{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,27]],"date-time":"2026-08-27T14:22:24Z","timestamp":1787840544802,"version":"build-2784847793"},"reference-count":65,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"4","license":[{"start":{"date-parts":[[2024,11,13]],"date-time":"2024-11-13T00:00:00Z","timestamp":1731456000000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-sa\/4.0"}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2026,4]]},"abstract":"<jats:p>JOURNAL\/nrgr\/04.03\/01300535-202604000-00043\/figure1\/v\/2026-04-21T135625Z\/r\/image-tiff<\/jats:p>\n                  <jats:p>\n                    Downregulation of the inwardly rectifying potassium channel Kir4.1 is a key step for inducing retinal M\u00fcller cell activation and interaction with other glial cells, which is involved in retinal ganglion cell apoptosis in glaucoma. Modulation of Kir4.1 expression in M\u00fcller cells may therefore be a potential strategy for attenuating retinal ganglion cell damage in glaucoma. In this study, we identified seven predicted phosphorylation sites in Kir4.1 and constructed lentiviral expression systems expressing Kir4.1 mutated at each site to prevent phosphorylation. Following this, we treated M\u00fcller glial cells\n                    <jats:italic toggle=\"yes\">in vitro<\/jats:italic>\n                    and\n                    <jats:italic toggle=\"yes\">in vivo<\/jats:italic>\n                    with the mGluR I agonist DHPG to induce Kir4.1 or Kir4.1 Tyr\n                    <jats:sup>9<\/jats:sup>\n                    Asp overexpression. We found that both Kir4.1 and Kir4.1 Tyr\n                    <jats:sup>9<\/jats:sup>\n                    Asp overexpression inhibited activation of M\u00fcller glial cells. Subsequently, we established a rat model of chronic ocular hypertension by injecting microbeads into the anterior chamber and overexpressed Kir4.1 or Kir4.1 Tyr\n                    <jats:sup>9<\/jats:sup>\n                    Asp in the eye, and observed similar results in M\u00fcller cells\n                    <jats:italic toggle=\"yes\">in vivo<\/jats:italic>\n                    as those seen\n                    <jats:italic toggle=\"yes\">in vitro<\/jats:italic>\n                    . Both Kir4.1 and Kir4.1 Tyr\n                    <jats:sup>9<\/jats:sup>\n                    Asp overexpression inhibited M\u00fcller cell activation, regulated the balance of Bax\/Bcl-2, and reduced the mRNA and protein levels of pro-inflammatory factors, including interleukin-1\u03b2 and tumor necrosis factor-\u03b1. Furthermore, we investigated the regulatory effects of Kir4.1 and Kir4.1 Tyr\n                    <jats:sup>9<\/jats:sup>\n                    Asp overexpression on the release of pro-inflammatory factors in a co-culture system of M\u00fcller glial cells and microglia. In this co-culture system, we observed elevated adenosine triphosphate concentrations in activated M\u00fcller cells, increased levels of translocator protein (a marker of microglial activation), and elevated interleukin-1\u03b2 mRNA and protein levels in microglia induced by activated M\u00fcller cells. These changes could be reversed by Kir4.1 and Kir4.1 Tyr\n                    <jats:sup>9<\/jats:sup>\n                    Asp overexpression in M\u00fcller cells. Kir4.1 overexpression, but not Kir4.1 Tyr\n                    <jats:sup>9<\/jats:sup>\n                    Asp overexpression, reduced the number of proliferative and migratory microglia induced by activated M\u00fcller cells. Collectively, these results suggest that the tyrosine residue at position nine in Kir4.1 may serve as a functional modulation site in the retina in an experimental model of glaucoma. Kir4.1 and Kir4.1 Tyr\n                    <jats:sup>9<\/jats:sup>\n                    Asp overexpression attenuated M\u00fcller cell activation, reduced ATP\/P2X receptor\u2013mediated interactions between glial cells, inhibited microglial activation, and decreased the synthesis and release of pro-inflammatory factors, consequently ameliorating retinal ganglion cell apoptosis in glaucoma.\n                  <\/jats:p>","DOI":"10.4103\/nrr.nrr-d-24-00461","type":"journal-article","created":{"date-parts":[[2024,11,13]],"date-time":"2024-11-13T06:40:58Z","timestamp":1731480058000},"page":"1628-1640","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":2,"title":["Overexpression of the inwardly rectifying potassium channel Kir4.1 or Kir4.1 Tyr9Asp in M\u00fcller cells exerts neuroprotective effects in an experimental glaucoma model"],"prefix":"10.4103","volume":"21","author":[{"given":"Fang","family":"Li","sequence":"first","affiliation":[{"name":"State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Institute of Brain Science, Fudan University, Shanghai, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhen","family":"Li","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Institute of Brain Science, Fudan University, Shanghai, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shuying","family":"Li","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Institute of Brain Science, Fudan University, Shanghai, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hong","family":"Zhou","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Institute of Brain Science, Fudan University, Shanghai, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yunhui","family":"Guo","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Institute of Brain Science, Fudan University, Shanghai, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yongchen","family":"Wang","sequence":"additional","affiliation":[{"name":"Institute of Neuroscience and Third Affiliated Hospital, Zhengzhou University, Zhengzhou, Henan Province, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bo","family":"Lei","sequence":"additional","affiliation":[{"name":"Institute of Neuroscience and Third Affiliated Hospital, Zhengzhou University, Zhengzhou, Henan Province, China"},{"name":"Henan Provincial People\u2019s Hospital, Henan Eye Institute, Henan Eye Hospital, People\u2019s Hospital of Zhengzhou University, Zhengzhou University, Zhengzhou, Henan Province, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3948-2943","authenticated-orcid":false,"given":"Yanying","family":"Miao","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Institute of Brain Science, Fudan University, Shanghai, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2279-6885","authenticated-orcid":false,"given":"Zhongfeng","family":"Wang","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Institute of Brain Science, Fudan University, Shanghai, 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