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Ongoing Cell Death and Immune Influences on Regeneration in the Vestibular Sensory Organs
Author(s) -
WARCHOL MARK E.,
MATSUI JONATHAN I.,
SIMKUS ELIZABETH L.,
OGILIVE JUDITH M.
Publication year - 2001
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2001.tb03733.x
Subject(s) - hair cell , microbiology and biotechnology , inner ear , biology , programmed cell death , regeneration (biology) , vestibular system , population , cochlea , immune system , immunology , apoptosis , neuroscience , medicine , genetics , environmental health
A bstract : Hair cells in the vestibular organs of birds have a relatively short life span. Mature hair cells appear to die spontaneously and are then quickly replaced by new hair cells that arise from the division of epithelial supporting cells. A similar regenerative mechanism also results in hair cell replacement after ototoxic damage. The cellular basis of hair cell turnover in the avian ear is not understood. We are investigating the signaling pathways that lead to hair cell death and the relationship between ongoing cell death and cell production. In addition, work from our lab and others has demonstrated that the avian inner ear contains a resident population of macrophages and that enhanced numbers of macrophages are recruited to sites of hair cells lesions.1–3 Those observations suggest that macrophages and their secretory products (cytokines) may be involved in hair cell regeneration. Consistent with that suggestion, we have found that treatment with the anti‐inflammatory drug dexamethasone reduces regenerative cell proliferation in the avian ear, and that certain macrophage‐secreted cytokines can influence the proliferation of vestibular supporting cells2 and the survival of statoacoustic neurons.4 Those results suggest a role for the immune system in the process of sensory regeneration in the inner ear. (For full refs. 1–4, see reference list to main paper.)