Oligodendrocyte maturation and progenitor cell proliferation are independently regulated by thyroid hormone

Baas, Dominique; Bourbeau, Denis; Sarliève, Louis L.; Ittel, Marie‐Elisabeth; Dussault, Jean H.; Puymirat, Jack

doi:10.1002/(sici)1098-1136(199704)19:4<324::aid-glia5>3.0.co;2-x

Cited by 158 publications

(111 citation statements)

References 60 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Thyroid hormones regulate brain development as attested by severe morphological, functional and cognitive impairments monitored in congenitally hypothyroid infants (Oppenheimer and Schwartz 1997). Particularly, they ensure normal oligodendrocyte maturation and myelination (McIntosh et al, 1981;Baas et al, 1997;Rodríguez-Peña 1999;Bury et al, 2002). There are two circulating thyroid hormones: thyroxin (T 4 ) and T 3 , and their action is transduced by thyroid hormone receptors (TRs), expressed in different cell types, including precursors and mature oligodendrocytes.…”

Section: Remyelination Induced By T 3 -Based Therapymentioning

confidence: 99%

“…Particularly, molecules implicated in oligodendrocyte differentiation and maturation may act in the generation of positive signals for recovery. Thyroid hormones (THs) are necessary for normal axonal myelination acting at multiple steps during oligodendrocytes development and myelination, via nuclear hormone receptors (Baas et al, 1997;Rodríguez-Peña, 1999;Jones et al, 2003;Sarliève et al, 2004;Schoonover et al, 2004;Kang et al, 2007), but no information are available about the role of TH in the induction of oligodendrocyte lineage in chronic demyelination. We therefore, explored the possibility of stimulating endogenous repair by triiodothyronine (T 3 ) administration in long-term cuprizone-treated mice.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Recovery from Chronic Demyelination by Thyroid Hormone Therapy: Myelinogenesis Induction and Assessment by Diffusion Tensor Magnetic Resonance Imaging

Harsan¹,

Steibel²,

Zaremba³

et al. 2008

J. Neurosci.

144

122

View full text Add to dashboard Cite

The failure of the remyelination processes in multiple sclerosis contributes to the formation of chronic demyelinated plaques that lead to severe neurological deficits. Long-term cuprizone treatment of C57BL/6 mice resulted in pronounced white matter pathology characterized by oligodendrocyte depletion, irreversible demyelination and persistent functional deficits after cuprizone withdrawal. The use of a combination of in vivo diffusion tensor magnetic resonance imaging (DT-MRI) and histological analyses allowed for an accurate longitudinal assessment of demyelination. Injection of triiodothyronine (T 3 ) hormone over a 3 week interval after cuprizone withdrawal progressively restored the normal DT-MRI phenotype accompanied by an improvement of clinical signs and remyelination. The effects of T 3 were not restricted to the later stages of remyelination but increased the expression of sonic hedgehog and the numbers of Olig2 ϩ and PSA-NCAM ϩ precursors and proliferative cells. Our findings establish a role for T 3 as an inducer of oligodendrocyte progenitor cells in adult mouse brain following chronic demyelination.

show abstract

Section: Remyelination Induced By T 3 -Based Therapymentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Recovery from Chronic Demyelination by Thyroid Hormone Therapy: Myelinogenesis Induction and Assessment by Diffusion Tensor Magnetic Resonance Imaging

Harsan¹,

Steibel²,

Zaremba³

et al. 2008

J. Neurosci.

144

122

View full text Add to dashboard Cite

show abstract

“…Similar to other neural cells (Walter, 1996;Baas et al, 1997;Lima et al, 1997), purified ameboid microglial cells respond to T3 exposure by increased extension of cell processes, an important step in their acquisition of a ramified phenotype. As for the effect on cell survival, it may be hypothesized that increased or decreased levels of T3 reaching microglial cells contribute to augment or reduce microglial process formation in hyperthyroid and hypothyroid rats, respectively.…”

Section: Pathways For Thyroid Hormone Influences On Microglia: Assessmentioning

confidence: 99%

Regulation of Microglial Development: A Novel Role for Thyroid Hormone

et al. 2001

View full text Add to dashboard Cite

The postnatal development of rat microglia is marked by an important increase in the number of microglial cells and the growth of their ramified processes. We studied the role of thyroid hormone in microglial development. The distribution and morphology of microglial cells stained with isolectin B4 or monoclonal antibody ED1 were analyzed in cortical and subcortical forebrain regions of developing rats rendered hypothyroid by prenatal and postnatal treatment with methyl-thiouracil. Microglial processes were markedly less abundant in hypothyroid pups than in age-matched normal animals, from postnatal day 4 up to the end of the third postnatal week of life. A delay in process extension and a decrease in the density of microglial cell bodies, as shown by cell counts in the developing cingulate cortex of normal and hypothyroid animals, were responsible for these differences. Conversely, neonatal rat hyperthyroidism, induced by daily injections of 3,5,3Ј-triiodothyronine (T3), accelerated the extension of microglial processes and increased the density of cortical microglial cell bodies above physiological levels during the first postnatal week of life.Reverse transcription-PCR and immunological analyses indicated that cultured cortical ameboid microglial cells expressed the ␣1 and ␤1 isoforms of nuclear thyroid hormone receptors. Consistent with the trophic and morphogenetic effects of thyroid hormone observed in situ, T3 favored the survival of cultured purified microglial cells and the growth of their processes. These results demonstrate that thyroid hormone promotes the growth and morphological differentiation of microglia during development.

show abstract

“…Unlike their viral homologue, the c-erbA gene products do not exert proliferative e ects but are implicated in the induction of various di erentiation processes such as those of muscle cells (Carnac et al, 1993), oligodendrocytes (Baas et al, 1997) and haematopoietic cells (Gandrillon et al, 1994). Each of the TRa genes produce several mRNAs.…”

Section: Introductionmentioning

confidence: 99%

Activation of the thyroid hormone receptor α gene promoter by the orphan nuclear receptor ERRα

et al. 1998

View full text Add to dashboard Cite

The superfamily of nuclear receptors comprises transcription factors that depend on a ligand for their activity. In addition, the superfamily includes a number of orphan receptors, for which no ligand is known. We report here that the orphan receptor estrogen receptor related alpha receptor (ERRa) stimulates the expression of the thyroid hormone receptor alpha (TRa) gene promoter. We characterized a responsive site that is both necessary and su cient for ERRa-induced transactivation. In addition, we show that both TRa and ERRa are coexpressed in embryonic intestine, brown fat and heart as well as in the adult gonads. In the testis, expression of both receptors can be found in the seminiferous tubes where it is totally restricted to spermatocytes I. Altogether this suggests that TRa is an in vivo target of ERRa.

show abstract

Oligodendrocyte maturation and progenitor cell proliferation are independently regulated by thyroid hormone

Cited by 158 publications

References 60 publications

Recovery from Chronic Demyelination by Thyroid Hormone Therapy: Myelinogenesis Induction and Assessment by Diffusion Tensor Magnetic Resonance Imaging

Recovery from Chronic Demyelination by Thyroid Hormone Therapy: Myelinogenesis Induction and Assessment by Diffusion Tensor Magnetic Resonance Imaging

Regulation of Microglial Development: A Novel Role for Thyroid Hormone

Activation of the thyroid hormone receptor α gene promoter by the orphan nuclear receptor ERRα

Contact Info

Product

Resources

About