Involvement of de novo ceramide biosynthesis in lymphotoxin-induced oligodendrocyte death

Plo, Isabelle; Ghandour, Saïd; Feutz, Anne-Catherine; Clanet, M.; Laurent, Guy; Bettaieb, Ali

doi:10.1097/00001756-199908020-00028

Cited by 25 publications

(17 citation statements)

References 4 publications

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“…TNF-a injected directly into the vitreous chamber of the eye induces demyelination of the optic nerve (Jenkins and Ikeda, 1992). In culture, both Lt-a and TNF-a are also cytotoxic to oligodendrocytes (Cammer, 2000;Plo et al, 1999), and TNF-a reduces oligodendrocyte proliferation and inhibits maturation into MBP-expressing oligodendrocytes (Cammer, 2000).…”

Section: Damage By Astrocytesmentioning

confidence: 99%

Astrocytes—Friends or foes in multiple sclerosis?

Williams

Piaton

Lubetzki

2007

Glia

254

216

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In multiple sclerosis (MS), the presence of demyelinating plaques has concentrated researchers' minds on the role of the oligodendrocyte in its pathophysiology. Recently, with the rediscovery of early and widespread loss of axons in the disease, new emphasis has been put on the role of axons and axon-oligodendrocyte interactions in MS. Despite the fact that, in 1904, Müller claimed that MS was a disease of astrocytes, more recently, astrocytes have taken a back seat, except as the cells that form the final glial scar after all hope of demyelination is over. However, perhaps it is time for the return of the astrocyte to popularity in the pathogenesis of MS, with recent reports on the dual role of astrocytes in aiding degeneration and demyelination, by promoting inflammation, damage of oligodendrocytes and axons, and glial scarring, but also in creating a permissive environment for remyelination by their action on oligodendrocyte precursor migration, oligodendrocyte proliferation, and differentiation. We review these findings to try to provide a cogent view of astrocytes in the pathology of MS.

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Section: Damage By Astrocytesmentioning

confidence: 99%

Astrocytes—Friends or foes in multiple sclerosis?

Williams

Piaton

Lubetzki

2007

Glia

254

216

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“…There are substantial data from both animal models and clinical studies that cytokines including TNF-α, IL-1β, IL-2, LTα, LTβ, and IFNγ are up-regulated in cerebrospinal fluid (CSF) and brain tissue of MS patients (Kunz & Ibrahim, 2009, Matei & Matei, 2002). A number of studies have demonstrated that some of these cytokines modulate phospholipid and sphingolipid metabolism (Plo et al , 1999, Singh et al , 1998). …”

Section: Multiple Sclerosis (Ms)mentioning

confidence: 99%

Sphingolipids in Multiple Sclerosis

Jana

Pahan

2010

Neuromol Med

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Multiple sclerosis (MS) is a chronic autoimmune demyelinating disease of the CNS. Oligodendrocytes, the myelin forming cells of the central nervous system (CNS), are target cells in MS. Although the etiology of MS is poorly known, new insights suggest oligodendrocyte apoptosis as one of the critical events followed by glial activation and infiltration of lymphocytes and macrophages. A major breakthrough in delineation of the mechanism of cell death, perivascular cuffing and glial activation came from elucidation of the sphingolipid signal transduction pathway. The sphingolipid signal transduction pathway induces apoptosis, differentiation, proliferation, and growth arrest depending upon cell and receptor types, and downstream targets. Sphingomyelin, a major component of myelin membrane formed by mature oligodendrocytes, is abundant in the CNS and ceramide, its primary catabolic product released by activation of either neutral or acidic sphingomyelinase, serves as a potential lipid second messenger or mediator molecule modulating diverse cellular signaling pathways. Similarly, under certain conditions, sphingosine produced from ceramide by ceramidase is phosphorylated by sphingosine kinases to sphingosine-1 phosphate, another potent second messenger molecule. Both ceramide and sphingosine-1 phosphate regulate life and death of many cell types including brain cells and participate in pathogenic processes of MS. In this review, we have made an honest attempt to compile recent findings made by others and us relating to the role of sphingolipids in the disease process of MS.

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“…For example inhibitors of the de novo pathway or of neutral sphingomyelinase can inhibit apoptosis in response to several chemotherapeutic agents, angiotensin II, and B cell activation (Hannun and Luberto, 2000;Mathias et al, 1998, Kroesen et al, 2001. In some cell types, the formation of Cer in response to extracellular agents (such as retinoic acid, etoposide, angiotensin II, IgM, or daunorubicin) is inhibited by Fumonisin Bl (FBI), an inhibitor of Cer synthase (Bose et al, 1995;Kalen et al, 1992;Plo et al, 1999;Liao et al, 1999;Lehtonen et al, 1999;Xu et al, 1998). This inhibitor also attenuates the apoptotic response of these agents, strongly suggesting an important role for Cer in apoptosis; 3) Ionizing radiation has been shown to cause Cer formation through activation of an acid sphingomyelinase, and animals deficient in this sphingomyelinase become resistant to high doses of irradiation, again demonstrating an important role for Cer in apoptosis (Santana et al, 1996a); and 4) In recent studies (Lavie et al, 1997;Liu et al, 1999), Cabot and co-workers have shown clearly that overexpression of glucosylceramide synthase, which utilizes Cer to generate cerebroside, attenuates the formation of Cer in response to and to several chemotherapeutic agents.…”

Section: Ceramide and Apoptosismentioning

confidence: 99%