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However, the potential mediators of pulmonary injury in PM\n                    <jats:sub>2.5<\/jats:sub>\n                    \u2010induced cardiovascular disorder are not fully understood. To investigate a potential cross talk between lung and heart upon PM\n                    <jats:sub>2.5<\/jats:sub>\n                    exposure, intratracheal instillation in vivo, organ culture ex vivo and human bronchial epithelial cells (Beas\u20102B) culture in vitro experiments were performed respectively. The exposed supernatants of Beas\u20102B were collected to treat primary neonatal rat cardiomyocytes (NRCMs). Upon intratracheal instillation, subacute PM\n                    <jats:sub>2.5<\/jats:sub>\n                    exposure caused cardiac dysfunction, which was time\u2010dependent secondary to lung injury in mice, thereby demonstrating a cross\u2010talk between lungs and heart potentially mediated via small extracellular vesicles (sEV). We isolated sEV from PM\n                    <jats:sub>2.5<\/jats:sub>\n                    \u2010exposed mice serum and Beas\u20102B supernatants to analyse the change of sEV subpopulations in response to PM\n                    <jats:sub>2.5<\/jats:sub>\n                    . Single particle interferometric reflectance imaging sensing analysis (SP\u2010IRIS) demonstrated that PM\n                    <jats:sub>2.5<\/jats:sub>\n                    increased CD63\/CD81\/CD9 positive particles. Our results indicated that respiratory system\u2010derived sEV containing miR\u2010421 contributed to cardiac dysfunction post\u2010PM\n                    <jats:sub>2.5<\/jats:sub>\n                    exposure. Inhibition of miR\u2010421 by AAV9\u2010miR421\u2010sponge could significantly reverse PM\n                    <jats:sub>2.5<\/jats:sub>\n                    \u2010induced cardiac dysfunction in mice. We identified that cardiac angiotensin converting enzyme 2 (ACE2) was a downstream target of sEV\u2010miR421, and induced myocardial cell apoptosis and cardiac dysfunction. In addition, we observed that GW4869 (an inhibitor of sEV release) or diminazene aceturate (DIZE, an activator of ACE2) treatment could attenuate PM\n                    <jats:sub>2.5<\/jats:sub>\n                    \u2010induced cardiac dysfunction in vivo. Taken together, our results suggest that PM\n                    <jats:sub>2.5<\/jats:sub>\n                    exposure promotes sEV\u2010linked miR421 release after lung injury and hereby contributes to PM\n                    <jats:sub>2.5<\/jats:sub>\n                    \u2010induced cardiac dysfunction via suppressing ACE2.\n                  <\/jats:p>","DOI":"10.1002\/jev2.12222","type":"journal-article","created":{"date-parts":[[2022,5,10]],"date-time":"2022-05-10T11:35:41Z","timestamp":1652182541000},"source":"Crossref","is-referenced-by-count":41,"title":["Extracellular vesicles enclosed\u2010miR\u2010421 suppresses air pollution (PM\n                    <sub>2.5<\/sub>\n                    )\u2010induced cardiac dysfunction via ACE2 signalling"],"prefix":"10.1002","volume":"11","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-2417-5924","authenticated-orcid":false,"given":"Hongyun","family":"Wang","sequence":"first","affiliation":[{"name":"Institute of Geriatrics (Shanghai University) Affiliated Nantong Hospital of Shanghai University (The Sixth People's Hospital of Nantong) School of Medicine Shanghai University  Nantong China"},{"name":"Cardiac Regeneration and Ageing Lab Institute of Cardiovascular Sciences Shanghai Engineering Research Center of Organ Repair School of Life Science Shanghai University  Shanghai China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tianhui","family":"Wang","sequence":"additional","affiliation":[{"name":"Institute of Geriatrics (Shanghai University) Affiliated Nantong Hospital of Shanghai University (The Sixth People's Hospital of Nantong) School of Medicine Shanghai University  Nantong China"},{"name":"Cardiac Regeneration and Ageing Lab Institute of Cardiovascular Sciences Shanghai Engineering Research Center of Organ Repair School of Life Science Shanghai University  Shanghai 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School of Medicine Shanghai University  Nantong China"},{"name":"Cardiac Regeneration and Ageing Lab Institute of Cardiovascular Sciences Shanghai Engineering Research Center of Organ Repair School of Life Science Shanghai University  Shanghai China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiao","family":"Zhang","sequence":"additional","affiliation":[{"name":"Institute of Geriatrics (Shanghai University) Affiliated Nantong Hospital of Shanghai University (The Sixth People's Hospital of Nantong) School of Medicine Shanghai University  Nantong China"},{"name":"Cardiac Regeneration and Ageing Lab Institute of Cardiovascular Sciences Shanghai Engineering Research Center of Organ Repair School of Life Science Shanghai University  Shanghai China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Longfei","family":"Guan","sequence":"additional","affiliation":[{"name":"China\u2010America Institute Neuroscience Beijing Luhe Hospital, Capital Medical University  Beijing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Guoping","family":"Li","sequence":"additional","affiliation":[{"name":"Cardiovascular Division of the Massachusetts General Hospital and Harvard Medical School  Boston Massachusetts USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhiyong","family":"Lei","sequence":"additional","affiliation":[{"name":"CDL Research University Medical Center Utrecht  Utrecht The Netherlands"},{"name":"Department of Cardiology Laboratory of Experimental Cardiology University Medical Center Utrecht  Utrecht The Netherlands"},{"name":"UMC Utrecht Regenerative Medicine Center University Medical Center Utrecht University  Utrecht The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Raymond M","family":"Schiffelers","sequence":"additional","affiliation":[{"name":"CDL Research University Medical Center Utrecht  Utrecht The 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