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eNOS Activity in CAV1 Knockout Mouse Eyes.

Yuan Lei1, Maomao Song2, Jihong Wu1

  • 1Research Centre Eye and ENT Hospital, Shanghai Medical College, Fudan University, Shanghai, China 2Key Laboratory of Myopia, Ministry of Health, Fudan University, Shanghai, China 3Shanghai Key Laboratory of Visual Impairment and Restoration, Eye and ENT H.

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Caveolin-1 knockout mice show higher intraocular pressure and reduced outflow facility, despite increased endothelial nitric oxide synthase (eNOS) activity. This suggests eNOS activity is not the sole factor in regulating intraocular pressure in these models.

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Area of Science:

  • Ophthalmology
  • Molecular Biology
  • Physiology

Background:

  • Caveolin-1 (CAV1) plays a role in regulating endothelial nitric oxide synthase (eNOS) activity.
  • The function of CAV1 in the eye's conventional outflow pathway and its impact on intraocular pressure (IOP) remain incompletely understood.

Purpose of the Study:

  • To investigate the role of CAV1 in regulating endothelial nitric oxide synthase (eNOS) activity.
  • To examine the effect of nitric oxide (NO) donors and a nitric oxide synthase (NOS) inhibitor on conventional outflow facility in CAV1 knockout (KO) mice.

Main Methods:

  • Intraocular pressure (IOP) was measured in CAV1 KO and wild-type (WT) mice.
  • Protein expression levels of CAV2, eNOS, phosphorylated eNOS, Akt, phosphorylated Akt, and nitrotyrosine were analyzed using Western blot.
  • Topical administration of NO donors (SNP, SNAP) or a NOS inhibitor (L-NAME) was performed.
  • Outflow facility was measured in enucleated eyes.

Main Results:

  • CAV1 KO mice exhibited elevated IOP and reduced conventional outflow facility compared to WT mice.
  • CAV1 deficiency led to increased eNOS activity, evidenced by higher eNOS-phospho Ser1177 and nitrotyrosine levels.
  • NO donors (SNP) reduced IOP in both WT and KO mice, while L-NAME increased IOP in KO mice.
  • NO donors enhanced pressure-dependent drainage in KO mice, whereas L-NAME reduced it.

Conclusions:

  • CAV1 deficiency, potentially with CAV2 loss, results in elevated IOP and decreased outflow facility despite increased eNOS activity.
  • The elevated IOP in KO mice may be linked to increased protein tyrosine nitration and impaired protein kinase K activity.
  • eNOS activity is not the sole determinant of conventional outflow facility and IOP regulation in the context of CAV1 deficiency.