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Effect of intransal C3a treatment on gene expression in mouse brain cortex in the post-acute phase of ischemic stroke.

ABSTRACT: The goal of this study was to gain insight into possible mechanisms of improved neural plasticity and functional recovery folowing ischemic stroke in mice confered by a delayed intranasal treatment with complement peptide C3a (reported previously in Stokowska et al., Brian, 2017). Differential expression analysis revealed that daily intranasal treatment between day 7 and 14 post-stroke is associated with downregualtion of genes involved in inflammatory responses and glial cells reactivity, primarily astrocytes. Further, cellular deconvolution analysis pointed to C3a-dependent reduction of fraction of astrocytes with gene expression profile charcterisitc for potentially neurotoxic disease-associated astrocytes (DAAs, orignially descreibed in Alzheimer disease) and increse in fraction of homeostatic astrocytes, with expression profile indicating supportive role for neuronal function and plasticity. We conclude that the C3a-C3aR signalling modulates post-stroke reactive astrogliosis in the manner favouring neural plasticity the peri-lesional cortex.

ORGANISM(S): Mus musculus

PROVIDER: GSE184917 | GEO | 2023/03/30

REPOSITORIES: GEO

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Deficiency of C3a receptor attenuates the development of diabetic nephropathy (Diabetic Group)

Project description:Diabetic nephropathy (DN) is the leading cause of chronic kidney disease and end-stage renal disease. Emerging evidence suggests that complement activation is involved in the pathogenesis of DN. The aim of this study was to investigate the pathogenic role of C3a and C3a receptor (C3aR) in DN. The expression of C3aR was examined in the renal specimen of DN patients. Using a C3aR gene knockout mice (C3aR-/-), we evaluated kidney injury in diabetic mice. The mouse gene expression microarray was performed to further explore the pathogenic role of C3aR. Then the underlying mechanism was investigated in vitro with macrophage treated with C3a. Compared with normal controls, the renal expression of C3aR was significantly increased in DN patients. C3aR-/- diabetic mice developed less severe diabetic renal damage compared with WT diabetic mice, exhibiting significantly lower level of albuminuria and milder renal pathological injury. Microarray profiling uncovered significantly suppressed inflammatory responses and T cell adaptive immunity in C3aR-/- diabetic mice compared with WT diabetic mice and this result was further verified by immunohistochemical staining of renal CD4+, CD8+ T cells and macrophages infiltration. In vitro study demonstrated C3a can enhance macrophages secreted cytokines which could induce inflammatory responses and differentiation of T cell lineage. In conclusion, C3aR deficiency could attenuate diabetic renal damage through suppressing inflammatory responses and T cell adaptive immunity, possibly by influencing macrophages secreted cytokines. Thus, C3aR may be a promising therapeutic target for DN.

2020-04-10 | GSE133597 | GEO

Deficiency of C3a receptor attenuates the development of diabetic nephropathy (Control Group)

2020-04-10 | GSE133596 | GEO

Generation of a C3a-specific monoclonal antibody and immunoapheresis of C3a/C3 and its associates

Project description:A high affine murine monoclonal antibody was generated against complement factor C3 and selected for binding to the C3a region to serve as immunoaffinity reagent. Subsequently, a C3a/C3 specific immunoaffinity column was developed and apheresis of C3a/C3 and its associates was performed. A proteomic analysis was carried out for identification of apheresis products.

2019-11-27 | PXD009829 | Pride

C3A Cells: Exposure vs Control [one-channel arrays]

Project description:Gene expression profiles comparing FCCP, CCCP, Dinoterb, Benzoapyrene, TCP, Medium control, 0,1% DMSO in C3A cells

2015-12-09 | GSE75783 | GEO

C3A Cells: Exposure vs Control [two-channel arrays]

Project description:Gene expression profiles comparing FCCP, CCCP, 6OH-BDE47, Ethylenglycol, TCP, PCP, Aniline, chloroaniline, DMSO in C3A cells

2015-12-09 | GSE75782 | GEO

Development of Specific Therapy Against Right Ventricular Failure

Project description:Right ventricular (RV) failure plays a critical role in any type of heart failure. However, there is no specific therapy developed for RV failure. To understand RV failure, we focused on the RV specific genes. Global gene expression analysis showed that alternative complement pathway-related genes including C3 and Cfd were significantly upregulated in right ventricle in murine heart. We generated the RV failure by right ventricle-specific pressure overload model mice, pulmonary artery constriction (PAC), which induces RV failure around 14 days. In C3 knockout (C3KO) mice, PAC-induced RV dysfunction and fibrosis were significantly attenuated. C3a is produced from C3 by C3 convertase complex including Cfd. Cfd knockout mice also attenuated PAC-induced RV failure. Moreover, C3a receptor (C3aR) antagonist dramatically improved PAC-induced RV dysfunction in wild type mice. Here we revealed the crucial role of C3-Cfd-C3a-C3aR axis in RV failure and highlight the potential therapeutic target for RV failure with no pharmacologic option.

2021-09-07 | GSE183504 | GEO

Expression data of CD11b+ cells isolated from WT and C3aR knockout mice after CTX injury

Project description:Regeneration of skeletal muscle following injury is accompanied by transient inflammation initiation and resolution. However, it is unclear what signals control these processes. To better understand the biological pathways by C3a-C3aR activation in monocyte druing muscle regeneration,we examined global transcriptional changes in macrophages from the muscle after CTX injury.Male C57BL/6J mice were used at 12 weeks of age. 30 ul 10uM Cardiotoxin (CTX) was injected to TA muscle to injury muscle. CD11b+ cells was isolated from WT and C3aR-/- muscle at 1 day after CTX injury by FACS , then total RNA obtained from these cells were used for the analysis of RNA-seq.

2017-08-31 | E-MTAB-5886 | biostudies-arrayexpress

HepG2/C3A cells cultured for 42 h in complete or leucine-devoid medium

Project description:HepG2/C3A cells cultured for 42 h in complete or leucine-devoid medium

2008-11-10 | GSE13142 | GEO

Effect of C3a treatment over cell death of pancreatic islets ex vivo

Project description:RNAseq of islets from WT mice treated in vehicle or palmitate conditions, wit or without recombinant C3a

2020-02-04 | GSE144709 | GEO

COMPLEMENT C3aR ACTS AS AN ONCOSUPPRESSOR IN COLORECTAL CANCER BY MODULATING GUT MICROBIOTA

Project description:Several lines of evidence suggest that inflammation plays a pivotal role in the development and progression of CRC and can be unleashed by the loss of innate immunosurveillance. The complement system is a well characterized first line of defense against pathogens and a central component of the immune responses. As such, the complement system is an important determinant in the maintenance of intestinal homeostasis and emerging evidences suggest that complement dysregulation is involved in the development and progression of CRC. Here we show that in CRC patients CpG island methylation occurs in the gene encoding for the complement anaphylatoxin C3a receptor (c3aR) and strong C3aR down-regulation resulted in decreased overall survival and events-free survival in CRC patients. Ablation of c3ar in mouse models of CRC resulted in the establishment of a pro-inflammatory microbial flora, which fostered strong Th1/Th17 immune responses and a striking increase in tumor incidence and growth that were both dependent on the microbiota. Our findings highlight a previously unrecognized tumor oncosuppressive role for C3aR in CRC that could be exploited as a biomarker for more effective therapeutic intervention.

2020-02-01 | E-MTAB-8500 | biostudies-arrayexpress

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