Immuno-Responsive Gene-1: A mitochondrial gene regulates pathogenic Th17 in CNS autoimmunity mouse model.

Pathogenic Th17 cells are crucial to CNS autoimmune diseases like multiple sclerosis (MS), though their control by endogenous mechanisms is unknown. RNAseq analysis of brain glial cells identified immuno-responsive gene 1 (), a mitochondrial-related enzyme-coding gene, as one of the highly upregulated gene under inflammatory conditions which were further validated in the spinal cord of animals with experimental autoimmune encephalomyelitis (EAE), an animal model of MS. Moreover, mRNA and protein levels in myeloid, CD4, and B cells were higher in the EAE group, raising questions about its function in CNS autoimmunity.

An early glycolysis burst in microglia regulates mitochondrial dysfunction in oligodendrocytes under neuroinflammation.

Metabolism and energy processes governing oligodendrocyte function during neuroinflammatory disease are of great interest. However, how varied cellular environments affect oligodendrocyte activity during neuroinflammation is unknown. We demonstrate that activated microglial energy metabolism controls oligodendrocyte mitochondrial respiration and activity.

Maresin-1 promotes neuroprotection and prevents disease progression in experimental models of multiple sclerosis through metabolic reprogramming and shaping innate and adaptive disease-associated cell types.

Multiple sclerosis (MS) is one of the most common inflammatory neurodegenerative diseases in young adults and causes neurological abnormalities and disability. We studied the effect of maresin 1 (MaR1) on the progression of disease in a relapsing-remitting form of experimental allergic encephalomyelitis (RR-EAE). Treatment with MaR1 in RR-EAE accelerated inflammation resolution, protected against neurological deficits, and delayed disease progression by decreasing immune cell infiltration (CD4+IL17+ and CD4+IFNγ+) into the CNS.

Temporal transcriptome analysis of neuronal commitment reveals the preeminent role of the divergent lncRNA biotype and a critical candidate gene during differentiation.

lncRNA genes can be genic or "intergenic". "Genic" RNAs can be further divided into six biotypes. Through genome-wide analysis of a publicly available data set on corticogenesis, we found that the divergent lncRNA (XH) biotype, comprising the lncRNA and the coding gene being in opposite directions in a head-to-head manner, was most prominent during neural commitment.

Shared Transcriptional Signatures in Major Depressive Disorder and Mouse Chronic Stress Models.

Background: Most of our knowledge of the biological basis of major depressive disorder (MDD) is derived from studies of chronic stress models in rodents. While these models capture certain aspects of the behavioral and neuroendocrine features of MDD, the extent to which they reproduce the molecular pathology of the human syndrome remains unknown.

Methods: We systematically compared transcriptional signatures in two brain regions implicated in depression-medial prefrontal cortex and nucleus accumbens-of humans with MDD and of 3 chronic stress models in mice: chronic variable stress, adult social isolation, and chronic social defeat stress.

Identification of lncRNAs Associated With Neuroblastoma in Cross-Sectional Databases: Potential Biomarkers.

Long non-coding RNAs (lncRNAs) have emerged as an important regulatory control in biological systems. Though the field of lncRNA has been progressing rapidly, a complete understanding of the role of lncRNAs in neuroblastoma pathogenesis is still lacking. To identify the abrogated lncRNAs in primary neuroblastoma and in the metastasized as well as the relapsed form of neuroblastoma, we analyzed an RNA-seq dataset on neuroblastoma that is available online to identify the lncRNAs that could potentially be contributing to the biology of neuroblastoma.

Molecular programs underlying differences in the expression of mood disorders in males and females.

Major depressive disorder (MDD) is a sexually dimorphic disease. This sexual dimorphism is believed to result from sex-specific molecular alterations affecting functional pathways regulating the capacity of males and females to cope with daily life stress differently. Transcriptional changes associated with epigenetic alterations have been observed in the brain of males and females with depression.

Gadd45b mediates depressive-like role through DNA demethylation.

Animal studies using chronic social defeat stress (CSDS) in mice showed that brain-derived neurotrophic factor (BDNF) signaling in the mesolimbic dopamine (DA) circuit is important for the development of social aversion. However, the downstream molecular targets after BDNF release from ventral tegmental area (VTA) DA terminals are unknown. Here, we show that depressive-like behaviors induced by CSDS are mediated in part by Gadd45b downstream of BDNF signaling in the nucleus accumbens (NAc).

Identification and epigenetic analysis of divergent long non-coding RNAs in multilineage differentiation of human Neural Progenitor Cells.

Long non-coding RNAs have emerged as an important regulatory layer in biological systems. Of the various types of lncRNAs, one class (designated as divergent RNAs/XH), which is in head-to-head overlap with the coding genes, has emerged as a critical biotype that regulates development and cellular differentiation. This work aimed to analyze previously published data on differential expression, epigenetic and network analysis in order to demonstrate the association of divergent lncRNAs, a specific biotype with the differentiation of human neural progenitor cells (hNPCs).