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Sedanolide alleviates LPS-induced depressive-like behaviors by modulating the C3a/C3aR signaling axis and microglial glycolysis

ABSTRACT: Depression is associated with neuroinflammation and microglial activation. This study investigated the effects of sedanolide in an LPS-induced mouse model of depressive-like behaviors. RNA sequencing of medial prefrontal cortex (mPFC) tissues was performed to identify transcriptomic changes associated with sedanolide treatment. Differential expression analysis revealed candidate genes involved in inflammatory pathways, including C3 and MMP9. Further validation demonstrated that sedanolide regulates neuroinflammation and microglial metabolic reprogramming through the C3a/C3aR signaling axis.

ORGANISM(S): Mus musculus

PROVIDER: GSE335983 | GEO | 2026/06/25

REPOSITORIES: GEO

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Microglia aggravate white matter injury via C3/C3aR pathway after experimental subrachnoid hemorrhage

Project description:Activation of microglia induces neuroinflammation in acute and chronic phase is closely related to the white matter injury (WMI) pathophysiologyafter subrachnoid hemorrhage (SAH). The complement C3a receptor (C3aR) has a dual role in regulating inflammation and plays a role in neurodevelopment, neuroplasticity and neurodegeneration, but it’s effect on WMI during SAH re'mairemains unknown. In this study, 175 male C57BL/6J mice received SAH by endovascular perforation. oxy-Hb was used to simulate SAH in vitro. Multiple technical approaches, including immunohistochemistry, transcriptome sequencing, neurological function assessment, and various molecular biotechnologies, were used to assess the activation of the C3-C3aR pathway after SAH and its effects on microglial polarizations and WMI after SAH. The results showed that abnormal microglial activation after SAH was accompanied by upregulation of complement C3 and C3aR. C3aR inhibition reduced abnormal microglial activation, attenuated neuroinflammation, ameliorated WMI and cognitive deficits after SAH. RNA-Seq revealed that C3aR inhibition downregulated several immune and inflammatory pathways and ameliorated cellular injury by downregulating Pidd1 expression. The adverse effects of C3-C3aR in SAH may be related to Endoplasmic reticulum (ER) stress-dependent cellular injury and formation of inflammasome. PERK agonists exacerbate cellular injury and neuroinflammation attenuated by C3aR inhibition. Intranasal C3a treatment during the subacute phase of SAH helps to reduce astrocyte reactivity and ameliorate cognitive deficits after SAH. In conclusion, these findings suggest that C3aR plays a critical role in the regulation of neuroinflammation and WMI after SAH, providing new therapeutic targets to ameliorate WMI and cognitive deficits after SAH.

2025-01-25 | GSE254320 | GEO

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

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

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

Complement C3aR depletion reverses HIF-1α induced metabolic impairment and improves microglial phagocytic and barrier function in response to Aβ pathology.

Project description:Complement C3aR is primarily expressed in microglial cells in the brain. Our study found elevated expression of C3aR in microglia in Alzheimer's disease. To understand the underlying molecular mechanism, we sorted microglia based on their C3aR expression from 9-month-old wild-type and APP-KI mice. Through RNA-seq analysis, we identified metabolic perturbations in C3aR-positive microglia from 9-month-old APP-KI mice. Furthermore, we performed RNA-seq on sorted microglial cells from wild-type, C3aR knockout, APP-KI, and APP-KI;C3aR knockout mice. This analysis revealed a dampening of metabolic dysfunction in the absence of C3aR.

2023-06-25 | GSE228258 | 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

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

Project description: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.

2023-03-30 | GSE184917 | GEO

PS19 and PS19/C3aR KO RNAseq data

Project description:Hippocampal tissue from 9 month old WT, C3aR KO, PS19 and PS19/C3aR KO mice was processed

2018-11-08 | GSE114910 | GEO

Complement C3aR deletion does not attenuate neurodegeneration in a tauopathy model or alter acute inflammation-induced gene expression changes in the brain

Project description:C3aR is highly expressed in microglia in the mouse brain and has been shown to play a role in neuroinflammation. This study examines single cell RNA expression profiles and cellularity changes in mouse hippocampi from WT or C3aRKO mice injected with PBS or LPS. The results from this study potentially provides a useful ScRNAseq dataset for LPS induced effects, critical insights for future C3aR inhibition efficacy readouts.

2026-03-23 | GSE291600 | 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

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