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Ca2+/calmodulin effects on cAMP response in cultured chick ciliary epithelial cells
H K Mishima1, H Nii, T Kurokawa
1Department of Ophthalmology, Hiroshima University School of Medicine, Japan.
Japanese Journal of Ophthalmology
|January 1, 1995
Summary
Elevated intracellular calcium (Ca2+) potentiates cyclic adenosine 3
Area of Science:
- Biochemistry
- Cell Biology
- Ophthalmology
Background:
- Intracellular calcium (Ca2+) and cyclic adenosine 3',5'-monophosphate (cAMP) are crucial second messengers in cellular signaling.
- The ciliary epithelium (CE) plays a vital role in aqueous humor production and intraocular pressure regulation.
Purpose of the Study:
- To investigate the influence of elevated intracellular Ca2+ on cAMP production in cultured chick embryo ciliary epithelium (CE).
- To elucidate the role of Ca2+/calmodulin signaling in receptor-mediated cAMP pathways within the CE.
Main Methods:
- Cultured chick embryo ciliary epithelium (CE) cells were used.
- The effects of calcium ionophore (A23187) on cAMP production were examined.
- Responses were measured after stimulation with vasoactive intestinal peptide (VIP), isoproterenol (ISO), sodium fluoride (NaF), or forskolin (FSK).
- Calmodulin antagonist (W-7) was employed to assess the role of calmodulin.
Main Results:
- A23187 alone did not affect basal or NaF/FSK-stimulated cAMP levels.
- A23187 significantly potentiated VIP- and ISO-stimulated cAMP production.
- The potentiating effect of A23187 was inhibited by the calmodulin antagonist W-7.
Conclusions:
- Ca2+/calmodulin signaling potentiates receptor-mediated cAMP pathways in the CE.
- This potentiation may involve Ca2+/calmodulin-dependent protein kinase.
- Findings suggest a novel regulatory mechanism for CE function involving calcium and cAMP.