Journal
CELL METABOLISM
Volume 29, Issue 2, Pages 335-+Publisher
CELL PRESS
DOI: 10.1016/j.cmet.2018.09.019
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Funding
- NHLBI HL [HL135124]
- NIH NIAMS [AR061593]
- ATS/Scleroderma Foundation Research Grant
- DOD [PR141319]
- BD Bioscience Immunology Research Grant
- NIH [HL076139, HL125940, AG049665, HL048129, HL071643, HL085534, ES015024, ES025644, ES026718, HL079190, HL124664, ES013995, BX000201, AR064546, HL134375, CA197532]
- Thoracic Surgery Foundation
- Society of University Surgeons
- American Association of Thoracic Surgery
- Parker B. Francis Research Opportunity Award [HL128867]
- Mabel Greene Myers Chair
- Flow Cytometry and Genomics NCI Cancer Center Support [P30 CA060553]
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Urban particulate matter air pollution induces the release of pro-inflammatory cytokines including inter-leukin-6 (IL-6) from alveolar macrophages, resulting in an increase in thrombosis. Here, we report that metformin provides protection in this murine model. Treatment of mice with metformin or exposure of murine or human alveolar macrophages to metformin prevented the particulate matter-induced generation of complex III mitochondrial reactive oxygen species, which were necessary for the opening of calcium release-activated channels (CRAC) and release of IL-6. Targeted genetic deletion of electron transport or CRAC channels in alveolar macrophages in mice prevented particulate matter-induced acceleration of arterial thrombosis. These findings suggest metformin as a potential therapy to prevent some of the premature deaths attributable to air pollution exposure worldwide.
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