Ophthalmology science · 2025
A Pilot Study Profiling Aqueous Humor-Derived Exosomal MicroRNA in Primary Open-Angle and Exfoliation Glaucoma.
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Zou Yunyun, Kim Jaeryung, Kim Taeun, Sung Soo-Eun, Han Jong Chul, Cha Soon Cheol, Park Do Young
Аннотация
OBJECTIVE: To profile aqueous humor (AH)-derived exosomal microRNAs (miRNAs) in primary open-angle glaucoma (POAG) and exfoliation glaucoma (XFG) and investigate their potential as diagnostic biomarkers and modulators of extracellular matrix (ECM) remodeling in glaucoma pathogenesis.
DESIGN: Prospective, comparative, observational pilot study.
SUBJECTS AND CONTROLS: Aqueous humor was obtained from 21 patients with POAG, 24 patients with XFG, and 14 healthy donors.
METHODS: Exosomes were isolated from pooled AH samples of patients with POAG, XFG, and healthy donors for small RNA sequencing. miR-29a, an ECM-targeting miRNA, was selected for functional validation in transforming growth factor-beta 2 (TGF-β2)- or dexamethasone (Dex)-induced collagen deposition models using human trabecular meshwork cells (HTMCs).
MAIN OUTCOME MEASURES: Identification of potential glaucoma- and subtype-specific exosomal miRNA biomarkers and evaluation of selected ECM-targeting miRNAs for their roles in modulating collagen expression in vitro.
RESULTS: A total of 130 and 145 miRNAs were differentially expressed in POAG/Healthy and XFG/Healthy comparisons, respectively, with 96 miRNAs commonly dysregulated. Upregulation of ECM-related miRNAs-miR-21-5p, miR-92b-3p, miR-99a-5p, miR-486-3p, miR-486-5p, and miR-1260a-constituted a glaucoma-specific signature, whereas miR-99b-5p and miR-125a-5p showed subtype-specific upregulation in POAG, and miR-26a-5p and miR-451a in XFG. miR-29a-3p, a known antifibrotic miRNA, was significantly downregulated in POAG, XFG, and in HTMCs treated with TGF-β2 or Dex. Functional assays demonstrated that overexpression of miR-29a-3p attenuated TGF-β2- and Dex-induced collagen deposition in HTMCs.
CONCLUSIONS: This study provides the first profile of AH-derived exosomal miRNAs in POAG and XFG, identifies potential miRNAs associated with ECM remodeling, and highlights their potential utility as biomarkers and therapeutic targets in glaucoma.
FINANCIAL DISCLOSURES: Proprietary or commercial disclosure may be found in the Footnotes and Disclosures at the end of this article.
DESIGN: Prospective, comparative, observational pilot study.
SUBJECTS AND CONTROLS: Aqueous humor was obtained from 21 patients with POAG, 24 patients with XFG, and 14 healthy donors.
METHODS: Exosomes were isolated from pooled AH samples of patients with POAG, XFG, and healthy donors for small RNA sequencing. miR-29a, an ECM-targeting miRNA, was selected for functional validation in transforming growth factor-beta 2 (TGF-β2)- or dexamethasone (Dex)-induced collagen deposition models using human trabecular meshwork cells (HTMCs).
MAIN OUTCOME MEASURES: Identification of potential glaucoma- and subtype-specific exosomal miRNA biomarkers and evaluation of selected ECM-targeting miRNAs for their roles in modulating collagen expression in vitro.
RESULTS: A total of 130 and 145 miRNAs were differentially expressed in POAG/Healthy and XFG/Healthy comparisons, respectively, with 96 miRNAs commonly dysregulated. Upregulation of ECM-related miRNAs-miR-21-5p, miR-92b-3p, miR-99a-5p, miR-486-3p, miR-486-5p, and miR-1260a-constituted a glaucoma-specific signature, whereas miR-99b-5p and miR-125a-5p showed subtype-specific upregulation in POAG, and miR-26a-5p and miR-451a in XFG. miR-29a-3p, a known antifibrotic miRNA, was significantly downregulated in POAG, XFG, and in HTMCs treated with TGF-β2 or Dex. Functional assays demonstrated that overexpression of miR-29a-3p attenuated TGF-β2- and Dex-induced collagen deposition in HTMCs.
CONCLUSIONS: This study provides the first profile of AH-derived exosomal miRNAs in POAG and XFG, identifies potential miRNAs associated with ECM remodeling, and highlights their potential utility as biomarkers and therapeutic targets in glaucoma.
FINANCIAL DISCLOSURES: Proprietary or commercial disclosure may be found in the Footnotes and Disclosures at the end of this article.