Nogo maintains muscle integrity and regulates muscle regeneration via modulating Nogo-A expression
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ABSTRACT:
PROVIDER: PRJNA545456 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR9159602_1.fastq.gz | Fastqsanger.gz | |||
| SRR9159602_2.fastq.gz | Fastqsanger.gz | |||
| SRR9159603_1.fastq.gz | Fastqsanger.gz | |||
| SRR9159603_2.fastq.gz | Fastqsanger.gz | |||
| SRR9159604_1.fastq.gz | Fastqsanger.gz |
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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:STAT3 maintains skin barrier integrity by modulating SPINK5 and KLK5 expression in keratinocytes
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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:The elevation of Nogo-B expression in T2DM mice and Nogo-B knockdown alleviated diabetic symptoms in db/db mice prompted us to further investigate the involvement of Nogo-B in the insulin signaling pathway and T2DM. The three isoforms of Nogo are derived from various RNA splicing events, so deleting Nogo-B exons 2-4 results in the deficiency of other Nogo members, resulting in Nogo knockout (Nogo-/-) mice. As the liver is the key organ in the systemic response to insulin and controls glucose and lipid metabolism, we conducted RNA-seq of livers isolated from 8-week-old Nogo-/- mice and WT littermates.
2023-07-24 | GSE236979 | 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.
2010-10-20 | GSE24218 | 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
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