Dimethylarginine dimethylaminohydrolase 1 protects PM_2.5 exposure-induced lung injury in mice by repressing inflammation and oxidative stress.

ABSTRACT:

Background

Airborne fine particulate matter with aerodynamic diameter ≤ 2.5 μm (PM_2.5) pollution is associated with the prevalence of respiratory diseases, including asthma, bronchitis and chronic obstructive pulmonary disease. In patients with those diseases, circulating asymmetric dimethylarginine (ADMA) levels are increased, which contributes to airway nitric oxide deficiency, oxidative stress and inflammation. Overexpression of dimethylarginine dimethylaminohydrolase 1 (DDAH1), an enzyme degrading ADMA, exerts protective effects in animal models. However, the impact of DDAH1/ADMA on PM_2.5-induced lung injury has not been investigated.

Methods

Ddah1^-/- and DDAH1-transgenic mice, as well as their respective wild-type (WT) littermates, were

SUBMITTER: Gao J 

PROVIDER: S-EPMC9569114 | biostudies-literature | 2022 Oct

REPOSITORIES: biostudies-literature