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  1. Book: The retinoids

    Dollé, Pascal / Niederreither, Karen

    biology, biochemistry, and disease

    2015  

    Author's details edited by Pascal Dollé and Karen Neiderreither
    MeSH term(s) Retinoids
    Language English
    Dates of publication 2015-2015
    Size xvii, 585 pages, 28 unnumbered pages of plates :, illustrations (some colour) ;, 25 cm
    Edition First edition.
    Document type Book
    Note The second editor's surname is Niederreither, but is misspelt as 'Neiderreither' on the title page.
    ISBN 9781118627983 ; 1118627989
    Database Catalogue of the US National Library of Medicine (NLM)

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  2. Article ; Online: Developmental expression of retinoic acid receptors (RARs).

    Dollé, Pascal

    Nuclear receptor signaling

    2009  Volume 7, Page(s) e006

    Abstract: Here, I review the developmental expression features of genes encoding the retinoic acid receptors (RARs) and the 'retinoid X' or rexinoid receptors (RXRs). The first detailed expression studies were performed in the mouse over two decades ago, following ...

    Abstract Here, I review the developmental expression features of genes encoding the retinoic acid receptors (RARs) and the 'retinoid X' or rexinoid receptors (RXRs). The first detailed expression studies were performed in the mouse over two decades ago, following the cloning of the murine Rar genes. These studies revealed complex expression features at all stages of post-implantation development, one receptor gene (Rara) showing widespread expression, the two others (Rarb and Rarg) with highly regionalized and/or cell type-specific expression in both neural and non-neural tissues. Rxr genes also have either widespread (Rxra, Rxrb), or highly-restricted (Rxrg) expression patterns. Studies performed in zebrafish and Xenopus demonstrated expression of Rar and Rxr genes (both maternal and zygotic), at early pre-gastrulation stages. The eventual characterization of specific enzymes involved in the synthesis of retinoic acid (retinol/retinaldehyde dehydrogenases), or the triggering of its catabolism (CYP26 cytochrome P450s), all of them showing differential expression patterns, led to a clearer understanding of the phenomenons regulated by retinoic acid signaling during development. Functional studies involving targeted gene disruptions in the mouse, and additional approaches such as dominant negative receptor expression in other models, have pinpointed the specific, versus partly redundant, roles of the RARs and RXRs in many developing organ systems. These pleiotropic roles are summarized hereafter in relationship to the receptors' expression patterns.
    MeSH term(s) Animals ; Cell Nucleus ; Gene Expression Regulation, Developmental/physiology ; Humans ; Mice ; Receptors, Retinoic Acid/physiology
    Chemical Substances Receptors, Retinoic Acid
    Language English
    Publishing date 2009-05-12
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2230618-3
    ISSN 1550-7629 ; 1550-7629
    ISSN (online) 1550-7629
    ISSN 1550-7629
    DOI 10.1621/nrs.07006
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: Meningeal retinoic acid contributes to neocortical lamination and radial migration during mouse brain development.

    Haushalter, Carole / Schuhbaur, Brigitte / Dollé, Pascal / Rhinn, Muriel

    Biology open

    2017  Volume 6, Issue 2, Page(s) 148–160

    Abstract: Retinoic acid (RA) is a diffusible molecule involved in early forebrain patterning. Its later production in the meninges by the retinaldehyde dehydrogenase RALDH2 coincides with the time of cortical neuron generation. A function of RA in this process has ...

    Abstract Retinoic acid (RA) is a diffusible molecule involved in early forebrain patterning. Its later production in the meninges by the retinaldehyde dehydrogenase RALDH2 coincides with the time of cortical neuron generation. A function of RA in this process has not been adressed directly as
    Language English
    Publishing date 2017-02-15
    Publishing country England
    Document type Journal Article
    ZDB-ID 2632264-X
    ISSN 2046-6390
    ISSN 2046-6390
    DOI 10.1242/bio.021063
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Retinoic acid receptor beta protects striatopallidal medium spiny neurons from mitochondrial dysfunction and neurodegeneration.

    Ciancia, Marion / Rataj-Baniowska, Monika / Zinter, Nicolas / Baldassarro, Vito Antonio / Fraulob, Valérie / Charles, Anne-Laure / Alvarez, Rosana / Muramatsu, Shin-Ichi / de Lera, Angel R / Geny, Bernard / Dollé, Pascal / Niewiadomska-Cimicka, Anna / Krężel, Wojciech

    Progress in neurobiology

    2022  Volume 212, Page(s) 102246

    Abstract: Retinoic acid is a powerful regulator of brain development, however its postnatal functions only start to be elucidated. We show that retinoic acid receptor beta (RARβ), is involved in neuroprotection of striatopallidal medium spiny neurons (spMSNs), the ...

