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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE291600 | GEO | 2026/03/23

REPOSITORIES: GEO

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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

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

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

| PRJNA1234217 | ENA

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

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

Project description: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.

2026-06-25 | GSE335983 | GEO

Complement C3aR Inactivation Attenuates Tau Pathology and Reverses an Immune Network Deregulated in Tauopathy Models and Alzheimer's Disease.

Project description: Not available

| S-EPMC6309202 | biostudies-literature

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

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

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

| PRJEB35288 | ENA

Complement Factor H maintains macrophage homeostasis through TRPM7 signaling

Project description:Factor H (FH) is a critical regulator of the alternative complement pathway preventing uncontrolled complement activation. Its role in mitigating complement-mediated injury is evident in diseases such as dense deposit disease and age related macular degeneration characterized by significant macrophage (Mo) infiltration. While primarily synthesized in the liver, FH is also produced by other cells, including monocytes and Mos. However, the influence of FH on these cells remains incompletely understood. This study explores the functions of FH in rodent bone marrow-derived Mos, revealing FH-dependent regulation of genes linked to proliferation and inflammation, including C3aR, the receptor for C3a generated on complement activation. Further, our findings demonstrate that intrinsic FH deficiency in Mos enhances proliferation, trafficking, migration, and reduces phagocytosis. FH-deficient Mos exhibit metabolic alterations characterized by reduced oxidative phosphorylation and glycolysis. Notably, our results show for the first time that FH in Mos influences non-canonical functions through downstream C3a/C3aR signaling, modulating calcium levels and the activity of transient receptor potential cation channel, subfamily M, member 7 (TRPM7). Inhibiting TRPM7 activity with FTY720 reduces Mo proliferation, and blocking C3a/C3aR signaling mitigates TRPM7-related alterations and proliferation in Mos. In summary, this study highlights FH's functional relevance in maintaining homeostasis in Mos, where it modulates functions in a cell-autonomous manner, regulating TRPM7 through C3a/C3aR signaling pathways, offering therapeutic avenues for kidney disease and other inflammatory conditions.

2026-05-05 | GSE279157 | GEO

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