A role for apolipoprotein E, apolipoprotein A-I, and low density lipoprotein receptors in cholesterol transport during regeneration and remyelination of the rat sciatic nerve.

Boyles, J K; Zoellner, Christian; Anderson, L J; Kosik, L M; Pitas, Robert E.; Weisgraber, Karl H.; Hui, David Y.; Mahley, Robert W.; Gebicke‐Haerter, Peter J.; Ignatius, Michael J.

doi:10.1172/jci113943

Cited by 500 publications

(293 citation statements)

References 47 publications

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“…In addition, they summon macrophages into the damaged tissue (11) . These macrophages function not only as phagocytes (20) but also serve as a reservoir for cholesterol derived from ingested myelin, which can then be used during remyelination of regenerating axons (21) .…”

Section: Leukocytes Microglia/macrophages and Dendritic Cells As Mementioning

confidence: 99%

Inflammation and spinal cord injury: Infiltrating leukocytes as determinants of injury and repair processes

Trivedi

Olivas

Noble-Haeusslein

2006

Clinical Neuroscience Research

184

138

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The immune response that accompanies spinal cord injury contributes to both injury and reparative processes. It is this duality that is the focus of this review. Here we consider the complex cellular and molecular immune responses that lead to the infiltration of leukocytes and glial activation, promote oxidative stress and tissue damage, influence wound healing, and subsequently modulate locomotor recovery. Immunomodulatory strategies to improve outcomes are gaining momentum as ongoing research carefully dissects those pathways, which likely mediate cell injury from those, which favor recovery processes. Current therapeutic strategies address divergent approaches including early immunoblockade and vaccination with immune cells to prevent early tissue damage and support a wound-healing environment that favors plasticity. Despite these advances, there remain basic questions regarding how inflammatory cells interact in the injured spinal cord. Such questions likely arise as a result of our limited understanding of immune cell/neural interactions in a dynamic environment that culminates in progressive cell injury, demyelination, and regenerative failure.

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Section: Leukocytes Microglia/macrophages and Dendritic Cells As Mementioning

confidence: 99%

Inflammation and spinal cord injury: Infiltrating leukocytes as determinants of injury and repair processes

Trivedi

Olivas

Noble-Haeusslein

2006

Clinical Neuroscience Research

184

138

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“…roles have been proposed for apoE in brain metabolism, including a lipid transport role based on both PNS and CNS studies (Ignatius et al, 1986;Boyles et al, 1989;Poirier et al, 1993). However, the critical functions of apoE in the CNS remain obscure Yankner, 1996).…”

mentioning

confidence: 99%

Novel Large Apolipoprotein E‐Containing Lipoproteins of Density 1.006–1.060 g/ml in Human Cerebrospinal Fluid

Guyton

Miller

Martin³

et al. 1998

Journal of Neurochemistry

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Abstract:Although the critical role of apolipoprotein F (apoE) allelic variation in Alzheimer's disease and in the outcome of CNS injury is now recognized, the functions of apoE in the CNS remain obscure, particularly with regard to lipid metabolism. We used density gradient ultracentrifugation to identify apoE-containing lipoproteins in human CSF. CSF apoE lipoproteins, previously identified only in the 1.063-1.21 g/ml density range, were also demonstrated in the 1.006-1.060 g/ml density range. Plasma lipoproteins in this density range include lowdensity lipoprotein and high-density lipoprotein (HDL) subfraction 1 (HDL 1). The novel CSF àpoE lipoproteins are designated HDL1. No immunoreactive apolipoprotein A-I (apo A-I) or B could be identified in the CSF HDL1 fractions. Large lipoproteins 18.3 ±6.6 nm in diameter (mean ±SD) in the HDL1 density range were demonstrated by electron microscopy. Following fast protein liquid chromatography of CSF at physiologic ionic strength, apoE was demonstrated in particles of average size greater than particles containing apoA-I. The largest lipoproteins separated by this technique contained apoE without apoA-I. Thus, the presence of large apoE-contaming lipoproteins was confirmed without ultracentrifugation. Interconversion between the more abundant smaller apoE-HDL subfractions 2 and 3 and the novel larger apoE-HDL1 is postulated to mediate a role in cholesterol redistribution in brain.

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“…ApoE is a major component of plasma and cerebrospinal fluid, and plays a fundamental role after CNS injury. 18,66 ApoE polymorphisms result in differences in the metabolism of ApoE-containing lipoprotein particles. 34 For example, it is possible that certain ApoE polymorphisms affect their ability to interact with lipoprotein lipase in the conversion of VLDL to LDL.…”

Section: Cholesterol Transport and Metabolismmentioning

confidence: 99%

Transport and Retinal Capture of Lutein and Zeaxanthin with Reference to Age-related Macular Degeneration

Loane

Nolan

O'Donovan

et al. 2008

Survey of Ophthalmology

100

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Abstract. Age-related macular degeneration (AMD) is the most common cause of irreversible blindness in the elderly population in the western world. The etiology and pathogenesis of this disease remain unclear. However, there is an increasing body of evidence supporting the hypothesis that the macular pigment carotenoids, lutein and zeaxanthin, play an important role in protection against AMD, by filtering out blue light at a pre-receptoral level, or by quenching free radicals. Lutein and zeaxanthin are dietary xanthophyll carotenoids, which are delivered to the retina via plasma lipoproteins. The biological mechanisms governing retinal capture and accumulation of lutein and zeaxanthin, to the exclusion of other carotenoids, are still poorly understood. Although these mechanisms remain unclear, it is possible that selective capture of these carotenoids is related to lipoprotein, or apolipoprotein, function and profile. Xanthophyll-binding proteins appear to play an important role in the retinal capture of the xanthophyll carotenoids. The Pi isoform of GSTP1 has been isolated as a specific binding protein for zeaxanthin. The binding protein responsible for retinal uptake of lutein remains elusive. This article reviews the literature germane to the mechanisms involved in the capture, accumulation and stabilization of lutein and zeaxanthin by the retina, and the processes involved in their transport in serum. (Surv Ophthalmol 53:68--81, 2008 The central retina, known as the macula, is responsible for central and color vision because of its high concentration of cone photoreceptors. The macula is characterized by a yellow color, attributable to the presence of macular pigment. 81 Macular pigment (MP) is composed of lutein and zeaxanthin, two hydroxycarotenoids, which are entirely of dietary origin. 17 The concentration of MP peaks at the center of the macula, known as the fovea, where zeaxanthin is the dominant carotenoid. In contrast, lutein dominates in the parafoveal region. 16,82 Dietary sources 68

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A role for apolipoprotein E, apolipoprotein A-I, and low density lipoprotein receptors in cholesterol transport during regeneration and remyelination of the rat sciatic nerve.

Cited by 500 publications

References 47 publications

Inflammation and spinal cord injury: Infiltrating leukocytes as determinants of injury and repair processes

Inflammation and spinal cord injury: Infiltrating leukocytes as determinants of injury and repair processes

Novel Large Apolipoprotein E‐Containing Lipoproteins of Density 1.006–1.060 g/ml in Human Cerebrospinal Fluid

Transport and Retinal Capture of Lutein and Zeaxanthin with Reference to Age-related Macular Degeneration

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