    Abstract Retinoic acid is a powerful regulator of brain development, however its postnatal functions only start to be elucidated. We show that retinoic acid receptor beta (RARβ), is involved in neuroprotection of striatopallidal medium spiny neurons (spMSNs), the cell type affected in different neuropsychiatric disorders and particularly prone to degenerate in Huntington disease (HD). Accordingly, the number of spMSNs was reduced in the striatum of adult Rarβ
    MeSH term(s) Animals ; Glutamic Acid/metabolism ; Huntington Disease ; Mice ; Mitochondria/metabolism ; Neurons/metabolism ; Receptors, Retinoic Acid
    Chemical Substances Receptors, Retinoic Acid ; retinoic acid receptor beta ; Glutamic Acid (3KX376GY7L)
    Language English
    Publishing date 2022-02-10
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 185535-9
    ISSN 1873-5118 ; 0301-0082
    ISSN (online) 1873-5118
    ISSN 0301-0082
    DOI 10.1016/j.pneurobio.2022.102246
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Meningeal retinoic acid contributes to neocortical lamination and radial migration during mouse brain development

    Carole Haushalter / Brigitte Schuhbaur / Pascal Dollé / Muriel Rhinn

    Biology Open, Vol 6, Iss 2, Pp 148-

    2017  Volume 160

    Abstract: Retinoic acid (RA) is a diffusible molecule involved in early forebrain patterning. Its later production in the meninges by the retinaldehyde dehydrogenase RALDH2 coincides with the time of cortical neuron generation. A function of RA in this process has ...

    Abstract Retinoic acid (RA) is a diffusible molecule involved in early forebrain patterning. Its later production in the meninges by the retinaldehyde dehydrogenase RALDH2 coincides with the time of cortical neuron generation. A function of RA in this process has not been adressed directly as Raldh2−/− mouse mutants are embryonic lethal. Here, we used a conditional genetic strategy to inactivate Raldh2 just prior to onset of its expression in the developing meninges. This inactivation does not affect the formation of the cortical progenitor populations, their rate of division, or timing of differentiation. However, migration of late-born cortical neurons is delayed, with neurons stalling in the intermediate zone and exhibiting an abnormal multipolar morphology. This suggests that RA controls the multipolar-to-bipolar transition that occurs in the intermediate zone and allows neurons to start locomotion in the cortical plate. Our work also shows a role for RA in cortical lamination, as deep layers are expanded and a subset of layer IV neurons are not formed in the Raldh2-ablated mutants. These data demonstrate that meninges are a source of extrinsic signals important for cortical development.
    Keywords Retinoids ; Cerebral cortex ; Neurons ; Radial migration ; Cortical layering ; Science ; Q ; Biology (General) ; QH301-705.5
    Subject code 571
    Language English
    Publishing date 2017-02-01T00:00:00Z
    Publisher The Company of Biologists
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

    Full text online

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  6. Article ; Online: Retinoic acid controls early neurogenesis in the developing mouse cerebral cortex.

    Haushalter, Carole / Asselin, Laure / Fraulob, Valérie / Dollé, Pascal / Rhinn, Muriel

    Developmental biology

    2017  Volume 430, Issue 1, Page(s) 129–141

    Abstract: A tight regulation of neuron production is required to generate a functional cerebral cortex and is achieved by a proper balance between proliferation and differentiation of progenitor cells. Though the vitamin A (retinol) active derivative retinoic acid ...

