Normal timing of oligodendrocyte development depends on thyroid hormone receptor alpha 1 (TRalpha1)

Billon, Noëlle

doi:10.1093/emboj/cdf662

Cited by 137 publications

(118 citation statements)

References 87 publications

(131 reference statements)

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“…OPCs and oligodendrocytes are the most obvious cellular targets to explain the effect of TH on remyelination in EAE, because oligodendrocyte development is under TH control (23). TH action at the cellular level is mediated by ligand-regulated transcription factors that belong to the family of nuclear receptors.…”

Section: Discussionmentioning

confidence: 99%

“…Thus, we may speculate that the disease itself, probably through cytokines and growth factors (32,44,45), released either from widespread inflammatory and glial cells (46) or from damaged axons after demyelination (47), induces adult OPCs to reenter the cell cycle after demyelination. This proliferative activity is believed to set the intrinsic timer in OPCs to become sensitive to TH, possibly through the expression of suitable amounts of nuclear receptors (23,48,49). A pulsed stimulus by TH at this time favors oligodendrocyte maturation.…”

Section: Discussionmentioning

confidence: 99%

“…To obtain further indications concerning the possible cellular substrate for T4 action in remyelination in EAE and particularly in restoring MBP content (see Discussion), we also tested T4-administration schedules different from the reference schema used in this study (acute phase of EAE), i.e., in the relapse phase (21,23, and 25 dpi in DA rats). We found that MBP content in the optic nerve increased when T4 was administered during the acute phase of EAE, but not during relapse (Fig.…”

Section: Th Increases Mbp Expression In Eaementioning

confidence: 99%

“…Cell-cycle stopping mechanism, terminal differentiation, and myelin production require TH (19). Studies in genetically modified animals (20,21), such as the analysis of myelination in hypo-and hyperthyroid animals (22), have provided abundant evidence that TH plays an important part in regulating oligodendrocyte lineage and maturation also in vivo and that the TH receptor ␣1 seems to be responsible for this process (23).…”

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Thyroid hormone administration enhances remyelination in chronic demyelinating inflammatory disease

Fernández

Giuliani

Pirondi

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

124

101

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Chronic disabilities in multiple sclerosis are believed to be due to neuron damage and degeneration, which follow remyelination failure. Due to the presence of numerous oligodendrocyte precursors inside demyelination plaques, one reason for demyelination failure could be the inability of oligodendrocyte precursor cells to turn into myelinating oligodendrocytes. In this study, we show that thyroid hormone enhances and accelerates remyelination in an experimental model of chronic demyelination, i.e., experimental allergic encephalomyelitis in congenic female Dark Agouti rats immunized with complete guinea pig spinal cord. Thyroid hormone, when administered during the acute phase of the disease, increases expression of platelet-derived growth factor ␣ receptor, restores normal levels of myelin basic protein mRNA and protein, and allows an early and morphologically competent reassembly of myelin sheaths. Moreover, thyroid hormone exerts a neuroprotective effect with respect to axonal pathology.neuroprotection ͉ multiple sclerosis ͉ oligodendrocyte precursor cells ͉ axonal pathology ͉ rat M ultiple sclerosis (MS) is a disorder of the central nervous system (CNS) that manifests as acute focal inflammatory demyelination with limited remyelination, usually culminating in chronic multifocal sclerotic plaques (1). Early axonal injury and loss followed by neuron distress (2) and death (3) occur in MS (4-6), accounting for brain and spinal cord atrophy. Irreversible axonal damage is an essential cause of nonremitting sensory, motor, and cognitive disabilities in MS (7). Although remyelination occurs in most experimental models of demyelination, this beneficial process is undoubtedly inadequate in MS. The reasons for this inadequacy are unknown, also because the oligodendrocyte precursor cells (OPCs), the cell population that is considered to be the most important source of remyelinating oligodendrocytes in the adult CNS (8-10), are present in early (fresh) demyelinating lesions in MS (11, 12).There are many possible speculative explanations for remyelination failure in MS (9, 10), including quantitatively inadequate recruitment and͞or differentiation of OPCs (13); axons not receptive to remyelination (14); and inappropriate support of growth factors by astrocytes and͞or other inflammatory cells (15), such as the extracellular microenvironment with regard to matrix proteins and adhesion molecules (16).Because the number of oligodendrocytes is greater than before demyelination in early MS, meaning that new oligodendrocytes are generated (17), another possibility is that OPCs are unable to turn into myelinating oligodendrocytes in chronic MS. Thus, extensive studies are under way to identify factors involved in OPC differentiation during remyelination. It is generally accepted that the process of remyelination represents a recapitulation of myelination during development, and so the key factors affecting the developmental maturation of OPCs into myelinating oligodendrocytes also should favor remyelination in the adult CNS. It ...

