Effect of Nogo deficiency on the insulin signaling pathway
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE236979 | GEO | 2023/07/24
REPOSITORIES: GEO
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Project description:Nogo, also called RTN4, functions through three isoforms including Nogo-A, -B, and -C. Although Nogo-A is a well-known CNS inhibitor and the level of Nogo-A is increased in muscles of ALS patients, its role in the regulation of skeletal muscle homeostasis and regeneration is still vague. In this study, we analyzed various pathological muscle condition of human and mouse model, and discovered significant increase of Nogo-A and myogenic factors. To understand the role of Nogo in skeletal muscle, muscle transcripts from Nogo+/+ and Nogo-/- mouse were analyzed and observed intensified gene expression involved in adipocyte differentiation and lipid metabolism, and reduced gene expression related to muscle differentiation and structure organization suggesting muscle disorder from muscle replacement with fat deposition. Skeletal muscle structure from Nogo null mice displayed dystrophic phenotypes including impaired myofiber structure and immune cell infiltrations, and dysregulated homeostatic features such as higher level of MyoD, procaspase 3, CHOP, and AKT compared to wild-type muscle. Notexin-injured Nogo deficient muscle resulted higher level of immune cell infiltration but defective in IL-6 production, a well-known myokine from immune cells, and abnormally upregulated regenerative muscle fibers than normal muscle. Therefore we hypothesized that increased Nogo-A in pathological conditions may regulate muscle regeneration. Then differentiating C2C12 cells and induced myogenic stem cells(iMSC) showed upregulated Nogo-A and Myogenin, and Nogo-A silencing in C2C12 cells abrogated the capability to differentiate into myotubes. In conclusion, Nogo functions to maintain muscle homeostasis and integrity, and altered Nogo-A expression in pathological muscle condition mediates muscle regeneration. These understanding suggests Nogo-A as a novel differentiation target for the treatment of myopathies at clinical set.
2019-05-31 | GSE131955 | GEO
Project description:In order to determine if there are any genetic differences among lungs of Nogo-A/B knockout mice which may explain their enhanced asthmatic-like responses, we have employed whole genome microarray expression profiling as a discovery platform to identify any genes that may be altered in the lung of Nogo-A/B knockout mice. RNA was isolated from three biological replicates of mouse lungs from naive WT and Nogo-A/B Knockout mice and run on agilent array. Two genes was significantly altered in Nogo-A/B Knockout lungs, SPLUNC1 and RTN4 (Nogo) which was significantly decreased and confirmed by real-time PCR. Gene expression in naïve mouse lungs of WT and Nogo-A/B knockout mice was measured in three individual biological replicates from each group.
2010-10-20 | E-GEOD-24218 | biostudies-arrayexpress
Project description:In order to determine if there are any genetic differences among lungs of Nogo-A/B knockout mice which may explain their enhanced asthmatic-like responses, we have employed whole genome microarray expression profiling as a discovery platform to identify any genes that may be altered in the lung of Nogo-A/B knockout mice. RNA was isolated from three biological replicates of mouse lungs from naive WT and Nogo-A/B Knockout mice and run on agilent array. Two genes was significantly altered in Nogo-A/B Knockout lungs, SPLUNC1 and RTN4 (Nogo) which was significantly decreased and confirmed by real-time PCR.