    Abstract A tight regulation of neuron production is required to generate a functional cerebral cortex and is achieved by a proper balance between proliferation and differentiation of progenitor cells. Though the vitamin A (retinol) active derivative retinoic acid (RA) has been implicated as one of the signals acting during mammalian forebrain neurogenesis, its function at the onset of neurogenesis as well as during establishment of cortical layers and neuronal subtypes remains elusive. One limitation is that murine mutants for genes encoding key enzymes involved in RA synthesis die during early embryonic development. We analysed corticogenesis in Rdh10 null mutants, in which an RA deficiency is generated as the intracellular retinol to retinaldehyde conversion is abolished. When analysed at the latest stage before lethality occurs (embryonic day [E]13.5), the mutants show smaller telencephalic vesicles and the thickness of their cortical plate is strongly reduced. The first progenitors formed in the cortical plate are radial glial (RG) cells which generate neurons either directly, or through an indirect mechanism involving the production of intermediate neuronal progenitors (INPs) which then give rise to neurons. We show that in absence of RA, the RG progenitors proliferate less and prematurely produce neurons, leading to their depletion at E11.5. Furthermore, we could demonstrate that lack of RA impairs the generation of INPs at E13.5 and affects the cell cycle exit of progenitor cells during corticogenesis, altogether leading to a deficit in projection neurons and to microcephaly.
    MeSH term(s) Alcohol Oxidoreductases/metabolism ; Animals ; Cell Cycle/drug effects ; Cerebral Cortex/drug effects ; Cerebral Cortex/embryology ; Cyclin D2/metabolism ; Ependymoglial Cells/drug effects ; Ependymoglial Cells/metabolism ; Gene Deletion ; Mice, Knockout ; Microcephaly/pathology ; Models, Biological ; Neurogenesis/drug effects ; Stem Cells/drug effects ; Stem Cells/metabolism ; Tretinoin/pharmacology
    Chemical Substances Cyclin D2 ; Tretinoin (5688UTC01R) ; Alcohol Oxidoreductases (EC 1.1.-) ; trans-retinol dehydrogenase (EC 1.1.1.-)
    Language English
    Publishing date 2017--01
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1114-9
    ISSN 1095-564X ; 0012-1606
    ISSN (online) 1095-564X
    ISSN 0012-1606
    DOI 10.1016/j.ydbio.2017.08.006
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Endogenous retinoic acid signaling is required for maintenance and regeneration of cornea.

    Kumar, Sandeep / Dollé, Pascal / Ghyselinck, Norbert B / Duester, Gregg

    Experimental eye research

    2017  Volume 154, Page(s) 190–195

    Abstract: Retinoic acid (RA) is a biologically active metabolite of vitamin A (retinol) that serves as an important signaling molecule in orchestrating diverse developmental processes including multiple roles during ocular development. Loss-of-function studies ... ...

    Abstract Retinoic acid (RA) is a biologically active metabolite of vitamin A (retinol) that serves as an important signaling molecule in orchestrating diverse developmental processes including multiple roles during ocular development. Loss-of-function studies using gene knockouts of RA-synthesizing enzymes encoded by Aldh1a1, Aldh1a2, and Aldh1a3 (also known as Raldh1, Raldh2, and Raldh3) have provided valuable insight into how RA controls eye morphogenesis including corneal development. However, it is unclear whether endogenous RA is required for maintenance and regeneration of adult cornea. Here, we investigated the role of Aldh1a genes in the adult cornea using a novel conditional Aldh1a1,2,3-flox/flox;Rosa26-CreERT2 loss-of-function mouse model to determine the biological function of RA. Our findings indicate that loss of RA synthesis results in corneal thinning characterized by reduced thickness of the stromal layer, impaired corneal epithelial cell proliferation, and increased apoptosis. Corneal thinning in Aldh1a-deficient mice was significantly rescued by RA administration, indicating an important role of endogenous RA signaling in adult corneal homeostasis and regeneration. Thus, Aldh1a1,2,3-flox/flox;Rosa26-CreERT2 mice provide a useful model for investigating the mechanistic role of RA signaling in adult corneal maintenance and could provide new insights into therapeutic approaches for controlling corneal repair to prevent vision loss.
    MeSH term(s) Animals ; Apoptosis ; Cell Proliferation ; Epithelium, Corneal/metabolism ; Epithelium, Corneal/pathology ; Mice ; Regeneration/physiology ; Signal Transduction ; Tretinoin/metabolism
    Chemical Substances Tretinoin (5688UTC01R)
    Language English
    Publishing date 2017-01
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 80122-7
    ISSN 1096-0007 ; 0014-4835
    ISSN (online) 1096-0007
    ISSN 0014-4835
    DOI 10.1016/j.exer.2016.11.009
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Retinoic acid signalling during development.

    Rhinn, Muriel / Dollé, Pascal

    Development (Cambridge, England)

    2012  Volume 139, Issue 5, Page(s) 843–858

    Abstract: Retinoic acid (RA) is a vitamin A-derived, non-peptidic, small lipophilic molecule that acts as ligand for nuclear RA receptors (RARs), converting them from transcriptional repressors to activators. The distribution and levels of RA in embryonic tissues ... ...

