Remyelination after cuprizone-induced demyelination in the rat is stimulated by apotransferrin

Adamo, Ana M.; Paez, Pablo M.; Cabrera, Oscar Enrique Escobar; Wolfson, Manuel Luis; Franco, Paula; Pasquini, Juana M.; Soto, Eduardo F.

doi:10.1016/j.expneurol.2005.12.027

Cited by 77 publications

(69 citation statements)

References 32 publications

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“…In the present work and in agreement with Adamo et al (2006), two weeks of cuprizone treatment resulted in very weak immunoreactivity for the mature OLG marker MBP in the CC as compared to the control group indicating damage of oligodendrocytes by the toxic effect of cuprizone.…”

Section: Discussionsupporting

confidence: 91%

“…at the dorsolateral aspect of the lateral ventricle in consistence with the result of Adamo et al (2006) using NG2 as a marker of OPCs and Franco et al (2008) using the neuroepithelial stem cell marker Nestin. The increased and scattered aspects of PDGFR␣ immunopositive cells can indicate proliferation and possible migration of OPCs which was induced by the lesion.…”

Section: Discussionmentioning

confidence: 89%

“…Group II (cuprizone treated) (n = 6): rats were fed standard rodent chow mixed with cuprizone (Sigma Aldrich) 0.6% (w/w) for two weeks (Adamo et al, 2006) then sacrificed at the end of the second week. Group III (+ve control) (n = 18): rats were fed standard rodent chow mixed with cuprizone 0.6% (w/w) for two weeks then returned to a normal diet.…”

Section: Experimental Designmentioning

confidence: 99%

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The effect of triiodothyronine on maturation and differentiation of oligodendrocyte progenitor cells during remyelination following induced demyelination in male albino rat

et al. 2016

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a b s t r a c tDemyelination was induced by two weeks cuprizone treatment. Rats of +ve control and triiodothyronine (T3) then received three subcutaneous injections of either saline or T3 day after day and sacrificed at the end of the third and fifth weeks. Animals in −ve control group received only standard rodent chow. After one week of cuprizone withdrawal the corpus callosum in +ve control and T3 treated rats was still demyelinated as revealed by MBP immunohistochemistry. The assay of PLP gene showed significant increase of T3 treated group compared to both the −ve control and +ve control groups. After three weeks, significant improvement in myelination was detected in T3-treated group compared to +ve control as detected by both MBP immunohistochemistry and electron microscopy. After one week of cuprizone withdrawal, PDGFR␣ positive cells and gene expression showed significant increase in +ve control and T3-treated groups as compared to −ve control with insignificant difference in between the former two groups. After three weeks of cuprizone withdrawal, PDGFR␣ positive cells in T3-treated and +ve control groups decreased to the control levels. These results suggest that T3 was effective in improving remyelination when administered during acute phase and might direct progenitor lineage toward oligodendrocytes.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 89%

Section: Experimental Designmentioning

confidence: 99%

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The effect of triiodothyronine on maturation and differentiation of oligodendrocyte progenitor cells during remyelination following induced demyelination in male albino rat

et al. 2016

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“…NB-3 triggers NICD nuclear translocation, promoting oligodendrogenesis from progenitor cells and OPC maturation via Deltex1 (Cui et al 2004). We found that the treatment of demyelinated rats with a single apotransferrin (aTf) (350 ng) injection at the time of CPZ withdrawal induces a marked increase in myelin deposition as compared to the spontaneous remyelination observed in control animals (Adamo et al 2006). Accordingly, different authors have reported the relevant role of aTf during myelination increasing brain myelin content, including proteins and their mRNAs (Escobar Cabrera et al 1997, regulating MBP gene transcription (Espinosa de los Monteros et al 1989Monteros et al , 1999, synergizing with insulin growth factor-1 (IGF-1), and enhancing myelination in myelin-deficient rats (Espinosa-Jeffrey et al 2002).…”

