{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,11,19]],"date-time":"2025-11-19T17:14:49Z","timestamp":1763572489295,"version":"3.41.2"},"reference-count":71,"publisher":"Portland Press Ltd.","issue":"2","license":[{"start":{"date-parts":[[2019,9,9]],"date-time":"2019-09-09T00:00:00Z","timestamp":1567987200000},"content-version":"vor","delay-in-days":220,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["portlandpress.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2019,2,28]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Connexins (Cxs) and pannexins (Panxs) are highly regulated large-pore channel-forming proteins that participate in cellular communication via small molecular exchange with the extracellular microenvironment, or in the case of connexins, directly between cells. Given the putative functional overlap between single membrane-spanning connexin hemichannels and Panx channels, and cardiovascular system prevalence, we generated the first Cx40\u2212\/\u2212Panx1\u2212\/\u2212 mouse with the anticipation that this genetic modification would lead to a severe cardiovascular phenotype. Mice null for both Cx40 and Panx1 produced litter sizes and adult growth progression similar to wild-type (WT), Cx40\u2212\/\u2212 and Panx1\u2212\/\u2212 mice. Akin to Cx40\u2212\/\u2212 mice, Cx40\u2212\/\u2212Panx1\u2212\/\u2212 mice exhibited cardiac hypertrophy and elevated systolic, diastolic, and mean arterial blood pressure compared with WT and Panx1\u2212\/\u2212 mice; however assessment of left ventricular ejection fraction and fractional shortening revealed no evidence of cardiac dysfunction between groups. Furthermore, Cx40\u2212\/\u2212, Panx1\u2212\/\u2212, and Cx40\u2212\/\u2212Panx1\u2212\/\u2212 mice demonstrated impaired endothelial-mediated vasodilation of aortic segments to increasing concentrations of methacholine (MCh) compared with WT, highlighting roles for both Cx40 and Panx1 in vascular endothelial cell (EC) function. Surprisingly, elevated kidney renin mRNA expression, plasma renin activity, and extraglomerular renin-producing cell populations found in Cx40\u2212\/\u2212 mice was further exaggerated in double knockout mice. Thus, while gestation and gross development were conserved in Cx40\u2212\/\u2212Panx1\u2212\/\u2212 mice, they exhibit cardiac hypertrophy, hypertension, and impaired endothelial-mediated vasodilation that phenocopies Cx40\u2212\/\u2212 mice. Nevertheless, the augmented renin homeostasis observed in the double knockout mice suggests that both Cx40 and Panx1 may play an integrative role.<\/jats:p>","DOI":"10.1042\/bsr20182350","type":"journal-article","created":{"date-parts":[[2019,2,11]],"date-time":"2019-02-11T17:44:49Z","timestamp":1549907089000},"update-policy":"https:\/\/doi.org\/10.1042\/crossmark_policy","source":"Crossref","is-referenced-by-count":6,"title":["Ablation of both Cx40 and Panx1 results in similar cardiovascular phenotypes exhibited in Cx40 knockout mice"],"prefix":"10.1042","volume":"39","author":[{"given":"Nicole\u00a0M.","family":"Novielli-Kuntz","sequence":"first","affiliation":[{"name":"Department of Anatomy and Cell Biology, University of Western Ontario, London, Canada"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Meghan","family":"Jelen","sequence":"additional","affiliation":[{"name":"Department of Anatomy and Cell Biology, University of Western Ontario, London, Canada"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kevin","family":"Barr","sequence":"additional","affiliation":[{"name":"Department of Anatomy and Cell Biology, University of Western Ontario, London, Canada"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Leon\u00a0J.","family":"DeLalio","sequence":"additional","affiliation":[{"name":"Robert M. Berne Cardiovascular Research Center, University of Virginia School of Medicine, Charlottesville, VA, U.S.A."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Qingping","family":"Feng","sequence":"additional","affiliation":[{"name":"Department of Physiology and Pharmacology London, ON, Canada"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Brant\u00a0E.","family":"Isakson","sequence":"additional","affiliation":[{"name":"Robert M. Berne Cardiovascular Research Center, University of Virginia School of Medicine, Charlottesville, VA, U.S.A."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Robert","family":"Gros","sequence":"additional","affiliation":[{"name":"Department of Physiology and Pharmacology London, ON, Canada"},{"name":"Robarts Research Institute, Schulich School of Medicine & Dentistry, University of Western Ontario, London, ON, Canada"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4568-3285","authenticated-orcid":false,"given":"Dale\u00a0W.","family":"Laird","sequence":"additional","affiliation":[{"name":"Department of Anatomy and Cell Biology, University of Western Ontario, London, Canada"},{"name":"Department of Physiology and Pharmacology London, ON, Canada"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"288","published-online":{"date-parts":[[2019,2,27]]},"reference":[{"key":"2021111619303872700_B1","doi-asserted-by":"publisher","first-page":"2045","DOI":"10.2174\/0929867033456927","article-title":"Transfer of biologically important molecules between cells through gap junction channels","volume":"10","author":"Alexander","year":"2003","journal-title":"Curr. 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