Oxidative stress disrupts oligodendrocyte maturation

French, Heather Morein; Reid, Mary; Mamontov, Polina; Simmons, Rebecca A.; Grinspan, Judith B.

doi:10.1002/jnr.22139

Cited by 194 publications

(172 citation statements)

References 73 publications

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“…(***p<0.001, CTX, CNTRL vs. EAE, non-parametric onetailed t test, t=12.64) can be mediated by different mechanisms. Either the precursor cells after leaving the niche die under severe oxidative conditions and affect the cell number [unpublished observations] or fail to mature into the glial lineage (French et al 2009). Chondroitin sulphate proteoglycans in general and CSPG3 has been demonstrated to inhibit neurite outgrowth (Garwood et al 1999) in vitro.…”

Section: Discussionmentioning

confidence: 97%

Upregulation of CSPG3 Accompanies Neuronal Progenitor Proliferation and Migration in EAE

et al. 2010

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The molecular identities of signals that regulate the CNS lesion remodeling remain unclear. Herein, we report for the first time that extracellular matrix chondroitin sulphate proteoglycan, CSPG3 (neurocan) is upregulated after primary inflammatory injury. EAE was induced using myelin oligodendrocyte glycoprotein (MOG) (35-55) which was characterized by massive polymorphonuclear cell infiltration and loss of myelin basic protein expression along with steep decrease of CNPase. Periventricular white matter (PVWM) and cortex presented with astrogliosis evidenced by increased Glial fibrillary acidic protein (GFAP) immunoreactivity 20 days post immunization (p.i). Neuronal progenitor cell (NPC) proliferation increased after first acute episode in the subventricular zone (SVZ), corpus callosum, and cortex, indicating migration of cells to structures other than rostral migration stream and olfactory bulb, which is indicative of cell recruitment for repair process and was confirmed by presence of thin myelin sheaths in the shadow plaques. Earlier CSPG3 has been demonstrated to impede regeneration. We observed neuroinflammation-induced up-regulation of the CSPG3 expression in two most affected regions viz. PVWM and cortex after proliferation and migration of NPCs. Our results show possible role of reactive astrogliosis in lesion remodeling and redefine the relation between inflammation and endogenous cellular repair which can aid in designing of newer therapeutic strategies.

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Section: Discussionmentioning

confidence: 97%

Upregulation of CSPG3 Accompanies Neuronal Progenitor Proliferation and Migration in EAE

et al. 2010

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“…Specifically, ROS may not only induce tissue injury and cellular death, but may also interfere with normal cellular functioning in the central nervous system. For instance, oxidative molecules, notably hydrogen peroxide, may disrupt oligodendrocyte maturation which may have consequences for endogenous repair mechanisms in MS (French et al, 2009). The enzymes responsible for the generation of ROS have been detected in tissue derived from patients with MS and experimental models of CNS inflammation.…”

Section: Discussionmentioning

confidence: 99%

“…Experimentally, ROS and their reactive products cause cellular injury to neurons (and their axons) and oligodendrocytes (Abarikwu et al, 2012;French et al, 2009;Li et al, 2005;Wilkins and Compston, 2005).In both pathological studies and animal models of CNS inflammation, ROS play a key role in promoting tissue damage (Cross et al, 1998;Haider et al, 2011;Smith et al, 1999;van Horssen et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

Oxidative injury in multiple sclerosis cerebellar grey matter

et al. 2016

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General rightsThis document is made available in accordance with publisher policies. Please cite only the published version using the reference above. AbstractCerebellar dysfunction is a significant contributor to disability in multiple sclerosis (MS). Both white matter (WM) and grey matter (GM) injury occurs within MS cerebellum and, within GM, demyelination, inflammatory cell infiltration and neuronal injury contribute to on-going pathology. The precise nature of cerebellar GM injury is, however, unknown. Oxidative stress pathways with ultimate lipid peroxidation and cell membrane injury occur extensively in MS and the purpose of this study was to investigate these processes in MS cerebellar GM. Post-mortem human cerebellar GM from MS and control subjects was analysed immunohistochemically, followed by semi-quantitative analysis of markers of cellular injury, lipid peroxidation and antioxidant enzyme expression. We have shown evidence for reduction in myelin and neuronal markers in MS GM, coupled to an increase in expression of a microglial marker. We also show that the lipid peroxidation product 4-hydroxynonenal co-localises with myelin and its levels negatively correlate to myelin basic protein levels. Furthermore, superoxide dismutase (SOD1 and 2) enzymes, localised within cerebellar neurons, are up-regulated, yet the activation of subsequent enzymes responsible for the detoxification of hydrogen peroxide, catalase and glutathione peroxidase are relatively deficient. These studies provide evidence for oxidative injury in MS cerebellar GM and further help define disease mechanisms within the MS brain.

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“…A explicação pode ser a produção excessiva de radicais livres após o nascimento, a qual é intensificada com a oxigenoterapia. Segundo French et al, 25 o estresse oxidativo pode contribuir para a hipomielinização difusa encontrada na lesão da matriz branca periventricular, a qual está associada à lesão neurológica crônica em recém-nascidos prematuros e, consequentemente, o atraso do desenvolvimento motor.…”

Section: Discussionunclassified