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Although mitochondria are acknowledged regulators of IP\n                      <jats:sub>3<\/jats:sub>\n                      \u2010mediated Ca\n                      <jats:sup>2+<\/jats:sup>\n                      release, how TRPV4\u2010mediated Ca\n                      <jats:sup>2+<\/jats:sup>\n                      signals are regulated by mitochondria is unknown. We show that depolarised mitochondria switch TRPV4 signalling from relying on Ca\n                      <jats:sup>2+<\/jats:sup>\n                      \u2010induced Ca\n                      <jats:sup>2+<\/jats:sup>\n                      release at IP\n                      <jats:sub>3<\/jats:sub>\n                      receptors to being independent of Ca\n                      <jats:sup>2+<\/jats:sup>\n                      influx and instead mediated by ATP release via pannexins.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Experimental Approach<\/jats:title>\n                    <jats:p>\n                      TRPV4\u2010evoked Ca\n                      <jats:sup>2+<\/jats:sup>\n                      signals were individually examined in hundreds of cells in the endothelium of rat mesenteric resistance arteries using the indicator Cal520.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Key Results<\/jats:title>\n                    <jats:p>\n                      TRPV4 activation with GSK1016790A (GSK) generated repetitive Ca\n                      <jats:sup>2+<\/jats:sup>\n                      oscillations that required Ca\n                      <jats:sup>2+<\/jats:sup>\n                      influx. However, when the mitochondrial membrane potential was depolarised, by the uncoupler CCCP or complex I inhibitor rotenone, TRPV4 activation generated large propagating, multicellular, Ca\n                      <jats:sup>2+<\/jats:sup>\n                      waves in the absence of external Ca\n                      <jats:sup>2+<\/jats:sup>\n                      . The ATP synthase inhibitor oligomycin did not potentiate TRPV4\u2010mediated Ca\n                      <jats:sup>2+<\/jats:sup>\n                      signals. GSK\u2010evoked Ca\n                      <jats:sup>2+<\/jats:sup>\n                      waves, when mitochondria were depolarised, were blocked by the TRPV4 channel blocker HC067047, the SERCA inhibitor cyclopiazonic acid, the PLC blocker U73122 and the inositol trisphosphate receptor blocker caffeine. The Ca\n                      <jats:sup>2+<\/jats:sup>\n                      waves were also inhibited by the extracellular ATP blockers suramin and apyrase and the pannexin blocker probenecid.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion and Implications<\/jats:title>\n                    <jats:p>\n                      These results highlight a previously unknown role of mitochondria in shaping TRPV4\u2010mediated Ca\n                      <jats:sup>2+<\/jats:sup>\n                      signalling by facilitating ATP release. When mitochondria are depolarised, TRPV4\u2010mediated release of ATP via pannexin channels activates plasma membrane purinergic receptors to trigger IP\n                      <jats:sub>3<\/jats:sub>\n                      \u2010evoked Ca\n                      <jats:sup>2+<\/jats:sup>\n                      release.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/bph.15687","type":"journal-article","created":{"date-parts":[[2021,10,5]],"date-time":"2021-10-05T01:07:24Z","timestamp":1633396044000},"page":"1017-1032","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":24,"title":["Mitochondria regulate TRPV4\u2010mediated release of ATP"],"prefix":"10.1111","volume":"179","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-0790-4291","authenticated-orcid":false,"given":"Xun","family":"Zhang","sequence":"first","affiliation":[{"name":"Strathclyde Institute of Pharmacy and Biomedical Sciences University of Strathclyde Glasgow UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8265-382X","authenticated-orcid":false,"given":"Matthew D.","family":"Lee","sequence":"additional","affiliation":[{"name":"Strathclyde Institute of Pharmacy and Biomedical Sciences University of Strathclyde Glasgow UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7961-4544","authenticated-orcid":false,"given":"Charlotte","family":"Buckley","sequence":"additional","affiliation":[{"name":"Strathclyde Institute of Pharmacy and Biomedical Sciences University of Strathclyde Glasgow UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2500-0632","authenticated-orcid":false,"given":"Calum","family":"Wilson","sequence":"additional","affiliation":[{"name":"Strathclyde Institute of Pharmacy and Biomedical Sciences University of Strathclyde Glasgow UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3302-3984","authenticated-orcid":false,"given":"John G.","family":"McCarron","sequence":"additional","affiliation":[{"name":"Strathclyde Institute of Pharmacy and Biomedical Sciences University of Strathclyde Glasgow UK"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2021,11,2]]},"reference":[{"key":"e_1_2_12_2_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbabio.2008.04.017"},{"key":"e_1_2_12_3_1","doi-asserted-by":"publisher","DOI":"10.1111\/bph.15538"},{"key":"e_1_2_12_4_1","doi-asserted-by":"publisher","DOI":"10.1111\/bph.15543"},{"key":"e_1_2_12_5_1","doi-asserted-by":"publisher","DOI":"10.1111\/bph.15539"},{"key":"e_1_2_12_6_1","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.0000247065.11756.19"},{"key":"e_1_2_12_7_1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0800793105"},{"key":"e_1_2_12_8_1","doi-asserted-by":"publisher","DOI":"10.1002\/bies.950161208"},{"key":"e_1_2_12_9_1","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.5.1.97"},{"key":"e_1_2_12_10_1","doi-asserted-by":"publisher","DOI":"10.1038\/nature01268"},{"key":"e_1_2_12_11_1","doi-asserted-by":"publisher","DOI":"10.1042\/bj2820309"},{"key":"e_1_2_12_12_1","doi-asserted-by":"publisher","DOI":"10.1111\/bph.14905"},{"key":"e_1_2_12_13_1","doi-asserted-by":"publisher","DOI":"10.1111\/bph.15329"},{"key":"e_1_2_12_14_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0968-0004(03)00053-7"},{"key":"e_1_2_12_15_1","doi-asserted-by":"publisher","DOI":"10.1242\/jcs.014522"},{"key":"e_1_2_12_16_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.ceca.2009.05.007"},{"key":"e_1_2_12_17_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.bpj.2012.11.2007"},{"key":"e_1_2_12_18_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2007.11.028"},{"key":"e_1_2_12_19_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.lfs.2011.08.003"},{"key":"e_1_2_12_20_1","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.200604016"},{"key":"e_1_2_12_21_1","doi-asserted-by":"publisher","DOI":"10.1111\/bph.14153"},{"key":"e_1_2_12_22_1","doi-asserted-by":"publisher","DOI":"10.1080\/15216540600794526"},{"issue":"6","key":"e_1_2_12_23_1","first-page":"1","article-title":"Pharmacological inhibitors of TRPV4 channels reduce cytokine production, restore endothelial function and increase survival in septic mice","volume":"61","author":"Dalsgaard T.","year":"2016","journal-title":"Scientific Reports"},{"key":"e_1_2_12_24_1","doi-asserted-by":"crossref","unstructured":"Daneva Z. 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