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Th Increases Mbp Expression In Eaementioning

confidence: 99%

mentioning

confidence: 99%

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Thyroid hormone administration enhances remyelination in chronic demyelinating inflammatory disease

Fernández

Giuliani

Pirondi

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

124

101

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“…All types of glial cells are sensitive to T3 in vitro (Durand and Raff, 2000;Lima et al, 2001;Adachi et al, 2002). However, the only glial defect reported for TR 1 -/-knockout mice was a slight delay in the post-natal differentiation of the oligodendrocyte precursor cells (OPC) for the optic nerve (Billon et al, 2002) and some long term persistence of OPC proliferation in the complete absence of TRs (TR 0/0 β -/-mice) (Baas et al, 2002). In the latter, myelin compaction was incomplete and, as a likely consequence, retinal ganglion cells degenerated in M a n u s c r i p t 7 some older animals.…”

Section: Data From Engineered Micementioning

confidence: 99%

Thyroid hormones and the control of cell proliferation or cell differentiation: Paradox or duality?

Kress

Samarut

Plateroti

2009

Molecular and Cellular Endocrinology

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Thyroid hormones and the control of cell proliferation or cell differentiation: paradox or duality?. Molecular and Cellular Endocrinology, Elsevier, 2009, 313 (1-2) This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. SummaryAmphibian metamorphosis perfectly illustrates a key paradox: thyroid hormones control diverse cellular processes depending on the tissue context. This point is also reinforced by a recent accumulation of evidence. For example, thyroid hormones and their nuclear receptor TRs have been described to function in different systems in synergy and/or in antagonism with other signaling pathways. This interaction helps explain their pleiotropic roles. This review summarizes the most important advances in this field, focusing in particular on the key action of thyroid hormones in controlling the balance between the processes of cell proliferation and cell differentiation in a few organs, with special attention paid to the intestine. We highlight similarities between the cellular and molecular events occurring during postnatal intestinal maturation at metamorphosis in amphibians, and comparable events observed at weaning in mice. 1-Introduction1.1 Thyroid hormone production Thyroid hormones (THs), L-thyroxine or T4 and 3,5,3'-L-triiodothyronine or T3, are essential for the development of several organs, including the central nervous system, skeleton, heart, intestine, skeletal muscle and sensory organs. Moreover, they also have important regulatory effects on oxygen consumption and metabolic rate (Oppenheimer et al., 1987). The follicular cells of the thyroid gland synthesize and secrete both hormones, but T4 is the most abundant. This process is under the control of circulating THs levels through the hypothalamuspituitary-thyroid feedback regulatory loop (rev. in Fredric and Wondisford, 2004). The intracellular concentration of T3 is dependent upon the uptake of T3 and T4, and their subsequent metabolism (Bianco and Kim, 2006). In fact, both hormones are actively transported across the cell membrane by specific transporter proteins, of which monocarboxylate transporter-8 is the best characterized (Dumitrescu et al., 2004;Friesema et al., 2004; rev. in Refetoff andDumitrescu, 2007 andVisser et al., 2007). Three iodothyronine deiodinase selenoenzymes (D1, D2 and D3) regulate TH activation and catabolism (Bianco and Kim, 2006). D1 and D2 catalyze the 5'-deiodination of T4 to its active metabolite T3. T3 is generated from the activity of D1, which is the main source of circulating T3. In contrast, D2 is the isoenzyme primarily responsible for local production of T3 in target cells. T3 derived from ...

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A Novel Approach to Increase Glial Cell Populations in Brain Microphysiological Systems

Morales Pantoja,

Ding,

Leite

et al. 2023

Advanced Biology

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Brain microphysiological systems (bMPS) recapitulate human brain cellular architecture and functionality more closely than traditional monolayer cultures and have become increasingly relevant for the study of neurological function in health and disease. Existing 3D brain models vary in reflecting the relative populations of different cell types present in the human brain. Most models consist mainly of neurons, while glial cells represent a smaller portion of the cell populations. Here, by means of a chemically defined glial‐enriched medium (GEM), an improved method to expand the population of astrocytes and oligodendrocytes without compromising neuronal differentiation in bMPS, is presented. An important finding is that astrocytes also change in morphology when cultured in GEM, more closely recapitulating primary culture astrocytes. GEM bMPS are electro‐chemically active and show different patterns of calcium staining and flux. Synaptic vesicles and terminals observed by electron microscopy are also present. No significant changes in neuronal differentiation are observed by gene expression, however, GEM enhanced neurite outgrowth and cell migration, and differentially modulated neuronal maturation in two different cell lines. These results have the potential to significantly improve functionality of bMPS for the study of neurological diseases and drug discovery, contributing to the unmet need for safe human models.

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Normal timing of oligodendrocyte development depends on thyroid hormone receptor alpha 1 (TRalpha1)

Cited by 137 publications

References 87 publications

Thyroid hormone administration enhances remyelination in chronic demyelinating inflammatory disease

Thyroid hormone administration enhances remyelination in chronic demyelinating inflammatory disease

Thyroid hormones and the control of cell proliferation or cell differentiation: Paradox or duality?

A Novel Approach to Increase Glial Cell Populations in Brain Microphysiological Systems

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