Section: Underlying Mechanisms In Demyelination/ Remyelination Processesmentioning

confidence: 93%

Nutritional factors and aging in demyelinating diseases

Adamo

2013

Genes Nutr

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Demyelination is a pathological process characterized by the loss of myelin around axons. In the central nervous system, oligodendroglial damage and demyelination are common pathological features characterizing white matter and neurodegenerative disorders. Remyelination is a regenerative process by which myelin sheaths are restored to demyelinated axons, resolving functional deficits. This process is often deficient in demyelinating diseases such as multiple sclerosis (MS), and the reasons for the failure of repair mechanisms remain unclear. The characterization of these mechanisms and the factors involved in the proliferation, recruitment, and differentiation of oligodendroglial progenitor cells is key in designing strategies to improve remyelination in demyelinating disorders. First, a very dynamic combination of different molecules such as growth factors, cytokines, chemokines, and different signaling pathways is tightly regulated during the remyelination process. Second, factors unrelated to this pathology, i.e., age and genetic background, may impact disease progression either positively or negatively, and in particular, age-related remyelination failure has been proven to involve oligodendroglial cells aging and their intrinsic capacities among other factors. Third, nutrients may either help or hinder disease progression. Experimental evidence supports the anti-inflammatory role of omega-6 and omega-3 polyunsaturated fatty acids through the competitive inhibition of arachidonic acid, whose metabolites participate in inflammation, and the reduction in T cell proliferation. In turn, vitamin D intake and synthesis have been associated with lower MS incidence levels, while vitamin D-gene interactions might be involved in the pathogenesis of MS. Finally, dietary polyphenols have been reported to mitigate demyelination by modulating the immune response.

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“…Two other proteins exhibiting decreased expression, transferrin and aspartoacylase, may also reflect a down regulation of myelin synthesis. Transferrin has been localized to oligodendrocytes and Schwann cells and experiments modulating levels of transferrin have supported its ability to enhance myelin synthesis either in normal animals or after demyelinating injury (44,45). Aspartoacylase is recognized to be important for the generation of acetyl groups from N-acetylaspartate for utilization in the synthesis of myelin lipids and a loss of function mutation for aspartoacylase results in Canavan's disease, a central nervous system myelinopathy that is typically fatal by 10 years of age (46)(47)(48).…”

Section: Discussionmentioning

confidence: 99%

Peripheral Nerve Protein Expression and Carbonyl Content in N,N-Diethlydithiocarbamate Myelinopathy

Viquez

Valentine

Friedman

et al. 2007

Chem. Res. Toxicol.

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Human exposure to dithiocarbamates results from their uses as pesticides, in manufacturing and as pharmaceutical agents. Neurotoxicity is an established hazard of dithiocarbamate exposure and has been observed in both humans and experimental animals. Previous studies have shown that the neurotoxicity of certain dithiocarbamates, including N,N-diethyldithiocarbamate (DEDC), disulfiram, and pyrrolidine dithiocarbamate can manifest as a primary myelinopathy of peripheral nerve. Because increased levels of copper in peripheral nerve and elevated levels of lipid peroxidation products accompany DEDC induced lesions it has been suggested that disruption of copper homeostasis and increased oxidative stress may contribute to myelin injury. To further assess the biological impact of DEDC-mediated lipid peroxidation in nerve the changes in protein expression levels resulting from DEDC exposure were determined. In addition, protein carbonyl content in peripheral nerve was also determined as an initial assessment of protein oxidative damage in DEDC neuropathy. Rats were exposed to DEDC by intraabdominal osmotic pumps for 8 weeks and proteins extracted from sciatic nerves of DEDC exposed animals and from non-exposed controls. The comparison of protein expression levels using two dimensional difference gel electrophoresis demonstrated significant changes in 56 spots of which 46 were identified by MALDI-TOF/MS. Among the proteins showing increased expression were three isoforms of glutathione transferase, important for detoxification of reactive αβ,-unsaturated aldehydes generated from lipid peroxidation. The increased expression of one isoform, glutathione transferase pi, was localized to the cytoplasm of Schwann cells using immunohistochemistry. Immunoassay for nerve protein carbonyls demonstrated a significant increase of approximately 2 fold for the proteins isolated from the DEDC exposed rats. These data support the ability of DEDC to promote protein oxidative damage in peripheral nerve and to produce sufficient lipid peroxidation in either myelin or another component of the Schwann cell to elicit a protective cellular response to oxidative stress.

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Remyelination after cuprizone-induced demyelination in the rat is stimulated by apotransferrin

Cited by 77 publications

References 32 publications

The effect of triiodothyronine on maturation and differentiation of oligodendrocyte progenitor cells during remyelination following induced demyelination in male albino rat

The effect of triiodothyronine on maturation and differentiation of oligodendrocyte progenitor cells during remyelination following induced demyelination in male albino rat

Nutritional factors and aging in demyelinating diseases

Peripheral Nerve Protein Expression and Carbonyl Content in N,N-Diethlydithiocarbamate Myelinopathy

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