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Updated: May 22, 2026
Application of Genetically Encoded Fluorescent Nitric Oxide (NO•) Probes, the geNOps, for Real-time Imaging of NO• Signals in Single Cells
Published on: March 16, 2017
Potential involvement of nitric oxide synthase but not inducible nitric oxide synthase in the development of
Yuan Chen1, Gao-Qin Liu, Pei-Rong Lu
1Department of Ophthalmology, the First Affiliated Hospital of Soochow University, Suzhou 215006, Jiangsu Province, China.
Aim:
To investigate the effect of nitric oxide and its synthetase on experimental corneal neovascularization (CRNV).
Methods:
CRNV was induced by alkali injury in mice, nitric oxide synthetase (NOS) was inhibited by NG-nitro-L-arginine (L-NAME) and inducible nitric oxide synthetase (iNOS) was inhibited by aminoguanidine hemisulfate salt (AG). The inhibitory effect was detected at day 2 and 4 after corneal alkali injury by reverse transcription polymerase chain reaction (RT-PCR). CRNV was compared between the control and the treated mice by microscopic observation and corneal whole mount CD31 immunostaining.
Results:
The inhibition of L-NAME to NOS and AG to iNOS after corneal injury was confirmed by RT-PCR (P<0.05). Compared with control mice, L-NAME treated mice exhibited significantly decreased CRNV areas (P<0.05). In contrast, AG treatment failed to attenuate alkali induced CRNV (P>0.05).
Conclusion:
Our findings suggest that NOS but not iNOS plays a critical role in alkali injury induced CRNV.
Insights
Nitric oxide synthetase (NOS) significantly reduces corneal neovascularization after alkali injury. Inhibiting inducible nitric oxide synthetase (iNOS) did not affect this neovascularization, suggesting NOS is critical.
Area of Science:
- Ophthalmology
- Vascular Biology
- Molecular Medicine
Background:
- Corneal neovascularization (CRNV) is a pathological process that can impair vision.
- Nitric oxide (NO) is implicated in various physiological and pathological processes, including inflammation and angiogenesis.
- The role of specific nitric oxide synthetase (NOS) isoforms in CRNV remains to be fully elucidated.
Purpose of the Study:
- To investigate the specific role of nitric oxide synthetase (NOS) and its inducible isoform (iNOS) in experimental corneal neovascularization (CRNV) following alkali injury.
Main Methods:
- CRNV was induced in mice using alkali injury.
- Nitric oxide synthetase (NOS) was inhibited using NG-nitro-L-arginine (L-NAME).
- Inducible nitric oxide synthetase (iNOS) was inhibited using aminoguanidine hemisulfate salt (AG).
- Inhibitory effects were confirmed via RT-PCR.
- CRNV was quantified using microscopy and CD31 immunostaining.
Main Results:
- Inhibition of NOS by L-NAME significantly reduced CRNV areas compared to controls (P<0.05).
- Inhibition of iNOS by AG did not significantly attenuate alkali-induced CRNV (P>0.05).
- RT-PCR confirmed effective inhibition of NOS and iNOS by L-NAME and AG, respectively.
Conclusions:
- Nitric oxide synthetase (NOS), but not its inducible form (iNOS), plays a critical role in the pathogenesis of alkali-induced corneal neovascularization.
- Targeting NOS may represent a therapeutic strategy for managing CRNV.
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