Fibrinogen mediates cadmium-induced macrophage activation and serves as a predictor of cadmium exposure in chronic obstructive pulmonary disease.
cadmium
chronic obstructive pulmonary disease (COPD)
fibrinogen
peptidylarginine deiminase 2 (PAD2)
plasminogen activator inhibitor 2 (PAI-2)
Journal
American journal of physiology. Lung cellular and molecular physiology
ISSN: 1522-1504
Titre abrégé: Am J Physiol Lung Cell Mol Physiol
Pays: United States
ID NLM: 100901229
Informations de publication
Date de publication:
01 04 2022
01 04 2022
Historique:
pubmed:
25
2
2022
medline:
9
4
2022
entrez:
24
2
2022
Statut:
ppublish
Résumé
The etiologies of chronic obstructive pulmonary disease (COPD) remain unclear. Cadmium (Cd) causes both pulmonary fibrosis and emphysema; however, the predictors for Cd exposure and the mechanisms by which Cd causes COPD remain unknown. We demonstrated that Cd burden was increased in lung tissue from subjects with COPD and this was associated with cigarette smoking. Fibrinogen levels increased markedly in lung tissue of patients with smoked COPD compared with never-smokers and control subjects. Fibrinogen concentration also correlated positively with lung Cd load, but inversely with the predicted % of FEV1 and FEV1/FVC. Cd enhanced the secretion of fibrinogen in a cdc2-dependent manner, whereas fibrinogen further mediated Cd-induced peptidylarginine deiminase 2 (PAD2)-dependent macrophage activation. Using lung fibroblasts from CdCl
Identifiants
pubmed: 35200041
doi: 10.1152/ajplung.00475.2021
pmc: PMC8993524
doi:
Substances chimiques
Toll-Like Receptor 4
0
Cadmium
00BH33GNGH
Fibrinogen
9001-32-5
Banques de données
figshare
['10.6084/m9.figshare.19342841']
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
L593-L606Subventions
Organisme : NIEHS NIH HHS
ID : P42 ES027723
Pays : United States
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