Circulating transforming growth factor-β1 facilitates remyelination in
                        the adult central nervous system

Hamaguchi, Maki; Muramatsu, Rieko; Fujimura, Harutoshi; Mochizuki, Hideki; Kataoka, Hirotoshi; Yamashita, Toshio

doi:10.7554/elife.41869

Cited by 55 publications

(52 citation statements)

References 41 publications

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“…In our experiment, an increase in the level of TGF-β in the examined rat brain structures could have a neuroprotective effect and serve as a mechanism to offset the chronic toxic action of neuroinflammation in brain cells. TGF-β is a highly anti-inflammatory cytokine [89][90][91] and protects brain cells against factors and diseases such as ischemia [92], β-amyloid (Aβ) [93,94], hypoxia [95], LPS-induced neuroinflammation [96] and multiple sclerosis [97][98][99]. TGF-β also supports nerve regeneration [100].…”

Section: Tgf-βmentioning

confidence: 99%

Pre- and Neonatal Exposure to Lead (Pb) Induces Neuroinflammation in the Forebrain Cortex, Hippocampus and Cerebellum of Rat Pups

Chibowska

Korbecki

Gutowska

et al. 2020

IJMS

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Lead (Pb) is a heavy metal with a proven neurotoxic effect. Exposure is particularly dangerous to the developing brain in the pre-and neonatal periods. One postulated mechanism of its neurotoxicity is induction of inflammation. This study analyzed the effect of exposure of rat pups to Pb during periods of brain development on the concentrations of selected cytokines and prostanoids in the forebrain cortex, hippocampus and cerebellum. Methods: Administration of 0.1% lead acetate (PbAc) in drinking water ad libitum, from the first day of gestation to postnatal day 21, resulted in blood Pb in rat pups reaching levels below the threshold considered safe for humans by the Centers for Disease Control and Prevention (10 µg/dL). Enzyme-linked immunosorbent assay (ELISA) method was used to determine the levels of interleukins IL-1β, IL-6, transforming growth factor-β (TGF-β), prostaglandin E2 (PGE2) and thromboxane B2 (TXB2). Western blot and quantitative real-time PCR were used to determine the expression levels of cyclooxygenases COX-1 and COX-2. Finally, Western blot was used to determine the level of nuclear factor kappa B (NF-κB). Results: In all studied brain structures (forebrain cortex, hippocampus and cerebellum), the administration of Pb caused a significant increase in all studied cytokines and prostanoids (IL-1β, IL-6, TGF-β, PGE2 and TXB2). The protein and mRNA expression of COX-1 and COX-2 increased in all studied brain structures, as did NF-κB expression. Conclusions: Chronic pre-and neonatal exposure to Pb induces neuroinflammation in the forebrain cortex, hippocampus and cerebellum of rat pups.

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Section: Tgf-βmentioning

confidence: 99%

Pre- and Neonatal Exposure to Lead (Pb) Induces Neuroinflammation in the Forebrain Cortex, Hippocampus and Cerebellum of Rat Pups

Chibowska

Korbecki

Gutowska

et al. 2020

IJMS

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“…This overexpression promotes OD differentiation and migration toward lesion site (Hinks and Franklin, 1999 ; Diemel et al, 2003 ; Traiffort et al, 2020 ). Furthermore, Hamaguchi et al ( 2019 ) recently proposed that circulating TGF-β1 enters the CNS and could contribute to RM. The study provided evidence that TGF-β1 administration promotes RM by stimulating human OD maturation and restore neurological function in MS (Hamaguchi et al, 2019 ).…”

Section: Role Of Microglia In Rmmentioning

confidence: 99%

Beneficial Roles of Microglia and Growth Factors in MS, a Brief Review

Pons

Rivest

2020

Front. Cell. Neurosci.

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Microglia are the brain resident immune cells; they can produce a large variety of growth factors (GFs) to prevent neuronal damages and promote recovery. In neurodegenerative diseases, microglia can play both benefic and deleterious roles, depending on different factors and disease context. In multiple sclerosis, microglia are involved in both demyelination (DM) and remyelination (RM) processes. Recent studies suggest a beneficial role of microglia in regenerative processes. These include the regenerative development of myelin after DM. This review gives an overlook of how microglia and GFs can influence the RM properties.

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“…An additional level of regulatory factors, mainly provided by microglia and astrocytes, is required to limit inflammation and demyelination and to clear myelin debris. More recent studies also point to a direct role of the systemic environment in efficient remyelination, i.e., both circulating TGFβ and regulatory T cells promote OPC differentiation [180,181]. This distinct regulation of developmental myelination and remyelination is reflected in the formation of shorter and thinner myelin sheaths on remyelinated axons compared to axons that are myelinated upon development.…”

Section: Regulation Of Remyelination: a Major Role Of Microglia And Amentioning

confidence: 99%

The emerging role of galectins in (re)myelination and its potential for developing new approaches to treat multiple sclerosis

Jong

Gabius

Baron

2019

Cell. Mol. Life Sci.

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Multiple sclerosis (MS) is an inflammatory, demyelinating and neurodegenerative disease of the central nervous system with unknown etiology. Currently approved disease-modifying treatment modalities are immunomodulatory or immunosuppressive. While the applied drugs reduce the frequency and severity of the attacks, their efficacy to regenerate myelin membranes and to halt disease progression is limited. To achieve such therapeutic aims, understanding biological mechanisms of remyelination and identifying factors that interfere with remyelination in MS can give respective directions. Such a perspective is given by the emerging functional profile of galectins. They form a family of tissue lectins, which are potent effectors in processes as diverse as adhesion, apoptosis, immune mediator release or migration. This review focuses on endogenous and exogenous roles of galectins in glial cells such as oligodendrocytes, astrocytes and microglia in the context of de-and (re)myelination and its dysregulation in MS. Evidence is arising for a cooperation among family members so that timed expression and/or secretion of galectins-1, -3 and -4 result in modifying developmental myelination, (neuro)inflammatory processes, de-and remyelination. Dissecting the mechanisms that underlie the distinct activities of galectins and identifying galectins as target or tool to modulate remyelination have the potential to contribute to the development of novel therapeutic strategies for MS.Publisher's Note Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

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Circulating transforming growth factor-β1 facilitates remyelination in the adult central nervous system

Cited by 55 publications

References 41 publications

Pre- and Neonatal Exposure to Lead (Pb) Induces Neuroinflammation in the Forebrain Cortex, Hippocampus and Cerebellum of Rat Pups

Pre- and Neonatal Exposure to Lead (Pb) Induces Neuroinflammation in the Forebrain Cortex, Hippocampus and Cerebellum of Rat Pups

Beneficial Roles of Microglia and Growth Factors in MS, a Brief Review

The emerging role of galectins in (re)myelination and its potential for developing new approaches to treat multiple sclerosis

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