypertension. • Exogenous PAI-2 attenuates monocrotaline induced pulmonary hypertension in rats. • PAI-2 inhibits pulmonary arterial smooth muscle proliferation via PI3K/Akt and ERK. The proliferation of pulmonary arterial smooth muscle cells (PASMCs) and subsequent pulmonary vascular remodeling leads to pulmonary arterial hypertension (PAH). Understanding the underlying mechanisms and identifying molecules that can suppress PASMCs proliferation is critical for developing effective pharmacological treatment. We previously showed that plasminogen activator inhibitor-2 (PAI-2) inhibited human PASMC (hPASMCs) proliferation in vitro. However, its inhibitory effect on PAH remains to be determined, and the mechanism remains to be illustrated.
- OSTI ID:
- 23195415
- Journal Information:
- Experimental Cell Research, Journal Name: Experimental Cell Research Journal Issue: 1 Vol. 398; ISSN 0014-4827; ISSN ECREAL
- Country of Publication:
- United States
- Language:
- English
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