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Updated: May 9, 2026
Quantitative Methods to Study Protein Arginine Methyltransferase 1-9 Activity in Cells
Published on: August 7, 2021
Inhibition of PRMT5 reduces angiogenesis in a corneal neovascularization model by blocking NLRP3-mediated pyroptosis
Jiewen Mao1, Siyu Ding1, Qian Deng1
1Department of Ophthalmology, Renmin Hospital of Wuhan University, 238 Jiefang Road, Wuchang District, Wuhan, 430061, China.
Abstract:
Protein arginine methyltransferase 5 (PRMT5) is a histone methyltransferase crucial for cell proliferation, differentiation, and inflammation. However, the biological functions of PRMT5 and its underlying molecular mechanisms in corneal neovascularization (CNV) remain unclear. This study utilized corneal alkali burn and vascular endothelial growth factor (VEGF)-induced HUVEC models to examine the role of PRMT5 in CNV. We found that PRMT5 expression was significantly upregulated following corneal alkali burn. Experiments both in vitro and in vivo showed that PRMT5 knockdown or inhibition lowered pyroptosis-related protein expression and reduced cell death. PRMT5 interacts with the NACHT domain of NOD-like receptor family pyrin domain-containing 3 (NLRP3) via its Rossmann fold, catalyzing arginine methylation at the R490 and R504 residues through its methyltransferase activity. This process modulates inflammation and pyroptosis, thereby influencing the formation of CNV. In conclusion, our findings provide evidence that inhibiting PRMT5 can alleviate angiogenesis in CNV models by blocking NLRP3-mediated pyroptosis.
Insights
Inhibiting protein arginine methyltransferase 5 (PRMT5) reduces corneal neovascularization (CNV) by blocking NLRP3-mediated pyroptosis and inflammation. This finding offers a potential therapeutic target for CNV.
Area of Science:
- Ophthalmology
- Molecular Biology
- Cell Biology
Background:
- Protein arginine methyltransferase 5 (PRMT5) is vital for cell functions but its role in corneal neovascularization (CNV) is unknown.
- Corneal neovascularization (CNV) is a pathological process involving inflammation and angiogenesis.
Purpose of the Study:
- To investigate the role and molecular mechanisms of PRMT5 in corneal neovascularization (CNV).
- To explore PRMT5 as a potential therapeutic target for CNV.
Main Methods:
- Utilized corneal alkali burn and VEGF-induced HUVEC models for in vitro and in vivo studies.
- Assessed PRMT5 expression, knockdown, and inhibition effects on pyroptosis and angiogenesis.
- Investigated the interaction between PRMT5 and NLRP3 inflammasome components.
Main Results:
- PRMT5 expression was significantly increased in corneal alkali burn models.
- PRMT5 knockdown/inhibition reduced pyroptosis, cell death, and CNV formation.
- PRMT5 directly interacts with NLRP3, catalyzing arginine methylation at R490/R504, modulating inflammation and pyroptosis.
Conclusions:
- PRMT5 plays a critical role in promoting CNV by mediating NLRP3-dependent pyroptosis and inflammation.
- Inhibiting PRMT5 demonstrates therapeutic potential for alleviating angiogenesis in CNV models.
