{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,29]],"date-time":"2026-07-29T10:55:24Z","timestamp":1785322524943,"version":"3.55.0"},"reference-count":61,"publisher":"Wiley","issue":"12","license":[{"start":{"date-parts":[[2024,5,25]],"date-time":"2024-05-25T00:00:00Z","timestamp":1716595200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["physoc.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[2024,6]]},"abstract":"<jats:sec><jats:title>Abstract<\/jats:title><jats:p>World Health Organisation data suggest that up to 99% of the global population are exposed to air pollutants above recommended levels. Impacts to health range from increased risk of stroke and cardiovascular disease to chronic respiratory conditions, and air pollution may contribute to over 7 million premature deaths a year. Additionally, mounting evidence suggests that <jats:italic>in utero<\/jats:italic> or early life exposure to particulate matter (PM) in ambient air pollution increases the risk of neurodevelopmental impairment with obvious lifelong consequences. Identifying brain\u2010specific cellular targets of PM is vital for determining its long\u2010term consequences. We previously established that microglial\u2010like BV2 cells were particularly sensitive to urban (U)PM\u2010induced damage including reactive oxygen species production, which was abrogated by a mitochondrially targeted antioxidant. Here we extend those studies to find that UPM treatment causes a rapid impairment of mitochondrial function and increased mitochondrial fragmentation. However, there is a subsequent restoration of mitochondrial and therefore cell health occurring concomitantly with upregulated measures of mitochondrial biogenesis and mitochondrial load. Our data highlight that protecting mitochondrial function may represent a valuable mechanism to offset the effects of UPM exposure in the neonatal brain.\n<jats:boxed-text content-type=\"graphic\" position=\"anchor\"><jats:graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" mimetype=\"image\/png\" position=\"anchor\" specific-use=\"enlarged-web-image\" xlink:href=\"graphic\/tjp16107-gra-0001-m.png\"><jats:alt-text>image<\/jats:alt-text><\/jats:graphic><\/jats:boxed-text><\/jats:p><\/jats:sec><jats:sec><jats:title>Key points<\/jats:title><jats:p><jats:list list-type=\"bullet\">\n<jats:list-item><jats:p>Air pollution represents a growing risk to long\u2010term health especially in early life, and the CNS is emerging a target for airborne particulate matter (PM).<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>We previously showed that microglial\u2010like BV2 cells were vulnerable to urban (U)PM exposure, which impaired cell survival and promoted reactive oxygen species production.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Here we find that, following UPM exposure, BV2 mitochondrial membrane potential is rapidly reduced, concomitant with decreased cellular bioenergetics and increased mitochondrial fission.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>However, markers of mitochondrial biogenesis and mitochondrial mass are subsequently induced, which may represent a cellular mitigation strategy.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>As mitochondria are more vulnerable in the developing brain, exposure to air pollution may represent a greater risk to lifelong health in this cohort; conversely, promoting mitochondrial integrity may offset these risks.<\/jats:p><\/jats:list-item>\n<\/jats:list><\/jats:p><\/jats:sec>","DOI":"10.1113\/jp285978","type":"journal-article","created":{"date-parts":[[2024,5,25]],"date-time":"2024-05-25T15:07:44Z","timestamp":1716649664000},"page":"2737-2750","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":7,"title":["Exposure to urban particulate matter (UPM) impairs mitochondrial dynamics in BV2 cells, triggering a mitochondrial biogenesis response"],"prefix":"10.1113","volume":"602","author":[{"given":"Rebecca H.","family":"Morris","sequence":"first","affiliation":[{"name":"Department of Comparative Biomedical Sciences Royal Veterinary College  London UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Serena J.","family":"Counsell","sequence":"additional","affiliation":[{"name":"Centre for the Developing Brain, School of Biomedical Engineering &amp; Imaging Sciences King's College London  London 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