    Abstract Retinoic acid (RA) is a vitamin A-derived, non-peptidic, small lipophilic molecule that acts as ligand for nuclear RA receptors (RARs), converting them from transcriptional repressors to activators. The distribution and levels of RA in embryonic tissues are tightly controlled by regulated synthesis through the action of specific retinol and retinaldehyde dehydrogenases and by degradation via specific cytochrome P450s (CYP26s). Recent studies indicate that RA action involves an interplay between diffusion (morphogen-like) gradients and the establishment of signalling boundaries due to RA metabolism, thereby allowing RA to finely control the differentiation and patterning of various stem/progenitor cell populations. Here, we provide an overview of the RA biosynthesis, degradation and signalling pathways and review the main functions of this molecule during embryogenesis.
    MeSH term(s) Alcohol Oxidoreductases/genetics ; Alcohol Oxidoreductases/metabolism ; Animals ; Brain/abnormalities ; Brain/embryology ; Brain/growth & development ; Brain/metabolism ; Cell Differentiation/physiology ; Embryo, Mammalian/anatomy & histology ; Embryo, Mammalian/physiology ; Embryonic Development/physiology ; Gene Expression Regulation ; Isoenzymes/genetics ; Isoenzymes/metabolism ; Receptors, Retinoic Acid/metabolism ; Response Elements ; Signal Transduction/physiology ; Stem Cells/cytology ; Stem Cells/physiology ; Tretinoin/chemistry ; Tretinoin/metabolism
    Chemical Substances Isoenzymes ; Receptors, Retinoic Acid ; Tretinoin (5688UTC01R) ; Alcohol Oxidoreductases (EC 1.1.-) ; retinol dehydrogenase (EC 1.1.1.105)
    Language English
    Publishing date 2012-03
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 90607-4
    ISSN 1477-9129 ; 0950-1991
    ISSN (online) 1477-9129
    ISSN 0950-1991
    DOI 10.1242/dev.065938
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Retinoic acid in development: towards an integrated view.

    Niederreither, Karen / Dollé, Pascal

    Nature reviews. Genetics

    2008  Volume 9, Issue 7, Page(s) 541–553

    Abstract: Retinoic acid (RA) has complex and pleiotropic functions during vertebrate development. Recent work in several species has increased our understanding of the roles of RA as a signalling molecule. These functions rely on a tight control of RA distribution ...

    Abstract Retinoic acid (RA) has complex and pleiotropic functions during vertebrate development. Recent work in several species has increased our understanding of the roles of RA as a signalling molecule. These functions rely on a tight control of RA distribution within embryonic tissues through the combined action of synthesizing and metabolizing enzymes, possibly leading to diffusion gradients. Also important is the switching of nuclear receptors from a transcriptionally repressing state to an activating state. In addition, cross-talk with other key embryonic signals, especially fibroblast growth factors (FGFs) and sonic hedgehog (SHH), is being uncovered. Some of these functions could be maintained throughout the life of an organism to regulate cell-lineage decisions and/or the differentiation of stem cell populations, highlighting possibilities for regenerative medicine.
    MeSH term(s) Animals ; Cell Differentiation ; Humans ; Stem Cells/cytology ; Tretinoin/metabolism ; Vertebrates/embryology ; Vertebrates/metabolism
    Chemical Substances Tretinoin (5688UTC01R)
    Language English
    Publishing date 2008
    Publishing country England
    Document type Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2035157-4
    ISSN 1471-0064 ; 1471-0056
    ISSN (online) 1471-0064
    ISSN 1471-0056
    DOI 10.1038/nrg2340
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article: Retinoic Acid Excess Impairs Amelogenesis Inducing Enamel Defects.

    Morkmued, Supawich / Laugel-Haushalter, Virginie / Mathieu, Eric / Schuhbaur, Brigitte / Hemmerlé, Joseph / Dollé, Pascal / Bloch-Zupan, Agnès / Niederreither, Karen

    Frontiers in physiology

    2017  Volume 7, Page(s) 673

    Abstract: Abnormalities of enamel matrix proteins deposition, mineralization, or degradation during tooth development are responsible for a spectrum of either genetic diseases ... ...

    Abstract Abnormalities of enamel matrix proteins deposition, mineralization, or degradation during tooth development are responsible for a spectrum of either genetic diseases termed
    Language English
    Publishing date 2017-01-06
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2564217-0
    ISSN 1664-042X
    ISSN 1664-042X
    DOI 10.3389/fphys.2016.00673
    Database MEDical Literature Analysis and Retrieval System OnLINE

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