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Titolo:
Oligodendrocytes in aging mice lacking myelin-associated glycoprotein are dystrophic but not apoptotic
Autore:
Weiss, MD; Hammer, J; Quarles, RH;
Indirizzi:
NINDS, Mol & Cellular Neurobiol Lab, NIH, Myelin & Brain Dev Sect, Bethesda, MD 20892 USA NINDS Bethesda MD USA 20892 elin & Brain Dev Sect, Bethesda, MD 20892 USA
Titolo Testata:
JOURNAL OF NEUROSCIENCE RESEARCH
fascicolo: 6, volume: 62, anno: 2000,
pagine: 772 - 780
SICI:
0360-4012(200012)62:6<772:OIAMLM>2.0.ZU;2-N
Fonte:
ISI
Lingua:
ENG
Soggetto:
MULTIPLE-SCLEROSIS LESIONS; CELL-ADHESION MOLECULE; CENTRAL-NERVOUS-SYSTEM; FYN TYROSINE KINASE; ANTERIOR MEDULLARY VELUM; BASIC-PROTEIN; MONOCLONAL-ANTIBODY; N-CAM; RAT; DEFICIENT;
Keywords:
2 ',3 '-cyclic nucleotide 3 '-phosphodiesterase; (CNPase); myelin; MAG-null mice; neural cell adhesion molecule (NCAM); oligodendrogliopathy;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
52
Recensione:
Indirizzi per estratti:
Indirizzo: Weiss, MD NINDS, Mol & Cellular Neurobiol Lab, NIH, Myelin & Brain Dev Sect, Bldg 49,Room 2A28, Bethesda, MD 20892 USA NINDS Bldg 49,Room 2A28 Bethesda MD USA 20892 esda, MD 20892 USA
Citazione:
M.D. Weiss et al., "Oligodendrocytes in aging mice lacking myelin-associated glycoprotein are dystrophic but not apoptotic", J NEUROSC R, 62(6), 2000, pp. 772-780

Abstract

Although MAG-null mice myelinate relatively normally except for subtle structural abnormalities in the periaxonal region of myelin sheaths, they develop more severe pathological changes as they age. The purpose of this studywas to further define the biochemical aspects of CNS pathology caused by an absence of MAG. Proteins associated with myelin and oligodendrocytes werequantified by densitometry of western blots in whole brain homogenates, aswell as in isolated myelinated axons and myelin. Neither myelin yields, nor levels of myelin basic protein and proteolipid protein, were decreased incomparison to control levels in 14-month-old MAG-null mice. On the other hand, 2',3'-cyclic nucleotide 3'-phosphodiesterase (CNPase) and the 120 kD neural cell adhesion molecule (N-CAM) were substantially reduced in whole brain, myelinated axons, and myelin. Tubulin, Na(+)K(+)ATPase and Fyn tyrosine kinase were also reduced significantly in myelin-related fractions, but not in whole brain homogenate. The decreased levels of these proteins suggest pathological abnormalities in oligodendrocytes. Furthermore, significant reductions of CNPase and 120 kD NCAM were also present at 2 months, indicating that the oligodendroglial abnormalities begin at a relatively early age. Neither TUNEL assays nov multiplex RT-PCR for mRNAs of apoptosis-related proteins in the aging MAG-null mice provided evidence for apoptotic oligodendrocytes. These biochemical findings suggest oligodendroglial damage in MAG-null mice and support the morphological observations pointing to a progressive "dying-back oligodendrogliopathy" as a consequence of MAG deficiency. (C) 2000 Wiley-Liss, Inc.

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Documento generato il 01/12/20 alle ore 07:33:03