Methods for the Identification and Characterization of Glycoproteins in Central and Peripheral Myelin

Quarles, Richard H.; Barbarash, Gary R.; MacIntosh, Tracy D.

doi:10.1007/978-1-4615-7760-7_10

Cited by 30 publications

(12 citation statements)

References 84 publications

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“…It is striking that the number of bilayers per fragment varies from fraction to fraction (summarized in Fig. 3), The denser fractions contain single-or double-bilayer fragments (Agrawal et al, 1970) and are rich in highmolecular weight proteins Waehneldt, 1978a,b;Quarles et al, 1985). The lower density fractions are correspondingly poor in the high-molecular weight proteins (Zgorzalewicz et al, 1974) and have four or more bilayers (Autilio et al, 1964;Wolfgram and Kotorii, 1968).…”

Section: Lipid/protein Ratio Determines Degree Of Myelin Vesiculationmentioning

confidence: 98%

Myelin vesicles: What we know and what we do not know

Sędzik

Blaurock²

1995

J of Neuroscience Research

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In the following review, we address difficulties that have arisen when attempting to convert the myelin multilayers into vesicles. The emphasis is on CNS myelin of adult mammals although both central nervous system (CNS) and peripheral nervous system (PNS) myelin are considered. The ability to prepare vesicle of myelin membrane has yet not been feasible. We hope to clarify some aspect of this problem and offer some possible approaches. Special attention is paid to myelin swelling phenomena because these indicate ways in which the myelin multilayer can break down. Images of isolated myelin are reviewed with special attention to the ways in which the multilayer actually breaks down. Attempts at reproducing a procedure for vesiculating myelin are summarized, and a critique is given to account for the inability to reproduce the published results. Finally, novel approaches for vesiculating myelin are proposed, which are based on well-characterized swelling phenomena.

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Section: Lipid/protein Ratio Determines Degree Of Myelin Vesiculationmentioning

confidence: 98%

Myelin vesicles: What we know and what we do not know

Sędzik

Blaurock²

1995

J of Neuroscience Research

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“…The blots were immunostained with anti-MAG monoclonal antibody D7E10 (Doberson et al, 1985) as described by Quarles et al (1985). The blots were immunostained with anti-MAG monoclonal antibody D7E10 (Doberson et al, 1985) as described by Quarles et al (1985).…”

Section: Gel Electrophoresis and Immunoblottingmentioning

confidence: 99%

Myelin‐Associated Calpain II

Yanagisawa

Sato

O’Shannessy

et al. 1988

Journal of Neurochemistry

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Anti-chicken muscle calpain (calcium-activated neutral protease) antibody (ACAb) was found to be absorbed by purified human brain myelin when titrated by enzyme-linked immunosorbent assay, suggesting the close association of the protease with myelin. To confirm this, calcium-dependent protease was extracted from myelin membrane and purified on a phenyl Sepharose CL 4B column. It was activated by calcium ion in the millimolar range, and therefore was determined to be calpain II. This enzyme fraction was electrophoresed and immunostained with ACAb, resulting in staining as a single band with apparent molecular weight of 80K. This protease degraded exogenous myelin-associated glycoprotein. From the present results, it is suggested that calpain is bound to myelin membrane and involved in the turnover of myelin proteins.

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“…Although the previous data do not support a major role for class II-restricted autoimmune T cell responses against MBP and PLP in the TMEV-induced demyelinating process, we could not exclude a possible role for autoimmune responses against minor myelin components, such as myelin-associated glycoprotein, myelin oligodendrocyte glycoprotein, or galactocerebroside (Rapport et al, 1964;Quarles et al, 1985;Linington and Lassmann, 1987), against altered neuroantigenic determinants, or against other nonmyelinassociated neuroantigens. In an attempt to address these possibilities, we employed two different experimental approaches.…”

Section: Discussionmentioning

confidence: 70%

Class II-restricted T cell responses in Theiler's murine encephalomyelitis virus (TMEV)-induced demyelinating disease

Miller¹,

Gerety²,

Kennedy³

et al. 1990

Journal of Neuroimmunology

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Intracerebral inoculation of Theiler's murine encephalomyelitis virus (TMEV) into susceptible mouse strains produces a chronic demyelinating disease in which mononuclear cell-rich infiltrates in the central nervous system (CNS) are prominent. Current evidence strongly supports an immune-mediated basis for myelin breakdown, with an effector role proposed for TMEV-specific, major histocompatibility complex (MHC) class II-restricted delayed-type hypersensitivity (DTH) responses in which lymphokine-activated macrophages mediate bystander demyelination. The present study examined the possibility that concomitant or later-appearing neuroantigen-specific autoimmune T cell responses, such as those demonstrated in chronic-relapsing experimental allergic encephalomyelitis (R-EAE), may contribute to the demyelinating process following TMEV infection. T cell responses against intact, purified major myelin proteins (myelin basic protein (MBP) and proteolipid protein (PLP], and against altered myelin constituents were readily demonstrable in SJL/J mice with R-EAE, but were not detectable in SJL/J mice with TMEV-induced demyelinating disease. TMEV-infected mice also did not display T cell responses against the peptide fragments of MBP(91-104) and PLP(139-151) recently shown to be encephalitogenic in SJL/J mice. In addition, induction of neuroantigen-specific tolerance to a heterogeneous mixture of CNS antigens, via the i.v. injection of syngeneic SJL/J splenocytes covalently coupled with mouse spinal cord homogenate, resulted in significant suppression of clinical and histologic signs of R-EAE and the accompanying MBP- and PLP-specific DTH responses. In contrast, neuroantigen-specific tolerance failed to alter the development of clinical and histologic signs of TMEV-induced demyelinating disease or the accompanying virus-specific DTH and humoral immune responses. These findings demonstrate that TMEV-induced demyelinating disease can occur in the apparent absence of neuroantigen-specific autoimmune responses. The relationship of the present results to the immunopathology of multiple sclerosis is discussed.

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Methods for the Identification and Characterization of Glycoproteins in Central and Peripheral Myelin

Cited by 30 publications

References 84 publications

Myelin vesicles: What we know and what we do not know

Myelin vesicles: What we know and what we do not know

Myelin‐Associated Calpain II

Class II-restricted T cell responses in Theiler's murine encephalomyelitis virus (TMEV)-induced demyelinating disease

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