Inhibition by brimonidine of forskolin-induced nitric oxide synthase expression in human ciliary bodies in vitro

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Renyi Wu1, Jinfu Yin, Ke Yao

  • 1Eye Center of the 2nd Affiliated Hospital, Medical College of Zhejiang University, Hangzhou, China. wubasel@hotmail.com

Molecular Vision
|April 10, 2007
PubMed
Abstract

Insights

Brimonidine, an ocular hypotensive drug, inhibits forskolin-induced upregulation of neuronal nitric oxide synthase (nNOS) in human ciliary bodies. This suggests a mechanism for brimonidine

Area of Science:

  • Ophthalmology
  • Molecular Biology
  • Pharmacology

Background:

  • Nitric oxide synthase (NOS) plays a role in ocular physiology.
  • The ciliary body is the site of aqueous humor production.
  • Understanding NOS regulation is crucial for developing ocular hypotensive agents.

Purpose of the Study:

  • To investigate nitric oxide synthase (NOS) mRNA and protein expression in human ciliary bodies.
  • To determine the effects of forskolin and brimonidine on NOS expression in vitro.
  • To elucidate the role of nNOS in the mechanism of action of ocular hypotensive agents.

Main Methods:

  • Human ciliary bodies were incubated with forskolin and/or brimonidine.
  • Reverse transcription-polymerase chain reaction (RT-PCR) was used to assess NOS mRNA expression.
  • Western blot analysis was performed to evaluate NOS protein expression.

Main Results:

  • All three NOS isoforms (nNOS, iNOS, eNOS) were detected at mRNA and protein levels.
  • Forskolin significantly upregulated neuronal NOS (nNOS) expression.
  • Brimonidine inhibited the forskolin-induced upregulation of nNOS.

Conclusions:

  • Brimonidine inhibits the forskolin-induced upregulation of nNOS expression in the human ciliary body.
  • This finding provides insights into the molecular mechanisms of brimonidine's ocular hypotensive effect.
  • nNOS may be a potential target for modulating aqueous humor production.

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