{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,23]],"date-time":"2026-07-23T16:15:20Z","timestamp":1784823320061,"version":"3.55.0"},"reference-count":77,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,1,30]],"date-time":"2026-01-30T00:00:00Z","timestamp":1769731200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Cell Dev. Biol."],"abstract":"<jats:sec>\n                    <jats:title>Purpose<\/jats:title>\n                    <jats:p>Fibrogenic changes in the trabecular meshwork (TM) are considered to be a major cause for the restriction in aqueous humor outflow from the anterior chamber associated with primary open angle glaucoma. In this study, we investigated whether integrin switching from \u03b15\u03b21 to \u03b1v\u03b23 integrin expression could initiate fibrotic-like changes in the TM that could restrict outflow.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Human TM cells were isolated from young (&amp;lt;40\u00a0years) and old (&amp;gt;50\u00a0years) donor eyes. RT-PCR, western blots and immunofluorescence microscopy were used to evaluate levels of integrin and \u03b1SMA expression. Lentiviral shRNA vectors were used to knockdown \u03b15 and \u03b23 integrin levels. Paraffin embedded anterior segments of young and old donor eyes were used to evaluate \u03b1SMA levels\n                      <jats:italic>in situ<\/jats:italic>\n                      .\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Studies revealed an age-related decrease in \u03b15 integrin mRNA expression in TM cells. This loss was accompanied by an increase in \u03b1SMA mRNA and protein levels and an increase in activated \u03b1v\u03b23 integrin levels. Knockdown of \u03b23 integrin mRNA and protein levels decreased the expression of \u03b1SMA mRNA and protein levels. Elevated mRNA levels of the EndMT biomarkers,\n                      <jats:italic>VIM<\/jats:italic>\n                      ,\n                      <jats:italic>SNAI2<\/jats:italic>\n                      , and\n                      <jats:italic>TWIST1<\/jats:italic>\n                      , observed in older TM cells were decreased when \u03b23 integrin was knockdown.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>These studies suggest that crosstalk between \u03b15\u03b21 and \u03b1v\u03b23 integrin signaling controls expression of \u03b1SMA mRNA and protein levels and that \u03b23 integrins may play a role in the development of the fibrogenic phenotype in TM cells and associated with POAG.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fcell.2025.1730542","type":"journal-article","created":{"date-parts":[[2026,1,30]],"date-time":"2026-01-30T06:44:06Z","timestamp":1769755446000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":1,"title":["A switch from \u03b15\u03b21 to \u03b1v\u03b23 integrin activity contributes to the development of a profibrotic mesenchymal phenotype in trabecular meshwork cells"],"prefix":"10.3389","volume":"13","author":[{"given":"Kassidy L.","family":"Johns","sequence":"first","affiliation":[{"name":"Department of Pathology & Laboratory Medicine, University of Wisconsin School of Medicine and Public Health","place":["Madison, WI, United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jennifer A.","family":"Faralli","sequence":"additional","affiliation":[{"name":"Department of Pathology & Laboratory Medicine, University of Wisconsin School of Medicine and Public Health","place":["Madison, WI, United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mark S.","family":"Filla","sequence":"additional","affiliation":[{"name":"Department of Pathology & Laboratory Medicine, University of Wisconsin School of Medicine and Public Health","place":["Madison, WI, United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nandini","family":"Shah","sequence":"additional","affiliation":[{"name":"Department of Pathology & Laboratory Medicine, University of Wisconsin School of Medicine and Public Health","place":["Madison, WI, United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kate E.","family":"Keller","sequence":"additional","affiliation":[{"name":"Casey Eye Institute, Oregon Health & Science University","place":["Portland, OR, United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Donna M.","family":"Peters","sequence":"additional","affiliation":[{"name":"Department of Pathology & Laboratory Medicine, University of Wisconsin School of Medicine and Public Health","place":["Madison, WI, United States"]},{"name":"Department of Ophthalmology & Visual Sciences, University of Wisconsin School of Medicine and Public Health","place":["Madison, WI, United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2026,1,30]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"610","DOI":"10.1111\/j.1600-0854.2012.01327.x","article-title":"Distinct recycling of active and inactive \u03b21 integrins","volume":"13","author":"Arjonen","year":"2012","journal-title":"Traffic"},{"key":"B2","doi-asserted-by":"publisher","first-page":"430","DOI":"10.1038\/nrm3599","article-title":"Integrin inactivators: balancing cellular functions in vitro and in vivo","volume":"14","author":"Bouvard","year":"2013","journal-title":"Nat. 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