2010-10-20 | GSE24218 | GEO
Project description:Purpose: Acute lung injury (ALI) is a severe clinical disorder characterized by diffused capillary-alveolar barrier damage and noncardiogenic lung edema induced by excessive inflammation reactions. Nogo-B, a member of the reticulon 4 protein family, plays a critical role in modulating macrophages and neutrophils’ function in inflammation. Its role in ALI remains unclear. Methods: Pulmonary expression of Nogo-B was investigated in a LPS-induced ALI mice model. The effects and the underline mechanisms of Nogo-B expression on the severity of lung injury was assessed using histological examination, Bronchoalveolar lavage fluid (BALF) protein and inflammatory cells and cytokines measurement, and microarray analysis. Results: Nogo-B was normally highly expressed in the lungs of naïve C57BL/6 mice. Intra-tracheal instillation of LPS significantly repressed the Nogo-B expression in lung tissues and BALF cells of ALI mice. In addition, over-expression of pulmonary Nogo-B using an adenovirus vector which expresses a Nogo-B-RFP-3-flag fusion protein (Ad-Nogo-B) significantly prolonged the survival time of mice challenged with lethal dose of LPS. Histological results and BALF protein measurement convinced that Ad-Nogo-B treated mice had less severity of lung injury and alveolar protein exudation, as compared with control adenovirus treated mice (Ad-RFP). They also had higher MCP-1 secretion and alveolar macrophages infiltration, but lower neutrophils infiltration. Finally, using microarray analysis, we identified a protective gene, PTX3, was highly elevated in Ad-Nogo-B treated mice. Conclusions: Nogo-B played a protective role in LPS-induced ALI, which might exert its role through modulation of inflammatory response and PTX3 secretion. A total of 12 samples from mice treated with or without LPS in the presence of Ad-Nogo-B or Ad-RFP transfection (n=3 for each group)
2013-07-12 | E-GEOD-48787 | biostudies-arrayexpress
Project description:Purpose: Acute lung injury (ALI) is a severe clinical disorder characterized by diffused capillary-alveolar barrier damage and noncardiogenic lung edema induced by excessive inflammation reactions. Nogo-B, a member of the reticulon 4 protein family, plays a critical role in modulating macrophages and neutrophils’ function in inflammation. Its role in ALI remains unclear. Methods: Pulmonary expression of Nogo-B was investigated in a LPS-induced ALI mice model. The effects and the underline mechanisms of Nogo-B expression on the severity of lung injury was assessed using histological examination, Bronchoalveolar lavage fluid (BALF) protein and inflammatory cells and cytokines measurement, and microarray analysis. Results: Nogo-B was normally highly expressed in the lungs of naïve C57BL/6 mice. Intra-tracheal instillation of LPS significantly repressed the Nogo-B expression in lung tissues and BALF cells of ALI mice. In addition, over-expression of pulmonary Nogo-B using an adenovirus vector which expresses a Nogo-B-RFP-3-flag fusion protein (Ad-Nogo-B) significantly prolonged the survival time of mice challenged with lethal dose of LPS. Histological results and BALF protein measurement convinced that Ad-Nogo-B treated mice had less severity of lung injury and alveolar protein exudation, as compared with control adenovirus treated mice (Ad-RFP). They also had higher MCP-1 secretion and alveolar macrophages infiltration, but lower neutrophils infiltration. Finally, using microarray analysis, we identified a protective gene, PTX3, was highly elevated in Ad-Nogo-B treated mice. Conclusions: Nogo-B played a protective role in LPS-induced ALI, which might exert its role through modulation of inflammatory response and PTX3 secretion.
2013-07-12 | GSE48787 | GEO
Project description:Nogo-A is a major regulator of neural development and regeneration in the central nervous system, but its role in tooth innervation remains largely unknown. Neurons of the trigeminal ganglion innervate the teeth. We showed that Nogo-A is expressed in the trigeminal ganglion and tooth-related nerve fibres. Nogo-A deletion in mice leads to a less complex neuronal network when compared to wild-type animals. Bulk RNA sequencing on the trigeminal ganglia of Nogo-A KO and wild-type mice revealed gene expression changes associated with alterations in neurotrophin signalling and neuronal synaptic formation during the development and maturation of the trigeminal neurons.
