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The molecular basis of neurotrophic keratitis
Author(s) -
Cavanagh H. Dwight,
Colley Ann M.
Publication year - 1989
Publication title -
acta ophthalmologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.534
H-Index - 87
eISSN - 1755-3768
pISSN - 1755-375X
DOI - 10.1111/j.1755-3768.1989.tb07103.x
Subject(s) - neurotrophin , mitosis , intracellular , microbiology and biotechnology , muscarinic acetylcholine receptor , cholinergic , stimulation , endocrinology , receptor , medicine , adrenergic receptor , denervation , chemistry , biology
Endogenous proliferation of corneal epithelial cells is regulated by a bidirectional control process characterized by an adrenergic, cAMP‐dependent ‘off’, and a cholinergic, muscarinic cGMP‐dependent ‘on’ response. The adrenergic receptor(s) are located in the plasma membrane (microsomal fraction), whereas the novel feature of the system is a cholinergic receptor specific for acetylcholine (ACH) located in the nuclear membrane. Exogenous substances which raise intracellular cAMP levels such as isoproterenol or PGE1, shut off epithelial mitosis; and, carbamylcholine or ACH raise intranuclear cGMP levels and increase mitosis by specific, regulatory stimulation of RNA‐polymerase II activity. We believe that this regulatory system explains the transitory mitotic suppression induced by superficial corneal wounding (interruption of adrenergic fibres, ‘chalone‐effect’); and the marked, permanent depression of epithelial mitosis associated with decreased intracellular ACH levels which are produced by total corneal denervation, and which results in neurotrophic keratitis.