1. The role of miRNA-155 in monocrotaline-induced pulmonary arterial hypertension through c-Fos/NLRP3/caspase-1
- Author
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Pei-Zhe Tang, Tao Liu, Shou-Dong Chai, Zhen-Kun Li, Mingfeng Dong, Rui Liu, Jiantang Wang, and Sheng-Jun Ma
- Subjects
0301 basic medicine ,Health, Toxicology and Mutagenesis ,Caspase 1 ,Inflammation ,Pharmacology ,Toxicology ,c-Fos ,Pathology and Forensic Medicine ,In vitro model ,03 medical and health sciences ,0302 clinical medicine ,Smooth muscle ,microRNA ,medicine ,Nisoldipine ,General Pharmacology, Toxicology and Pharmaceutics ,integumentary system ,biology ,Chemistry ,Cell growth ,Public Health, Environmental and Occupational Health ,030104 developmental biology ,030220 oncology & carcinogenesis ,biology.protein ,medicine.symptom ,medicine.drug - Abstract
Nisoldipine can effectively suppress pulmonary arterial smooth muscle cell proliferation and c-Fos expression. To identify the mechanism of the anti-inflammatory effects in monocrotaline-induced pulmonary arterial hypertension (PAH), focusing on the c-Fos/NLRP3/caspase-1 pathway. In a mice model of monocrotaline-induced PAH, miRNA-155 expression was increased. In an in vitro model, overexpression of miRNA-155 promoted inflammation and induced c-Fos, NLRP3, and caspase-1 protein expression. The inhibition of c-Fos reduced the effects of miRNA-155 on inflammation in an in vitro model of monocrotaline-induced PAH. The inhibition of NLRP3 reduced the effects of miRNA-155 on inflammation in an in vitro model of monocrotaline-induced PAH. miRNA-155 increased inflammation in monocrotaline-induced PAH through c-Fos/NLRP3/caspase-1.
- Published
- 2020
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