2024-12-04 | GSE283391 | GEO
Project description:Nogo-A localized on myelin adaxonal membrane in the adult CNS is well known for its role as neurite outgrowth inhibitor following a lesion. Nogo-A KO mice show enhanced regenerative/compensatory fiber growth following CNS lesion. However, changes undergoing in their intact CNS have not been studied. Moreover, Nogo-A in the intact adult CNS in also expressed in some neuronal subpopulations, e.g. in the hippocampus, olfactory bulbs and dorsal root ganglia. We compared the intact adult CNS (spinal cord) of Nogo-A KO mice in order to identify: potential compensating molecules which could be interesting new inhibitory neurite outgrowth candidates, possible molecules involved in the up to now not yet clarified downstream signalling pathway of Nogo-A, additional new functions for myelin or neuronal Nogo-A in the intact adult CNS. Keywords: gene expression, Nogo-A KO, spinal cord, adult, naive, unlesioned
2010-11-01 | GSE11276 | GEO
Project description:Nogo-A localized on myelin adaxonal membrane in the adult CNS is well known for its role as neurite outgrowth inhibitor following a lesion. Nogo-A KO mice show enhanced regenerative/compensatory fiber growth following CNS lesion. However, changes undergoing in their intact CNS have not been studied. Moreover, Nogo-A in the intact adult CNS in also expressed in some neuronal subpopulations, e.g. in the hippocampus, olfactory bulbs and dorsal root ganglia. We compared the intact adult CNS (spinal cord) of Nogo-A KO mice in order to identify: potential compensating molecules which could be interesting new inhibitory neurite outgrowth candidates, possible molecules involved in the up to now not yet clarified downstream signalling pathway of Nogo-A, additional new functions for myelin or neuronal Nogo-A in the intact adult CNS. Keywords: gene expression, Nogo-A KO, spinal cord, adult, naive, unlesioned Spinal cords from 3 adult C57Bl/6 wild type and Nogo-A KO mice have been explanted. Total RNA has been extracted and processed for hybridization on Mouse 430 2.0 Affymetrix GeneChips. Following scanning and first analysis with MAS 5.0, further analysis was performed by GeneSpring 7.2 (Silicon Genetics, Redwood City, CA). A present call filter (2 out of 3 present calls in at least one out of the different studied conditions) was applied. Normalization was run per chip as well as per gene to the median of the control replicates. Data were statistical restricted through a 1-way Anova (p=0.05). A final threshold of =1.2 folds of increase or decrease in the expression level of each single transcript was applied. Regulated transcripts have been assigned to functional categories according to GeneOntology as well as literature and database mining (Pubmed and Bioinformatics Harvester EMBL Heidelberg).
2010-11-01 | E-GEOD-11276 | biostudies-arrayexpress
Project description:Sarcopenia has been recognized as an emerging complication of type 2 diabetes mellitus (T2DM). Currently, the pathogenesis of T2DM-related sarcopenia remains unclear. The aim of this study was to investigate the molecular mechanisms and potential therapeutic targets for T2DM-related sarcopenia. In this study, a T2DM-related sarcopenia mouse model was established using db/db mice. Proteins extracted from the gastrocnemius muscles of db/db mice and littermate control db/m mice were analyzed by a 4D label-free quantitative proteomics approach. A total of 131 upregulated and 68 downregulated proteins were identified as differentially expressed proteins (DEPs). Bioinformatics analysis revealed that DEPs were significantly enriched in lipid metabolism. Protein–protein interaction network analysis revealed that six hub proteins, including ACOX1, CPT2, ECI2, ACADVL, ACADL, and ECH1, were involved in the fatty acid oxidation. The hub protein-transcription factor-miRNA network was also constructed through the NetworkAnalyst tool. Finally, the hub proteins were validated by western blotting and immunohistochemistry and further confirmed to be significantly negatively correlated with the muscle mass and grip strength. Our study suggested that lipid metabolism, especially excessive fatty acid oxidation, may be a crucial contributor to the progression of T2DM-related sarcopenia and a common cause of the interrelationship between T2DM and sarcopenia.
2024-10-17 | PXD051462 | Pride
Project description:Effect of Nogo deficiency on the insulin signaling pathway
| PRJNA993241 | ENA