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Titolo:
Myocilin is associated with mitochondria in human trabecular meshwork cells
Autore:
Wentz-Hunter, K; Ueda, J; Shimizu, N; Yue, BYJT;
Indirizzi:
Univ Illinois, Dept Ophthalmol & Visual Sci, Coll Med, Chicago, IL 60612 USA Univ Illinois Chicago IL USA 60612 l Sci, Coll Med, Chicago, IL 60612 USA Keio Univ, Sch Med, Dept Mol Biol, Tokyo, Japan Keio Univ Tokyo JapanKeio Univ, Sch Med, Dept Mol Biol, Tokyo, Japan
Titolo Testata:
JOURNAL OF CELLULAR PHYSIOLOGY
fascicolo: 1, volume: 190, anno: 2002,
pagine: 46 - 53
SICI:
0021-9541(200201)190:1<46:MIAWMI>2.0.ZU;2-5
Fonte:
ISI
Lingua:
ENG
Soggetto:
OPEN-ANGLE GLAUCOMA; GLUCOCORTICOID RESPONSE PROTEIN; SCHLEMMS CANAL CELLS; EXTRACELLULAR-MATRIX; ENDOPLASMIC-RETICULUM; GOLGI-APPARATUS; AQUEOUS-HUMOR; CILIARY BODY; LOCALIZATION; APOPTOSIS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
56
Recensione:
Indirizzi per estratti:
Indirizzo: Yue, BYJT Univ Illinois, Dept Ophthalmol & Visual Sci, Coll Med, 1855 W Taylor St, Chicago, IL 60612 USA Univ Illinois 1855 W Taylor St Chicago IL USA 60612 IL 60612 USA
Citazione:
K. Wentz-Hunter et al., "Myocilin is associated with mitochondria in human trabecular meshwork cells", J CELL PHYS, 190(1), 2002, pp. 46-53

Abstract

The trabecular meshwork (TM) is a specialized tissue located at the chamber angle of the eye next to the cornea. This tissue is believed to be responsible for regulation of the aqueous humor outflow and control of the intraocular pressure (IOP). Alterations in functions of the TM may lead to IOP elevation and development of glaucoma, a major cause of blindness. The myocilin gene has recently been directly linked to open-angle glaucomas. The geneproduct was originally identified as a protein inducible in TM cells by treatment with glucocorticoids such as dexamethasone (DEX) and termed TIGR (TM inducible-glucocorticoid response). The exact nature and function of the myocilin protein so far still remain elusive. In this study, myocilin was localized to the perinuclear region of both DEX-treated and control TM cells. Its distribution overlapped considerably with that of mitochondria. Subcellular fractionation and Western blot analyses suggested a rather extensiveassociation of myocilin with mitochondria. The DEX-treated TM cells were found to undergo apoptosis, when exposed to anti-Fas antibody, to a significantly higher degree than the untreated control cells. It appears that the TM cell integrity remains intact after DEX treatment. However, the induced myocilin or myocilin-mitochondria association seems to render the cells moresusceptible to a second stress or challenge. This vulnerability may be thebasis that ultimately leads to pathological consequences. (C) 2002 Wiley-Liss, Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/12/20 alle ore 12:56:02