{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T16:20:07Z","timestamp":1790698807834,"version":"4.1.0"},"reference-count":69,"publisher":"MDPI AG","issue":"11","license":[{"start":{"date-parts":[[2021,6,4]],"date-time":"2021-06-04T00:00:00Z","timestamp":1622764800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100013126","name":"Psoriasis Association","doi-asserted-by":"publisher","award":["ST3 15"],"award-info":[{"award-number":["ST3 15"]}],"id":[{"id":"10.13039\/100013126","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["IJMS"],"abstract":"<jats:p>Background: Psoriasis, a chronic inflammatory disease affecting 2\u20133% of the population, is characterised by epidermal hyperplasia, a sustained pro-inflammatory immune response and is primarily a T-cell driven disease. Previous work determined that Connexin26 is upregulated in psoriatic tissue. This study extends these findings. Methods: Biopsies spanning psoriatic plaque (PP) and non-involved tissue (PN) were compared to normal controls (NN). RNA was isolated and subject to real-time PCR to determine gene expression profiles, including GJB2\/CX26, GJB6\/CX30 and GJA1\/CX43. Protein expression was assessed by immunohistochemistry. Keratinocytes and fibroblasts were isolated and used in 3D organotypic models. The pro-inflammatory status of fibroblasts and 3D cultures was assessed via ELISA and RnD cytokine arrays in the presence or absence of the connexin channel blocker Gap27. Results: Connexin26 expression is dramatically enhanced at both transcriptional and translational level in PP and PN tissue compared to NN (&gt;100x). In contrast, CX43 gene expression is not affected, but the protein is post-translationally modified and accumulates in psoriatic tissue. Fibroblasts isolated from psoriatic patients had a higher inflammatory index than normal fibroblasts and drove normal keratinocytes to adopt a \u201cpsoriatic phenotype\u201d in a 3D-organotypic model. Exposure of normal fibroblasts to the pro-inflammatory mediator peptidoglycan, isolated from Staphylococcus aureus enhanced cytokine release, an event protected by Gap27. Conclusion: dysregulation of the connexin26:43 expression profile in psoriatic tissue contributes to an imbalance of cellular events. Inhibition of connexin signalling reduces pro-inflammatory events and may hold therapeutic benefit.<\/jats:p>","DOI":"10.3390\/ijms22116060","type":"journal-article","created":{"date-parts":[[2021,6,4]],"date-time":"2021-06-04T11:12:13Z","timestamp":1622805133000},"page":"6060","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":10,"title":["Dysregulation of Connexin Expression Plays a Pivotal Role in Psoriasis"],"prefix":"10.3390","volume":"22","author":[{"given":"Erin M.","family":"O\u2019Shaughnessy","sequence":"first","affiliation":[{"name":"Department of Biological and Biomedical Sciences, School of Health and Life Sciences, Glasgow Caledonian University, Glasgow G4 0BA, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"William","family":"Duffy","sequence":"additional","affiliation":[{"name":"Department of Dermatology, University Hospital Crosshouse, Kilmarnock KA2 0BE, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Laura","family":"Garcia-Vega","sequence":"additional","affiliation":[{"name":"Department of Biological and Biomedical Sciences, School of Health and Life Sciences, Glasgow Caledonian University, Glasgow G4 0BA, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Keith","family":"Hussey","sequence":"additional","affiliation":[{"name":"Department of Vascular Surgery, Queen Elizabeth University Hospital, Glasgow G51 4TF, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"A. David","family":"Burden","sequence":"additional","affiliation":[{"name":"Institute of Infection Immunity and Inflammation, University of Glasgow, Glasgow G12 8TA, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mozheh","family":"Zamiri","sequence":"additional","affiliation":[{"name":"Department of Dermatology, University Hospital Crosshouse, Kilmarnock KA2 0BE, UK"},{"name":"Department of Dermatology, Queen Elizabeth University Hospital, Glasgow G51 4TF, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0890-8059","authenticated-orcid":false,"given":"Patricia E.","family":"Martin","sequence":"additional","affiliation":[{"name":"Department of Biological and Biomedical Sciences, School of Health and Life Sciences, Glasgow Caledonian University, Glasgow G4 0BA, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2021,6,4]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","unstructured":"Rendon, A., and Sch\u00e4kel, K. 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