Fine particulate matter exposure promotes M2 macrophage polarization through inhibiting histone deacetylase 2 in the pathogenesis of chronic obstructive pulmonary disease.

ABSTRACT:

Background

Chronic obstructive pulmonary disease (COPD) is a major cause of morbidity and mortality globally. Fine particulate matter (PM2.5) has been indicated to be a major detrimental risk factor for COPD by numerous epidemiological studies. Histone deacetylase 2 (HDAC2), a critical regulator of chromatin remodeling, plays a pivotal role in the development of COPD. However, the underlying mechanisms regarding the relationship between PM2.5 and HDAC2 in the pathogenesis of COPD have yet to be elucidated. In the present study, we aim to investigate the role and the underlying mechanism of HDAC2 in the development of PM2.5-induced COPD.

Methods

The effects of PM2.5 exposure on M2 macrophage polarization and the expression levels of HDAC2 were examined in vitro. The in

SUBMITTER: Jiang Y 

PROVIDER: S-EPMC7661902 | biostudies-literature | 2020 Oct

REPOSITORIES: biostudies-literature