The coregulator Alien

Papaioannou, Maria; Melle, Christian; Baniahmad, Aria

doi:10.1621/nrs.05008

Cited by 12 publications

(8 citation statements)

References 76 publications

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“…Early in development, TH functions as an instructive agent, triggering OPCs (O-2A cell) cell cycle exit in close cooperation with platelet-derived growth factor (PDGF; Durand et al 1997, Durand & Raff 2000, Lu et al 2008. According to the hypothesis developed by Raff's group for OL generation and maturation (Durand & Raff 2000, Raff 2006) and further confirmed by other groups for different cell types (Papaioannou et al 2007, Tsui et al 2008, T 3 is a major component of the molecular machinery that regulates OPC proliferation and differentiation through a mitogen-dependent intrinsic cell timer. When OPCs proliferate, they become sensitive to T 3 after eight cell divisions (or corresponding time), probably because of a cell cycle-dependent expression of TRs (Maruvada et al 2004).…”

Section: Th and Cns Myelinationmentioning

confidence: 83%

Cellular approaches to central nervous system remyelination stimulation: thyroid hormone to promote myelin repair via endogenous stem and precursor cells

Calzà¹,

Fernández²,

Giardino³

2009

Journal of Molecular Endocrinology

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Brain and spinal cord repair is a very difficult task in view of the extremely limited repair capability of the mature central nervous system (CNS). Thus, cellular therapies are regarded as a new frontier for both acute and chronic neurological diseases characterized by neuron or oligodendroglia degeneration. Although cell replacement has been considered as the primary goal of such approaches, in recent years greater attention has been devoted to the possibility that new undifferentiated cells in damaged nervous tissue might also act in autocrine-paracrine fashion, regulating the microenvironment through the release of growth factor and cytokines, also regulating immune response and local inflammation. In this review, repair of demyelinating disease using endogenous cells will be discussed in view of the critical role played by thyroid hormones (THs) during developmental myelination, focusing on the following points: 1) endogenous stem and precursor cells during demyelinating diseases; 2) TH homeostasis in the CNS; 3) cellular and molecular mechanism regulated by TH during developmental myelination and 4) a working hypothesis to develop a rationale for the use of THs to improve remyelination through endogenous stem and precursor cells in the course of demyelinating diseases.

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Section: Th and Cns Myelinationmentioning

confidence: 83%

Cellular approaches to central nervous system remyelination stimulation: thyroid hormone to promote myelin repair via endogenous stem and precursor cells

Calzà¹,

Fernández²,

Giardino³

2009

Journal of Molecular Endocrinology

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“…The Drosophila homolog of Alien, COUP-TF1, is a corepressor reported to bind EcR but not USP. 47,48 Out of the current transcriptional cofactors known to bind EcR and USP, histone methyltransferases TRR, 49 dSet2, 50 dG9a, 51 nucleosome remodeling factor NURF 52 and Taiman, 53 all of them act as co-activators, rather than co-repressors. In any event, assuming co-repressors, in the light of the current data, the search for them should be conducted in the PG.…”

Section: Discussionmentioning

confidence: 99%

Ligand-independent requirements of steroid receptors EcR and USP for cell survival

