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The role of miRNA-155 in monocrotaline-induced pulmonary arterial hypertension through c-Fos/NLRP3/caspase-1

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Abstract

Background

Nisoldipine can effectively suppress pulmonary arterial smooth muscle cell proliferation and c-Fos expression.

Objective

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.

Results

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.

Conclusions

miRNA-155 increased inflammation in monocrotaline-induced PAH through c-Fos/NLRP3/caspase-1.

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Correspondence to Sheng-Jun Ma.

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Chai, SD., Li, ZK., Liu, R. et al. The role of miRNA-155 in monocrotaline-induced pulmonary arterial hypertension through c-Fos/NLRP3/caspase-1. Mol. Cell. Toxicol. 16, 311–320 (2020). https://doi.org/10.1007/s13273-020-00083-9

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  • DOI: https://doi.org/10.1007/s13273-020-00083-9

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