GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE318nnn/GSE318434/primaryOK200TranscriptomicsMus musculusExpression profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE318434GEOGSEfalseEndothelial TGFβ signaling regulates choroidal neovascularization severity via myeloid–endothelial interactionThe blood-retinal barrier (BRB) is essential for maintaining retinal homeostasis, yet its disruption contributes to pathological angiogenesis in diseases such as neovascular age-related macular degeneration (nAMD). Here, we investigated how endothelial TGF-β signaling interacts with microglia to regulate choroidal neovascularization (CNV). Using a laser-induced CNV model in mice with endothelial-specific Tgfbr2 deletion (Tgfbr2∆EC) and concomitant microglia depletion via PLX5622, we demonstrate that loss of endothelial TGF-β signaling significantly exacerbates CNV, an effect fully rescued by microglia depletion. Bulk RNA sequencing and RNAscope analyses of CNV lesions identified fibrinogen alpha chain (Fga) as a microglia-derived factor upregulated exclusively in Tgfbr2∆EC mice. These findings suggest a TGF-β-dependent interaction between endothelial cells and microglia that promotes angiogenesis through microglia derived Fga expression.2026/07/15GSE318434GSM9494505GSM9494527GSM9494504GSM9494526GSM9494525GSM9494503GSM9494502GSM9494524GSM9494509GSM9494508GSM9494507GSM9494529GSM9494528GSM9494506GSM9494530GSM9494534GSM9494512GSM9494511GSM9494533GSM9494510GSM9494532GSM9494531GSM9494516GSM9494538GSM9494537GSM9494515GSM9494514GSM9494536GSM9494513GSM9494535GSM9494519GSM9494518GSM9494517GSM9494539GSM9494540GSM9494501GSM9494523GSM9494522GSM9494521GSM949452030172318434Mus musculus[42433372]