{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,17]],"date-time":"2026-09-17T20:14:15Z","timestamp":1789676055444,"version":"4.0.1"},"reference-count":72,"publisher":"Molecular Vision","license":[{"start":{"date-parts":[[2026,8,19]],"date-time":"2026-08-19T00:00:00Z","timestamp":1787097600000},"content-version":"vor","delay-in-days":68,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2026,6,12]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Purpose<\/jats:title>\n                    <jats:p>Inflammatory processes in the aged retina may be exacerbated by systemic infection with viruses and bacteria, potentially aggravating age-related macular degeneration (AMD). Toll-like receptors (TLR) are key mediators in detecting pathogen-associated molecular patterns (PAMPs) and host-derived damage-associated molecular patterns (DAMPs). This study aimed to investigate TLR gene expression in cultured retinal pigment epithelial (RPE) cells, focusing particularly on TLR9.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>TLR gene expression was assessed using semiquantitative qPCR, while protein expression was evaluated through western blotting, immunocytochemistry, and ELISA. Hypoxic conditions were simulated using CoCl2 or by incubation in a 0.1% O2 atmosphere. RPE cell proliferation and viability were examined using bromodeoxyuridine (BrdU) and MTT assays. Cell necrosis and apoptosis were analyzed with a cellular DNA fragmentation ELISA.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Among the TLRs analyzed, TLR9 showed the most pronounced upregulation under hypoxic conditions. TLR9 protein expression was similarly induced by CoCl2 as well as in a 0.1% O2 atmosphere. Hypoxia increased the protein levels of \u03b3H2A.X, a marker for DNA damage and cellular senescence. The TLR9 agonist ODN 1826 induced the gene expression of downstream signaling molecules (MYD88, IRF7, RELA), inflammatory factors (IFNA, COX2), and MMP9 as well as the secretion of TGF-\u03b21. These effects were reversed by TLR9 inhibitors (ODN 2088 and ODN INH-18). Transforming growth factor (TGF)-\u03b21 significantly suppressed the TLR9 expression at both the mRNA and protein levels. This suppressive effect was reversed at the RNA level by inhibiting components of the TGF-\u03b21 signaling pathway, including activin receptor-like kinase (ALK), Smad3, p38 mitogen-activated protein kinase (p38 MAPK), c-Jun N-terminal kinase (JNK), and phosphatidylinositol 3-kinase (PI3K) under hypoxic conditions.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>TLR9 activation under hypoxic conditions initiates pro-inflammatory pathways in RPE cells. In the aging retina, viral and bacterial infections and\/or DAMPs may further amplify these responses, worsening retinal degeneration. TGF-\u03b21 may exert protective, anti-inflammatory effects by downregulating TLR9 expression.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.63500\/mv_v32_210","type":"journal-article","created":{"date-parts":[[2026,8,19]],"date-time":"2026-08-19T19:02:56Z","timestamp":1787166176000},"page":"210-230","source":"Crossref","is-referenced-by-count":0,"title":["Toll-like receptor 9 in retinal pigment epithelial cells: Expression, function and the role of TGF-\u03b21"],"prefix":"10.63500","volume":"32","author":[{"given":"Elisabeth","family":"Esser","sequence":"first","affiliation":[{"name":"Department of Ophthalmology and Eye Hospital, University of Leipzig, Leipzig, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Heidrun","family":"Kuhrt","sequence":"additional","affiliation":[{"name":"Institute of Anatomy, University of Leipzig, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Focke","family":"Ziemssen","sequence":"additional","affiliation":[{"name":"Department of Ophthalmology and Eye Hospital, University of Leipzig, Leipzig, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Margrit","family":"Hollborn","sequence":"additional","affiliation":[{"name":"Department of Ophthalmology and Eye Hospital, University of Leipzig, Leipzig, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"52877","published-online":{"date-parts":[[2026,6,12]]},"reference":[{"key":"2026091715583037900_r1","doi-asserted-by":"crossref","first-page":"348","DOI":"10.1016\/j.preteyeres.2009.06.001","article-title":"Para-inflammation in the aging retina","volume":"28","author":"Xu","year":"2009","journal-title":"Prog Retin Eye Res"},{"key":"2026091715583037900_r2","doi-asserted-by":"crossref","DOI":"10.1155\/2014\/930671","article-title":"Age-related macular degeneration in 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