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Updated: Feb 15, 2026

Purification of Ubiquitinated p53 Proteins from Mammalian Cells
Published on: March 21, 2022
MicroRNA regulation of MDM2-p53 loop in pterygium
Yufei Teng1, Gary Hin-Fai Yam2, Na Li3
1Department of Ophthalmology & Visual Sciences, The Chinese University of Hong Kong, Hong Kong, China; Beijing Institute of Ophthalmology, Beijing Tongren Eye Center, Beijing Tongren Hospital, Capital Medical University, Beijing Ophthalmology and Visual Sciences Key Laboratory, Beijing, China; Beijing Tongren Eye Center, Beijing Tongren Hospital, Capital Medical University, Beijing Ophthalmology and Visual Sciences Key Laboratory, Beijing, China.
Purpose:
The pathogenesis of pterygium has been linked to limbal stem cell damage, abnormal apoptosis and cellular proliferation. In this study, we investigated the epigenetic regulation through microRNA expression in the pathogenesis of pterygium.
Methods:
Human full-length primary pterygia were microdissected into head and body regions. Specific microRNA and mRNA expression was assayed by TaqMan® real-time quantitative polymerase chain reaction (qPCR). Tissue localization of target microRNAs was performed by LNA-based in situ hybridization. MicroRNA-145 (miR-145) mimics were transfected to primary culture of human pterygial cells, followed by analyses of cell cycle changes, apoptosis, p53 and MDM2 expression using flow cytometry and qPCR.
Results:
The expression of miR-145 was markedly higher in primary human pterygium than in limbus and conjunctiva. Both miR-143 and miR-145 were predominantly expressed in the basal pterygial epithelium. Oncogene MDM2 expression was abundant in pterygial epithelium and stroma, while the expression pattern was opposite to that of miR-145. Ectopic expression of miR-145 in pterygial cells induced G1 arrest, down-regulated MDM2 and elevated p53 expression.
Conclusions:
Our study showed that miR-145 suppressed MDM2 expression, which subsequently influenced the p53-related cell growth pattern in pterygial epithelium. The regulatory miR-145/MDM2-p53 loop can serve as a potential target for treatment of pterygium.
Insights
MicroRNA-145 (miR-145) is elevated in pterygium, suppressing MDM2 and influencing p53. This miR-145/MDM2-p53 pathway presents a potential therapeutic target for pterygium treatment.
Area of Science:
- Ophthalmology
- Molecular Biology
- Epigenetics
Background:
- Pterygium pathogenesis involves limbal stem cell damage, abnormal apoptosis, and cellular proliferation.
- Epigenetic regulation via microRNA expression is implicated in pterygium development.
Purpose of the Study:
- To investigate the role of microRNA expression in pterygium pathogenesis.
- To explore the epigenetic regulation of pterygium through microRNA analysis.
Main Methods:
- MicroRNA and mRNA expression analyzed using quantitative polymerase chain reaction (qPCR).
- MicroRNA tissue localization performed via in situ hybridization.
- Functional effects of microRNA-145 (miR-145) on pterygial cells assessed through transfection, cell cycle analysis, apoptosis assays, and gene expression analysis (p53, MDM2).
Main Results:
- miR-145 expression was significantly higher in pterygium tissue compared to limbus and conjunctiva.
- miR-145 and miR-143 were predominantly expressed in the basal pterygial epithelium.
- Ectopic miR-145 expression in pterygial cells induced cell cycle arrest (G1), downregulated MDM2, and upregulated p53.
Conclusions:
- miR-145 suppresses MDM2 expression, impacting p53-mediated cell growth in pterygial epithelium.
- The miR-145/MDM2-p53 regulatory loop is a potential therapeutic target for pterygium treatment.
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