Retinoic Acid Induces Ubiquitination-Resistant RIP140/LSD1 Complex to Fine-Tune <i>P</i>
                  <i>ax6</i> Gene in Neuronal Differentiation

Wu, Cheng‐Ying; Persaud, Shanta J.; Wei, Li‐Na

doi:10.1002/stem.2190

Cited by 16 publications

(13 citation statements)

References 40 publications

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“…Instead, they may be the result of insufficient generation of OPCs from the SVZ. This could be related to the increased death of Nestin ϩ cells in the Raldh2 cKO SVZ, a finding that aligns with reports that RA is necessary for NSC survival (Crandall et al, 2004;Jacobs et al, 2006;Rajaii et al, 2008;Harrison-Uy et al, 2013;Mishra et al, 2016;Wu et al, 2016). The reduction in OPCs may also follow from reduced Gli1, indicative of decreased SHH signaling, in the subcallosal SVZ, where SHH is required for OPC production during early postnatal life (Tong et al, 2015;Sanchez and Armstrong, 2018;Winkler et al, 2018).…”

Section: Raldh2 Is Required For Opc Production and Differentiationsupporting

confidence: 75%

Retinoic Acid Is Required for Oligodendrocyte Precursor Cell Production and Differentiation in the Postnatal Mouse Corpus Callosum

Morrison

Smith

Huang

2019

eNeuro

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Myelination of the CNS relies on the production and differentiation of oligodendrocyte (OL) precursor cells (OPCs) into mature OLs. During the first month of postnatal life, OPCs that populate the corpus callosum (CC) arise from neural stem cells (NSCs) in the subcallosal subventricular zone (SVZ), and then differentiate to generate myelinating OLs. However, the signals that regulate these processes are not fully understood. In this study, we show that endogenous expression of the retinoic acid (RA)-synthesizing enzyme retinaldehyde dehydrogenase 2 (RALDH2) is required for OPC generation and differentiation in the postnatal subcortical white matter. In male and female pups, conditional deletion of Raldh2 reduced OPC numbers and differentiation. Moreover, decreased OPC numbers coincided with reductions in NSC survival and expression of the sonic hedgehog (SHH) signaling effector protein Gli1 in the SVZ. Additionally, GFAP expression in the CC was decreased, and cortical neuron numbers were altered. Our work suggests a role for endogenous RALDH2-dependent RA synthesis in OPC production and differentiation in the CC, as well as in the development of other cell types derived from NSCs in the embryonic ventricular zone (VZ) and SVZ, as well as the postnatal subcallosal SVZ.

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Section: Raldh2 Is Required For Opc Production and Differentiationsupporting

confidence: 75%

Retinoic Acid Is Required for Oligodendrocyte Precursor Cell Production and Differentiation in the Postnatal Mouse Corpus Callosum

Morrison

Smith

Huang

2019

eNeuro

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“…PAX6 is a highly conserved multifunctional transcription factor, which has been demonstrated to be a key protein in neurogenesis and neuronal plasticity by influencing cascades of gene expression (Mishra et al, 2015). In retinoic acid-induced neuronal differentiation, PAX6 was found to be repressed by the recruitment of histone modifier lysine-specific demethylase 1 (Wu et al, 2016). Our results showed that Pax6 is a key gene in neuronal differentiation and neuronal development.…”

Section: Discussionmentioning

confidence: 56%

Identification of neuron-related genes for cell therapy of neurological disorders by network analysis

Song

et al. 2017

J. Zhejiang Univ. Sci. B

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Bone mesenchymal stem cells (BMSCs) differentiated into neurons have been widely proposed for use in cell therapy of many neurological disorders. It is therefore important to understand the molecular mechanisms underlying this differentiation. We screened differentially expressed genes between immature neural tissues and untreated BMSCs to identify the genes responsible for neuronal differentiation from BMSCs. GSE68243 gene microarray data of rat BMSCs and GSE18860 gene microarray data of rat neurons were received from the Gene Expression Omnibus database. Transcriptome Analysis Console software showed that 1248 genes were up-regulated and 1273 were down-regulated in neurons compared with BMSCs. Gene Ontology functional enrichment, protein-protein interaction networks, functional modules, and hub genes were analyzed using DAVID, STRING 10, BiNGO tool, and Network Analyzer software, revealing that nine hub genes, Nrcam, Sema3a, Mapk8, Dlg4, Slit1, Creb1, Ntrk2, Cntn2, and Pax6, may play a pivotal role in neuronal differentiation from BMSCs. Seven genes, Dcx, Nrcam, sema3a, Cntn2, Slit1, Ephb1, and Pax6, were shown to be hub nodes within the neuronal development network, while six genes, Fgf2, Tgfβ1, Vegfa, Serpine1, Il6, and Stat1, appeared to play an important role in suppressing neuronal differentiation. However, additional studies are required to confirm these results.

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“…Interestingly, recent studies have begun to demonstrate that vitamin A, especially its most active metabolite, atRA, can also elicit specific non-canonical (RAR/RXR-independent) activities beyond regulating gene expression [23,24,25,26,27]. Using genetic tools, it has been established that most of these non-canonical activities are mediated by a specific, highly conserved, cellular binding protein for atRA named CRABP1 that serves as a cytosolic signal modulator/integrator or functions as an RA-regulated signal scaffold [27].…”

Section: Introductionmentioning

confidence: 99%

All-trans Retinoic Acid as a Versatile Cytosolic Signal Modulator Mediated by CRABP1

Nagpal

2019

IJMS

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All-trans retinoic acid (AtRA), an active metabolite of vitamin A, is recognized for its classical action as an endocrine hormone that triggers genomic effects mediated through nuclear receptors RA receptors (RARs). New evidence shows that atRA-mediated cellular responses are biphasic with rapid and delayed responses. Most of these rapid atRA responses are the outcome of its binding to cellular retinoic acid binding protein 1 (CRABP1) that is predominantly localized in cytoplasm and binds to atRA with a high affinity. This review summarizes the most recent studies of such non-genomic outcomes of atRA and the role of CRABP1 in mediating such rapid effects in different cell types. In embryonic stem cells (ESCs), atRA-CRABP1 dampens growth factor sensitivity and stemness. In a hippocampal neural stem cell (NSC) population, atRA-CRABP1 negatively modulates NSC proliferation and affects learning and memory. In cardiomyocytes, atRA-CRABP1 prevents over-activation of calcium-calmodulin-dependent protein kinase II (CaMKII), protecting heart function. These are supported by the fact that CRABP1 gene knockout (KO) mice exhibit multiple phenotypes including hippocampal NSC expansion and spontaneous cardiac hypertrophy. This indicates that more potential processes/signaling pathways involving atRA-CRABP1 may exist, which remain to be identified.

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Retinoic Acid Induces Ubiquitination-Resistant RIP140/LSD1 Complex to Fine-Tune P ax6 Gene in Neuronal Differentiation

Cited by 16 publications

References 40 publications

Retinoic Acid Is Required for Oligodendrocyte Precursor Cell Production and Differentiation in the Postnatal Mouse Corpus Callosum

Retinoic Acid Is Required for Oligodendrocyte Precursor Cell Production and Differentiation in the Postnatal Mouse Corpus Callosum

Identification of neuron-related genes for cell therapy of neurological disorders by network analysis

All-trans Retinoic Acid as a Versatile Cytosolic Signal Modulator Mediated by CRABP1

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