Current eye research · 2026
STOM Promotes Retinal Angiogenesis in Diabetic Retinopathy via the ERK1/2/VEGFA Pathway.
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Chi Jingyi, Liu Xinyu, Song Weichen, Chen Wen, Xue Xiaoxiao, Zhang Yongqi, Zhu Wenwen
Аннотация
PURPOSE: Diabetic retinopathy (DR) is a leading cause of blindness, but its underlying molecular mechanisms remain poorly understood. This study aimed to investigate the role of STOM in DR-related retinal angiogenesis and to elucidate its potential signaling mechanism.
METHODS: A streptozotocin-induced diabetic rat model and human retinal microvascular endothelial cells (HRMECs) exposed to high glucose were employed. The expression levels of STOM, vascular endothelial growth factor A (VEGFA), and extracellular signal-regulated kinase (ERK1/2) pathway-related molecules were detected by quantitative real-time polymerase chain reaction (qRT-PCR), Western blotting (WB), and immunohistochemistry (IHC). Functional assays including Cell Counting Kit-8 (CCK-8), Direct cell counting, wound healing, Transwell migration, and Matrigel tube formation were performed to assess the effects of STOM knockdown or overexpression on HRMECs. The ERK1/2 inhibitor U0126 was applied to verify pathway dependence.
RESULTS: STOM expression was significantly upregulated in the retinas of diabetic rats and in HRMECs under high glucose conditions. STOM silencing suppressed high glucose-induced proliferation, migration, and angiogenic tube formation in HRMECs. Whereas STOM overexpression enhanced these pathological behaviors. Mechanistically, STOM promoted VEGFA upregulation and angiogenesis through activation of the ERK1/2 signaling pathway.
CONCLUSIONS: STOM facilitates pathological retinal angiogenesis in diabetic retinopathy via the ERK1/2/VEGFA signaling pathway. These findings identify STOM as a potential therapeutic target for DR.
METHODS: A streptozotocin-induced diabetic rat model and human retinal microvascular endothelial cells (HRMECs) exposed to high glucose were employed. The expression levels of STOM, vascular endothelial growth factor A (VEGFA), and extracellular signal-regulated kinase (ERK1/2) pathway-related molecules were detected by quantitative real-time polymerase chain reaction (qRT-PCR), Western blotting (WB), and immunohistochemistry (IHC). Functional assays including Cell Counting Kit-8 (CCK-8), Direct cell counting, wound healing, Transwell migration, and Matrigel tube formation were performed to assess the effects of STOM knockdown or overexpression on HRMECs. The ERK1/2 inhibitor U0126 was applied to verify pathway dependence.
RESULTS: STOM expression was significantly upregulated in the retinas of diabetic rats and in HRMECs under high glucose conditions. STOM silencing suppressed high glucose-induced proliferation, migration, and angiogenic tube formation in HRMECs. Whereas STOM overexpression enhanced these pathological behaviors. Mechanistically, STOM promoted VEGFA upregulation and angiogenesis through activation of the ERK1/2 signaling pathway.
CONCLUSIONS: STOM facilitates pathological retinal angiogenesis in diabetic retinopathy via the ERK1/2/VEGFA signaling pathway. These findings identify STOM as a potential therapeutic target for DR.
Предметные рубрики MeSH
AnimalsDiabetic RetinopathyVascular Endothelial Growth Factor ARatsRetinal NeovascularizationBlotting, WesternHumansDiabetes Mellitus, ExperimentalCells, CulturedMaleRats, Sprague-DawleyMAP Kinase Signaling SystemCell MovementReal-Time Polymerase Chain ReactionCell ProliferationImmunohistochemistryRetinal VesselsGene Expression RegulationMitogen-Activated Protein Kinase 3