2015

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The active form of the Drosophila steroid hormone ecdysone, 20-hydroxyecdysone (20E), binds the heterodimer EcR/USP nuclear receptor to regulate target genes that elicit proliferation, cell death and differentiation during insect development. Although the 20E effects are relatively well known, the physiological relevance of its receptors remains poorly understood. We show here that the prothoracic gland (PG), the major steroid-producing organ of insect larvae, requires EcR and USP to survive in a critical period previous to metamorphosis, and that this requirement is 20E-independent. The cell death induced by the downregulation of these receptors involves the activation of the JNK-encoding basket gene and it can be rescued by upregulating EcR isoforms which are unable to respond to 20E. Also, while PG cell death prevents ecdysone production, blocking hormone synthesis or secretion in normal PG does not lead to cell death, demonstrating further the ecdysone-independent nature of the receptor-deprivation cell death. In contrast to PG cells, wing disc or salivary glands cells do not require these receptors for survival, revealing their cell and developmental time specificity. Exploring the potential use of this feature of steroid receptors in cancer, we assayed tumor overgrowth induced by altered yorkie signaling. This overgrowth is suppressed by EcR downregulation in PG, but not in wing disc, cells. The mechanism of all these cell death features is based on the transcriptional regulation of reaper. These novel and context-dependent functional properties for EcR and USP receptors may help to understand the heterogeneous responses to steroid-based therapies in human pathologies. Steroid hormones control multiple biological processes and, consequently, their faulty regulation underlies many pathologies. 1,2 The main Drosophila steroid hormone, ecdysone, is synthesized in the larval prothoracic gland (PG) using dietary sterols and cytochrome P450 enzymes. 3 Following its pulsated secretion into the hemolymph, peripheral tissues convert ecdysone into biologically active 20-hydroxyecdysone (20E) to control larval molting and metamorphosis. 4 The 20E signal is transduced by heterodimers of two nuclear receptors, ecdysone receptor (EcR) and Ultraspiracle (USP). 5 USP exhibits a single form throughout development. By contrast, EcR encodes three protein isoforms (EcRA, EcRB1 and EcRB2). These show common DNA-and hormone-binding domains but different N-termini although all of them can heterodimerize USP. 6,7 Each EcR isoform is hypothesized to have specific functions based on their distinct spatial and temporal patterns and N-termini. [8][9][10] EcR and USP DNA-binding domains recognize ecdysone response sequences which are short palindromes. 11 Like its vertebrate counterparts, 12 the ligand-EcR/USP complex activates transcription, whereas the unliganded receptor act as a repressor. [13][14][15] The in vivo validation of repressor activities for unliganded complexes, however, is mostly indirect. For example, EcR or USP loss...

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“…deficiency negatively impacts on oligodendroglial differentiation and maturation, as oligodendrocytes are cultured in T3-deprived conditions characterized by less extensive processes than controls (Younes-Rapozo et al, 2006). According to the hypothesis developed by Raff's group for oligodendrocyte generation and maturation (Durand and Raff, 2000;Raff, 2006) and further confirmed by other groups for different cell types (Papaioannou et al, 2007;Tsui et al, 2008), TH is a major component of the molecular machinery that regulate OPC proliferation and differentiation through a mitogen-dependent intrinsic cell timer. When OPCs proliferate, they become sensitive to TH, probably because of a cell cycle-dependent expression of TRs (Maruvada et al, 2004).…”

Section: Neurospheres Derived From the Svz Of Adult Non-pathological mentioning

confidence: 93%

Thyroid hormone induces glial lineage of primary neurospheres derived from non‐pathological and pathological rat brain: implications for remyelination‐enhancing therapies

Fernández

Paradisi

Vecchio

et al. 2009

Intl J of Devlp Neuroscience

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Thyroid hormone exerts a critical role in developmental myelination, acting on the production and maturation of oligodendrocyte, and on the expression of genes encoding for myelin protein. Since remyelination is considered a recapitulation of cellular and molecular events occurring during development, we tested the possibility of stimulating the oligodendroglial lineage and maturation in neurospheres derived from the subventricular zone of adult rats using 3,5,3'-L-triiodothyronine (T3). Both non-pathological and pathological brains derived from rats affected by the inflammatory-demyelinating disease experimental allergic encephalomyelitis (EAE) were included in the study. We investigated the effect of in vitro T3 exposure on: (i) the expression of nuclear thyroid hormone receptors; (ii) proliferation rate; (iii) differentiation into neurons, astrocytes and oligodendrocytes, focusing our attention on oligodendrocyte maturation. T3 reduced the proliferation rate of neurospheres when cultured in the presence of mitogens, shifting towards oligodendroglial lineage as indicated by increased expression of olig-1, and also favoring oligodendrocyte maturation, as indicated by the expression of antigens associated with different maturation stages. Neurospheres derived from EAE rats show a strong limitation in oligodendrocyte generation, which is completely restored by T3 treatment. These results indicate that T3 is a key factor in regulating neurosphere biology, when derived either from non-pathological or pathological adult brains, suggesting that T3 might be an important factor in favoring remyelination in demyelinating disorders.

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The coregulator Alien

Cited by 12 publications

References 76 publications

Cellular approaches to central nervous system remyelination stimulation: thyroid hormone to promote myelin repair via endogenous stem and precursor cells

Cellular approaches to central nervous system remyelination stimulation: thyroid hormone to promote myelin repair via endogenous stem and precursor cells

Ligand-independent requirements of steroid receptors EcR and USP for cell survival

Thyroid hormone induces glial lineage of primary neurospheres derived from non‐pathological and pathological rat brain: implications for remyelination‐enhancing therapies

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