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RORα coordinates thalamic and cortical maturation to instruct barrel cortex development.

ABSTRACT: The retinoic acid orphan receptor alpha (RORα) is well known for its role in cerebellar development and maturation as revealed in the stagerrer (Stg) mutant mouse line. However it’s potential involvement for the development of other brain regions has not been assessed. Here we describe a new role of RORα in the development of the thalamic and cortical circuits that leads to the assembly of columnar barrel structures in the primary somatosensory cortex. Microarray analyses comparing gene expression in the thalamus and cortex of the Stg, showed a down-regulation of genes that have been involved in the control of TCA or cellular maturation of layer IV neurons. Overall, our study outlines a new role of RORα for the coordinated maturation of the thalamus and cortex during early postnatal life, and shows that it is required to initiate the transcription of genes involved in barrel formation.

ORGANISM(S): Mus musculus

PROVIDER: GSE80317 | GEO | 2017/09/30

SECONDARY ACCESSION(S): PRJNA318576

REPOSITORIES: GEO

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Mus musculus

Project description:RORα coordinates thalamic and cortical maturation to instruct barrel cortex development.

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The identification of genes altered by RORα in progression of non-alcoholic steatohepatitis (NASH)

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RORɣt and RORα Signature Genes in Human Th17 Cells

Project description:In an effort to study gene expression modulated by RORɣt and RORα in human Th17 cells, global gene expression of human CD4 T cells activated under Th17 skewing conditions was profiled by RNA sequencing. RORɣt and RORα signature genes were identified in these Th17 cells treated with specific siRNAs to knock down RORɣt or RORα expression. In addition, selective small molecule RORɣt modulators were also utilized as pharmacological tools in RORɣt signature gene identification.

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Cortical, hippocampal and thalamic whole genome transcriptome data from controls and G72 schizophrenia mice of both sexes

Project description:G72 transgenic (TG, transgenic mice carrying the G72/G30 locus) and wildtype (WT) mice with a CD1 background were used for transcriptome data acquisition. Importantly, three different brain regions, i.e., the retrosplenial cortex, the hippocampus and thalamus, of animals from both sexes were investigated. In total, eight WT control animals (four ♂, age: 23.14 ± 0.00 wks; four ♀, age: 23.46 ± 0.11 wks) and eight G72 transgenic mice (four ♂, age: 23.14 ± 0.00 wks; four ♀, age: 23.14 ± 0.00 wks) were used for dissection of the cortex, thalamus and hippocampus for subsequent transcriptome analysis. Our data allow new insight into relevant alterations in gene transcript levels in G72 mice and allow the reader/user to carry out additional complex analyses to characterize potential sex-, age- and brain-region-specific profiles in gene expression and related pathways. These analyses could trigger biomarker identification and drug research and development in schizophrenia research in the future.

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2021-07-28 | GSE168217 | GEO

RORα is critical for mTORC1 activity in T cell-mediated colitis [RNA-seq]

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Project description:Chronic pain is a major health care problem with great social and economic consequences. Although the medial prefrontal cortex (mPFC) and the thalamus have been implicated in regulating pain, whether and how these regions may involve in pain chronification process have remained largely unknown. Here, we show that Foxp2+ neurons in mPFC, which are corticothalamic (CT) neurons representing the major mPFC output to thalamus, are deactivated in chronic inflammatory pain. Interestingly, prolonged, but not short-term, inactivation of the Foxp2+ neurons in mPFC increases the sensitivity to noxious stimulations. Conversely, chemogenetic activation of this neuronal cluster induces robust antinociceptive effects in both naïve mice and mice with chronic inflammatory pain. Furthermore, we found that the mPFC Foxp2+ neurons project to several thalamic relay nuclei and that activation of the mPFC to the parataenial nucleus of thalamus (PTN) circuit relieves pain. Finally, RNA-seq of the mPFC Foxp2+ neurons revealed that many genes related to neuronal activity are dysregulated in mice with chronic inflammatory pain. Collectively, our studies revealed that Foxp2+ neurons in mPFC that project to thalamus play a critical role in somatosensory processing and pain chronification.

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RORα is critical for mTORC1 activity in T cell-mediated colitis [16S rRNA-seq]

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Inhibition of nuclear receptor RORα attenuates cartilage damage in osteoarthritis by modulating IL-6/STAT3 pathwa

Project description:Osteoarthritis is characterized by cartilage destruction, chronic inflammation, and subchondral sclerosis. Evidence showed that nuclear receptor family is closely associated with cartilage damage in an unclear molecular mechanism. Here, we investigated the role and molecular mechanism of the retinoic acid receptor-related orphan receptor-α (RORα), an important member of nuclear receptor, in regulating cartilage degradation and osteoarthritis pathogenesis. Investigation to osteoarthritis clinical specimen showed that the degree of RORα elevation is positively correlated with the severity of osteoarthritis and cartilage damage. In an in vivo osteoarthritis models induced by anterior crucial ligament transaction, intraarticularly injection of siRora adenovirus reversed the cartilage damage. RORα knock-down increased the protein expression level of anabolic factor such as type II collagen, Aggrecan, and decreased the expression of catabolic factor. RNA-seq data suggested IL-6/STAT3 pathway is significantly down-regulated. Mechanistically, RORα knock-down decreased the expression level of both IL-6 and phosphorylated STAT3. RORα exerted its effect on IL-6/STAT3 signaling in two different ways, which includes interaction with STAT3 and IL6 promoter. Taken together, our findings indicated the pivotal role of RORα/IL-6/STAT3 axis in osteoarthritis progression and confirmed RORα knock-down exerted therapeutic effect in human chondrocyte thus providing a potential drug target in osteoarthritis therapy.

2021-04-20 | GSE172291 | GEO

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