Complement and clusterin in the injured nervous system

Törnqvist, Elin; Liu, L.; Aldskogius, H.; Holst, Hans von; Svensson, Mikael

doi:10.1016/0197-4580(96)00120-0

Cited by 27 publications

(19 citation statements)

References 73 publications

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“…Complement factors mediate a variety of inflammatory processes and promote phagocytosis and cell lysis. Increased levels of complement have been found in microglial cells after direct injury to the central nervous system (Pasinetti et al 1992), in the vicinity of axotomized central neurons, or near degenerating central terminals of axotomized peripheral neurons (Tornqvist et al 1996). However, complement activation is not observed during Wallerian degeneration in spinal white matter, and recent studies argue against an involvement of clusterin in complement inhibition (Hochgrebe et al 1999).…”

Section: Putative Functions Of Clusterin Following Spinal Cord Injurymentioning

confidence: 97%

Regulation of clusterin expression following spinal cord injury

Klimaschewski

Obermüller

Witzgall

2001

Cell and Tissue Research

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We have investigated the localization and regulation of a putative extracellular chaperone, clusterin, in the rat spinal cord after lesion. In control animals, clusterin is expressed in motoneurons, in meningeal and ependymal cells, and in astrocytes mainly located beneath the pial surface. Beginning at day 2 after hemisection at segmental level C6, clusterin levels increase in GFAP-positive astrocytes within the lesioned segment. Three weeks after trauma, clusterin mRNA and protein are elevated in neurons close to the lesion site and in glial elements within scar tissue and within degenerating fiber tracts rostral and caudal to the lesion. This study provides evidence for a role of clusterin in the subacute and late phase of spinal cord injury.

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Section: Putative Functions Of Clusterin Following Spinal Cord Injurymentioning

confidence: 97%

Regulation of clusterin expression following spinal cord injury

Klimaschewski

Obermüller

Witzgall

2001

Cell and Tissue Research

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“…ApoJ, the major apolipoprotein in these particles, has been implicated in cell death, particularly apoptotic cell death (47). Following injury, apoJ expression is upregulated at sites undergoing tissue remodeling occurring in conjunction with apoptosis (47)(48)(49)(50). The apoJ carried on these microglial particles might subserve a function to protect against neuronal injury.…”

Section: Discussionmentioning

confidence: 99%

Isolation and Characterization of Apolipoproteins from Murine Microglia

Xu¹,

Li²,

Sanan³

et al. 2000

Journal of Biological Chemistry

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Amyloid A␤ deposition is a neuropathologic hallmark of Alzheimer's disease. Activated microglia are intimately associated with plaques and appear to facilitate A␤ deposition, an event believed to contribute to pathogenesis. It is unclear if microglia can modulate pathogenesis of Alzheimer's disease by secreting lipoprotein particles. Here we show that cultured BV2 murine microglial cells, like astrocytes, secrete apolipoprotein E (apoE) and apolipoprotein J (apoJ) in a time-dependent manner. To isolate and identify BV2 microglial particles, gel filtration chromatography was employed to fractionate BV2-conditioned medium. Analyses by Western blot, lipid determination, electron microscopy, and native gel electrophoresis demonstrate that BV2 microglial cells release spherical low density lipoprotein (LDL)-like lipid-containing particles rich in apoJ but poor in apoE. These microglial particles are dissimilar in size, shape, and lipoprotein composition to astrocytederived particles. The microglial-derived particles were tested for functional activity. Under conditions of suppressed de novo cholesterol synthesis, the LDL-like particles effectively rescued primary rat cortical neurons from mevastatin-induced neurotoxicity. The particles were also shown to bind A␤. We speculate that the LDLlike apoJ-rich apoE-poor microglial lipoproteins preferentially bind the lipoprotein receptor, recognizing apoJ, which is abundant in the choroid plexus, facilitating A␤ clearance from the brain. BV2 cells also secrete an apoErich lipid-poor species that binds A␤. Consistent with the role of apoE in A␤ fibril formation and deposition, this microglial species may promote plaque formation.

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“…Recently, a great deal of interest has been given to the relationship between clusterin and various aspects of neural degeneration and regeneration (May and Finch, 1992;Törnqvist et al, 1996). Clusterin has complement inhibitory properties, but is involved in a number of other biological functions as well, such as cell-cell interaction and lipid transport (Rosenberg et al, 1993) The purpose of the present study was to examine the glial cell response and the possible expression of complement and clusterin during Wallerian degeneration in the central nervous system following dorsal rhizotomy and, furthermore, to compare these reactions to those occurring in the corresponding areas after injury to the peripheral processes of dorsal root ganglion cells.…”

Section: Introductionmentioning

confidence: 99%