ArticleInternational journal of ophthalmology2025
Co-host ncRNA MIR503HG/miR-503-5p antagonistically interfere with the crosstalk between fibroblasts and microvascular endothelial cells by affecting the production of LMW FGF2 in pterygium.
Article in International journal of ophthalmology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
aimTo explore the effect of co-host non-coding RNA (ncRNA) MIR503HG/miR-503-5p on the angiogenesis of pterygium.
methodsMIR503HG/miR-503-5p/fibroblast growth factor 2 (FGF2) expression levels in pterygium tissues, control conjunctival tissues, and human pterygium fibroblasts (HPF) were examined by reverse transcription-polymerase chain reaction (qRT-PCR) and immunohistochemical methods. Effects of MIR503HG/miR-503-5p on low molecular weight FGF2 (LWM FGF2), migration and angiogenesis of human retinal microvascular endothelial cells (HRMEC) were determined in an HPF and HRMEC co-culture model using Western blots, wound healing assay, Matrigel-based tube formation assay, and Transwell assay.
resultsMIR503HG/miR-503-5p/FGF2 pathway was actively increased in pterygium tissue and there was a negative correlation between the expression of the two ncRNAs. FGF2 expression level was positively correlated with MIR503HG and negatively correlated with miR-503-5p. Overexpressed MIR503HG/miR-503-5p did not affect the migration and angiogenesis of HRMECs cultured separately, but significantly affected migration and angiogenesis of HRMEC in HPF and HRMEC co-culture models. Western blotting revealed that MIR503HG/miR-503-5p overexpression significantly increased LMW FGF2 expression in HPF.
conclusionMIR503HG/miR-503-5p inhibits HRMEC migration and angiogenic function by interfering with the interaction between HPF and endothelial cells
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