Thyroid hormone triggers the developmental loss of axonal regenerative capacity via TR α 1 and KLF 9 in Purkinje cells

نویسندگان

  • Hasan X. Avci
  • Clement Lebrun
  • Rosine Wehrlé
  • Mohamed Doulazmi
  • Fabrice Chatonnet
  • Marie-Pierre Morel
  • Masatsugu Ema
  • Guilan Vodjdani
  • Constantino Sotelo
  • Frédéric Flamant
  • Isabelle Dusart
چکیده

UPMC Univ Paris 06, UMR 7102, NPA, Bat B, 6eme, Case 12, 9 Quai Saint Bernard, 75005 Paris, France, CNRS, UMR 7102, NPA, Bat B, 6eme, Case 12, 9 Quai Saint Bernard, 75005 Paris, France Université de Lyon, CNRS, INRA, École Normale, Supérieure de Lyon, Institut de Génomique Fonctionnelle de Lyon, 46 allée d’Italie 69007 Lyon, France Graduate School of Comprehensive Human Sciences, University of Tsukuba, Ibaraki, Japan CRICM, UPMC Univ Paris 06/ UMR7225-CNRS / UMRS975-INSERM, Bât CERVI, 83 bd de l’Hôpital, 75013, Paris, France Cátedra de Neurobiología del Desarrollo "Remedios Caro Almela," Instituto de Neurociencias, Universidad Miguel Hernández–CSIC, 03550 San Juan de Alicante, Spain.

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The developmental loss of the ability of Purkinje cells to regenerate their axons occurs in the absence of myelin: an in vitro model to prevent myelination.

Axonal regeneration in the mammalian CNS is a property of immature neurons that is lost during development. Using organotypic culture of cerebellum, we have shown that in vitro Purkinje cells lose their regenerative capacity in parallel with the process of myelination. We have investigated whether myelination is involved in the age-dependent loss of regeneration of these neurons. By applying a ...

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Disruption of Thyroid Hormone Receptor–Mediated Transcription and Thyroid Hormone–Induced Purkinje Cell Dendrite Arborization by Polybrominated Diphenyl Ethers

BACKGROUND Polybrominated diphenyl ethers (PBDEs) have been used as flame retardants and are becoming a ubiquitous environmental contaminant. Adverse effects in the developing brain are of great health concern. OBJECTIVE We investigated the effect of PBDEs/hydroxylated PBDEs (OH-PBDEs) on thyroid hormone (TH) receptor (TR)-mediated transcription and on TH-induced dendrite arborization of cere...

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Thyroid hormone induces cerebellar Purkinje cell dendritic development via the thyroid hormone receptor alpha1.

The thyroid hormone l-3,3',5-triiodothyronine (T3) plays an important role during cerebellar development. Perinatal T3 deficiency leads to severe cellular perturbations, among them a striking reduction in the growth and branching of Purkinje cell dendritic arborization. The molecular mechanisms underlying these effects are poorly understood. Despite the well documented broad expression of thyro...

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Liganded Thyroid Hormone Receptor Inhibits Phorbol 12-O-Tetradecanoate-13-Acetate-Induced Enhancer Activity via Firefly Luciferase cDNA

Thyroid hormone receptor (TR) belongs to the nuclear hormone receptor (NHR) superfamily and regulates the transcription of its target genes in a thyroid hormone (T3)-dependent manner. While the detail of transcriptional activation by T3 (positive regulation) has been clarified, the mechanism of T3-dependent repression (negative regulation) remains to be determined. In addition to naturally occu...

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Deletion of the thyroid hormone receptor alpha 1 prevents the structural alterations of the cerebellum induced by hypothyroidism.

Thyroid hormone (T3) controls critical aspects of cerebellar development, such as migration of postmitotic granule cells and terminal differentiation of Purkinje cells. T3 acts through nuclear receptors (TR) of two types, TRalpha1 and TRbeta, that either repress or activate gene expression. We have analyzed the cerebellar structure of developing mice lacking the TRalpha1 isoform, which normally...

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تاریخ انتشار 2012