CX3CR1 (Extracellular Loop) Peptide
- Known as:
- CX3CR1 (Extracellular Loop) Peptide
- Catalog number:
- 2201P
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- CX3CR1 (Extracellular Loop) Peptide
Related genes to: CX3CR1 (Extracellular Loop) Peptide
- Gene:
- CX3CR1 NIH gene
- Name:
- C-X3-C motif chemokine receptor 1
- Previous symbol:
- GPR13, CMKBRL1
- Synonyms:
- CMKDR1, V28, CCRL1
- Chromosome:
- 3p22.2
- Locus Type:
- gene with protein product
- Date approved:
- 1998-01-12
- Date modifiied:
- 2016-10-05
Related products to: CX3CR1 (Extracellular Loop) Peptide
Related articles to: CX3CR1 (Extracellular Loop) Peptide
- To investigate the efficacy of sacral neuromodulation (SNM) in alleviating neuropathic pelvic pain (NPP) and its underlying neuroimmune mechanisms, focusing on microglial activation and the CX3CL1-CX3CR1 pathway. A rat model of NPP was established via pelvic nerve crush (PNC), followed by SNM intervention. Pain behaviors were assessed using von Frey filaments and thermal withdrawal latency testing. Microglial activation, inflammatory factor expression, and signaling pathway dynamics in the spinal dorsal horn were analyzed using immunofluorescence, Western blot, qRT-PCR, and ELISA. Transcriptome sequencing was used to identify key pathways modulated by SNM. Exogenous CX3CL1, LPS, minocycline, and PLX5622 were employed to validate the roles of microglia and the CX3CL1-CX3CR1 axis in SNM-induced analgesia. PNC rats exhibited stable lower abdominal mechanical hypersensitivity, accompanied by significant microglial activation and increased expression of pro-inflammatory cytokines (TNF-α, IL-1β, and IL-6) in the spinal dorsal horn. SNM treatment ameliorated pain behaviors, suppressed microglial activation, reduced pro-inflammatory cytokine expression, and inhibited p38 and p65 phosphorylation. Transcriptome analysis revealed that SNM remodeled inflammation-related transcriptional profiles, notably suppressing the CX3CL1-CX3CR1 signaling axis. Exogenous CX3CL1 or LPS partially reversed SNM-induced analgesia and anti-inflammatory effects. Microglial depletion attenuated the PNC-induced pain phenotype, with no significant synergistic effect observed when combined with SNM. SNM alleviates NPP by inhibiting CX3CL1-CX3CR1-mediated microglial activation and downstream inflammatory signaling, thereby remodeling the spinal cord immune microenvironment. This study provides new evidence for the central immunological mechanism underlying SNM in treating chronic pelvic pain and suggests the CX3CL1-CX3CR1 axis as a potential target for combined neuromodulation therapy. - Source: PubMed
Publication date: 2026/09/16
Zuo JinmingWang YangYang LixinHu YueshiZhang FutianWang QiangCao ZhihuaDuan Qixin - General anesthesia exposure in early life may disrupt the normal progression of developmental myelination, but the underlying mechanisms remain unclear. Early postnatal microglia in developing white matter exhibit diverse transcriptional and functional states, including a population with pronounced phagocytic activity. This study aims to investigate whether sevoflurane impairs oligodendrocyte myelination by promoting microglial phagocytosis of oligodendrocyte precursor cells (OPCs). Mice received either a single 2-h exposure to 3.3% sevoflurane on postnatal day 2 (P2) or repeated 2-h exposures on P2, P3, and P4. Neurobehavioral tests were used to assess cognitive and fine motor functions. The effects of microglial phagocytosis of OPCs on cerebral myelination were assessed using three-dimensional reconstruction and related biochemical analysis. Our findings indicate that repeated sevoflurane exposure, rather than a single exposure, induced hypomyelination and was associated with persistent cognitive and fine motor deficits. Repeated sevoflurane exposures promoted microglial activation and excessive phagocytosis of OPCs, thereby decreasing the number of oligodendrocytes and impairing developmental myelination. Mechanistically, repeated sevoflurane exposure enhanced CX3CL1/CX3CR1 signaling in neonatal brain tissue. In cultured microglial cells, sevoflurane altered Rac1-related cytoskeletal regulation and increased phagocytic activity. CX3CR1 knockout attenuated the phagocytic ability of microglia and rescued oligodendrocyte myelination and neurobehaviors. This study indicates that CX3CL1/CX3CR1-dependent microglial phagocytosis of OPCs might contribute to sevoflurane-induced myelination impairments in neonatal mice, and provides a potential therapeutic target for preventing anesthesia-induced developmental neurotoxicity. - Source: PubMed
