
Claudin localization in cilia of the retinal pigment epithelium
Author(s) -
Nishiyama Kazutoshi,
Sakaguchi Hirokazu,
Hu Jane G.,
Bok Dean,
Hollyfield Joe G.
Publication year - 2002
Publication title -
the anatomical record
Language(s) - English
Resource type - Journals
eISSN - 1097-0185
pISSN - 0003-276X
DOI - 10.1002/ar.10102
Subject(s) - cilium , retinal pigment epithelium , microbiology and biotechnology , biology , ciliogenesis , immunocytochemistry , claudin , epithelium , retina , tight junction , retinal , microtubule , endocrinology , neuroscience , biochemistry , genetics
Using immunocytochemistry and confocal microscopy we demonstrate that claudin‐immunoreactivity is a novel marker for retinal pigment epithelial cilia. Claudin‐immunoreactivity obtained by polyclonal anti‐claudin 1 antibody, which could crossreact with claudin 3, was colocalized with acetylated tubulin‐immunoreactivity in cultured human retinal pigment epithelial cells. Claudin‐immunoreactivity associated with the retinal pigment epithelium (RPE) cilia was more intense than was claudin‐immunoreactivity in the junctional complex. Approximately two‐thirds of the RPE cells in the rat contain cilia that are immunoreactive with acetylated tubulin on postnatal day 1, and a significant portion of these cilia label with the anti‐claudin 1 antibody. Cilia decrease in frequency over subsequent postnatal days, and are absent by postnatal day 30. As RPE cilia decrease in number during postnatal rat development, claudin‐immunoreactivity is lost earlier than acetylated tubulin, suggesting that the loss of claudin may initiate RPE cilium degeneration. Claudin‐immunoreactivity was not evident in cilia of photoreceptor cells, epithelia of nasal mucosa, small intestine, or colon, suggesting that claudin may be a unique molecule in RPE cilia. These data suggest that cilia of the RPE, unlike cilia on other cell types, contain claudin, and that this molecule may play an important and specific role in the function and/or maintenance of RPE cilia. Anat Rec 267:196–203, 2002. © 2002 Wiley‐Liss, Inc.