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Consistent with data from obese, hypertensive humans, mice with an endothelial cell\u2013specific deficiency in<jats:italic>Panx3<\/jats:italic>had spontaneous systemic hypertension without obvious changes in channel function, as assessed by Ca<jats:sup>2+<\/jats:sup>handling, ATP amounts, or Golgi luminal pH. Panx3 bound to Bcl6, and its absence reduced Bcl6 protein abundance, suggesting that the interaction with Panx3 stabilized Bcl6 by preventing its degradation.<jats:italic>Panx3<\/jats:italic>deficiency was associated with increased expression of the gene encoding the H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub>-producing enzyme Nox4, which is normally repressed by Bcl6, resulting in H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub>-induced oxidative damage in the vasculature. Catalase rescued impaired vasodilation in mice lacking endothelial Panx3. Administration of a newly developed peptide to inhibit the Panx3-Bcl6 interaction recapitulated the increase in<jats:italic>Nox4<\/jats:italic>expression and in blood pressure seen in mice with endothelial<jats:italic>Panx3<\/jats:italic>deficiency. Panx3-Bcl6-Nox4 dysregulation occurred in obesity-related hypertension, but not when hypertension was induced in the absence of obesity. Our findings provide insight into a channel-independent role of Panx3 wherein its interaction with Bcl6 determines vascular oxidative state, particularly under the adverse conditions of obesity.<\/jats:p>","DOI":"10.1126\/scisignal.adg2622","type":"journal-article","created":{"date-parts":[[2024,1,30]],"date-time":"2024-01-30T18:58:11Z","timestamp":1706641091000},"update-policy":"https:\/\/doi.org\/10.34133\/aaas_crossmark","source":"Crossref","is-referenced-by-count":13,"title":["Pannexin-3 stabilizes the transcription factor Bcl6 in a channel-independent manner to protect against vascular oxidative stress"],"prefix":"10.1126","volume":"17","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-4169-3697","authenticated-orcid":true,"given":"Abigail G.","family":"Wolpe","sequence":"first","affiliation":[{"name":"Robert M. 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