Publication date: 2026/08/06
Lv JiangmingXia ZhangtingWang XinZhao PingWu Ziyi - Little is known about the functional consequences of real-time changes to innate immune-cell states. While chemogenetic tools have become increasingly used for probing immune-brain interactions, the consequences of manipulating myeloid cell activity states remain poorly understood. In this study, we found that acute activation of Gi-coupled DREADDs (hM4Di) in Cx3cr1⁺ myeloid cells severely supresses cardiac function and induces a predominantly anti-inflammatory signalling state in mice. This surprising finding prompted further investigation. Using high-resolution ultrasound and electrocardiography, we show that although Cx3cr1⁺ mice have some reduced cardiac function already prior intervention, activation of hM4Di in Cx3cr1+ cells markedly reduces cardiac output and ejection fraction, and induces arrhythmias and increased heart-rate variability, which is absent in Cx3cr1Cre controls. hM4Di activation leads to decreased soma size, but not number, of IBA1⁺ microglia in the hypothalamus, while sections containing nucleus of the solitary tract remained unaffected. Plasma proteomic profiling using the Olink Mouse Exploratory panel revealed increased IL-10 alongside reductions in IL-23R and CCL20, indicating a shift toward systemic anti-inflammatory signalling. Furthermore, Olink analysis revealed a complex systemic signalling profile characterized by changes in several proteins associated with extracellular matrix remodelling, vascular regulation, and cell death pathways. Collectively, these findings demonstrate that Gi-DREADD inhibition of Cx3cr1⁺ myeloid cells produce coordinated central and peripheral immune changes and causes fatal cardiac dysfunction. - Source: PubMed
Publication date: 2026/09/14
Holde FrederikPedersen Tina MyhreFrandsen Sofie LetThomsen BjarkeMatchkov VladimirKlawonn Anna Mathia - White matter preservation is a rate-limiting factor in neurological recovery after ischemic stroke and depends on efficient clearance of myelin debris by microglia/macrophages. Our prior work demonstrated that microglia/macrophage-specific SIK3 (salt-inducible kinase) knockout (SIK3-mKO) promotes an anti-inflammatory subset, enhances myelin phagocytosis, and limits white matter injury, yet the downstream molecular mechanisms remain undefined. Here, we elucidate a previously unrecognized signaling axis underlying these protective effects. - Source: PubMed
Publication date: 2026/09/11
Mao LeileiWang ChenranWang KeZhong ChenxiShi ZiyuYuan YiwenZheng JiananWu JingjingHe MiaoSun ZeyuGao Yanqin - Microglia play essential yet poorly understood roles in brain development, including axon guidance, regulation of neurogenesis, and pruning of neuronal projections. Congenital hydrocephalus (CH), characterized by enlarged cerebrospinal fluid (CSF)-filled ventricles, is a leading cause of pediatric brain surgery, but its molecular mechanisms remain unclear. We have identified what we believe to be novel, recurrent, damaging missense variants in the SH3-binding domain of the adaptor protein Growth Factor Receptor-Bound Protein 2 (GRB2) in unrelated patients with CH. GRB2 is significantly co-expressed with one of its known upstream receptor tyrosine kinase partners, CSF1R, in the developing human brain, particularly in a microglial subtype associated with regulation of neural stem cells. Immunoprecipitation validated GRB2-CSF1R binding in mouse microglial cells and human monocyte cell line. Cx3cr1-Grb2fl/fl mice engineered with conditional deletion of Grb2 in microglia exhibit congenital absence of microglia and early postnatal severe communicating (non-obstructive) hydrocephalus, mimicking GRB2-mutant patients. The severe ventriculomegaly of Cx3cr1-Grb2fl/fl mice is associated with both depletion of cerebral cortical neurons and impairment of glia-lymphatic-mediated CSF flow. Together, these findings implicate a role of GRB2 in microglia that could be essential for brain development and CSF homeostasis. - Source: PubMed
Publication date: 2026/09/10
Duy Phan QReeves Benjamin CSun HuanxingPeng XueyanKalailingam PazhanichamyAllington GarrettDennis EvanThi Hao LeWang LeiRufino-Ramos DavidZhao ShujuanLi QiangMehta Neel HDavalan William CBlacker MasonPiscopo Anthony JHaider ShozebFan BaojianMekbib Kedous YShao ShuaiNelson-Williams CarolLam TuKiet TKleinstiver Benjamin PMusolino Patricia LAlper Seth LJin Sheng ChihHerzog Erica LKahle Kristopher T