What question did this study set out to answer?

The aim is to explore how NEAT1 and miR-28-3p impact human scleral fibroblasts in the context of high myopia.

March 19, 2026Turkish Journal of Biochemistry0 citationsOpen Access

NEAT1 promotes the development of high myopia by targeting miR-28-3p to regulate human scleral fibroblasts

LXLifei XuTongde Hospital of Zhejiang Province WLWenwei LiTongde Hospital of Zhejiang Province RJRuting JiangTongde Hospital of Zhejiang Province

Key Points

The aim is to explore how NEAT1 and miR-28-3p impact human scleral fibroblasts in the context of high myopia.
Included 102 patients with high myopia and 100 with myopia.
Assessed expression levels using RT-qPCR for NEAT1, miR-28-3p, TGF-β1, and collagen I.
Utilized CCK-8 and flow cytometry to evaluate cell proliferation and apoptosis.
Conducted dual luciferase reporter and RNA immunoprecipitation assays to explore target-binding interactions.
NEAT1 levels were higher and miR-28-3p levels were lower in the high myopia group compared to the control.
NEAT1 was found to bind to miR-28-3p, with an inverse correlation in their expression.
Elevated NEAT1 suppressed the activity of human scleral fibroblasts and reduced TGF-β1 and collagen I levels.
Knockdown of NEAT1 increased miR-28-3p expression, enhancing cell proliferation and reducing apoptosis.

Abstract

Abstract Objectives High myopia (HM) can lead to serious complications that are hazardous to the health of adolescents. LncRNA nuclear-enriched abundant transcript 1 (NEAT1) and miR-28-3p exhibit abnormal expression in multiple ocular structures. Investigating the effects of NEAT1 and miR-28-3p on human corneal fibroblasts (HSF) may provide new theoretical foundations and directions for myopia management. Methods 102 patients with HM and 100 patients with myopia were included. The expression of NEAT1, miR-28-3p, transforming growth factor-β 1 (TGF-β1) and collagen Ι in aqueous humor was assessed by RT-qPCR. Cell Counting Kit-8 (CCK-8) and flow cytometry were used to detect cell proliferation and apoptosis, respectively. Dual luciferase reporter (DLR) and RNA Immunoprecipitation (RIP) assays were detected the target-binding relationship of NEAT1 and miR-28-3p. Results NEAT1 levels were higher and miR-28-3p levels were notably downregulated in the HM group than control. NEAT1 binds to miR-28-3p target and the levels were negatively correlated. Elevated NEAT1 suppressed cellular activity, markedly reducing TGF-β1 and collagen I levels. Knockdown of NEAT1 increased miR-28-3p expression, enhanced cell proliferation, reduced apoptosis, and boosted extracellular matrix synthesis. Conversely, silencing miR-28-3p significantly decreased cellular viability and extracellular matrix production. Conclusions Patients with HM have elevated levels of NEAT1. High NEAT1 levels suppress cellular activity and inhibit extracellular matrix production. Following NEAT1 silencing, miR-28-3p levels increase, thereby enhancing HSF cellular activity and promoting extracellular matrix production. This may delay HM progression.

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