Human CX3CL1 ELISA Kit
- Known as:
- Human CX3CL1 Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- 55r-1578
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- Human CX3CL1 ELISA Kit
Related genes to: Human CX3CL1 ELISA Kit
- Gene:
- CX3CL1 NIH gene
- Name:
- C-X3-C motif chemokine ligand 1
- Previous symbol:
- SCYD1
- Synonyms:
- NTN, C3Xkine, ABCD-3, CXC3C, CXC3, fractalkine, neurotactin
- Chromosome:
- 16q21
- Locus Type:
- gene with protein product
- Date approved:
- 1997-08-22
- Date modifiied:
- 2016-10-05
Related products to: Human CX3CL1 ELISA Kit
Related articles to: Human CX3CL1 ELISA Kit
- Arteriogenic erectile dysfunction (AED) results from insufficient arterial filling of the corpus cavernosum. Its complex pathophysiology is poorly understood, and current treatments have limitations. While electrical stimulation (ES) has been widely applied clinically for male diseases, its therapeutic targets in AED remain unexplored. This study aimed to investigate the hypothesis that ES ameliorates AED by improving the local immune microenvironment and inhibiting the pathological phenotypic transformation of cavernous smooth muscle cells (SMCs). An AED rat model was established via cuff-induced endothelial injury and a high-fat diet. Erectile function, histology, and molecular mechanisms were assessed using intracavernous pressure measurement, infrared thermography, immunohistochemistry, co-immunoprecipitation, and an in vitro macrophage-corpus cavernosum smooth muscle cells (CCSMCs) co-culture system. Our findings demonstrate that ES treatment significantly improved erectile function in the AED rat model. We discovered that macrophages were polarized towards the anti-inflammatory M2 phenotype following ES treatment. This polarization was directly associated with the upregulation of cylindromatosis (CYLD) and the subsequent inhibition of CX3CL1 release. Concurrently, Th2 cytokines released from these M2 macrophages further enhanced P300/Myocardin (Myocd) acetylation in SMCs, which critically inhibited their transformation towards a synthetic phenotype and prevented adverse vascular remodeling. This study demonstrates that crosstalk between macrophages and SMCs is an essential mechanism in ES-treated AED. We verify that ES-induced M2 macrophage polarization inhibits the detrimental phenotypic switching of CCSMCs, thereby preserving vascular integrity and improving erectile function. This process is pivotally regulated by the upregulation of CYLD and reduction of CX3CL1. - Source: PubMed
Publication date: 2026/06/15
Wang GuanboZang ZhenjieLi RuiyuFeng ChenHang XiaomengLiu ShuaiFu Qiang - Epithelial ovarian cancer (EOC) is characterized by aggressive peritoneal dissemination and an immunosuppressive tumor microenvironment in which tumor-associated macrophages (TAMs) play a central role. Chemokine signaling pathways regulate macrophage recruitment and function; however, the contribution of the CX3CL1-CX3CR1 axis to ovarian cancer progression and TAM-mediated effector mechanisms remains unclarified. This study aimed to clarify the role of CX3CL1-CX3CR1 signaling in ovarian cancer progression, focusing on macrophage-derived pro-tumorigenic factors. CX3CL1 and CX3CR1 expression was examined in human EOC and healthy ovarian tissues by real-time polymerase chain reaction and immunohistochemistry. Functional effects of CX3CL1 on ovarian cancer cells were evaluated via migration and proliferation assays in the murine ID8 cell line. An intraperitoneal syngeneic ovarian cancer model was established by injecting ID8 cells into wild-type and Cx3cr1-deficient mice. Tumor burden, ascites formation, survival, macrophage infiltration, and expression levels of matrix metalloprotease-2 (MMP-2) and transforming growth factor-β (TGF-β) were assessed by histological, immunohistochemical, and molecular analyses. CX3CL1 and CX3CR1 expression was significantly upregulated in human EOC tissues and associated with marked macrophage infiltration. CX3CL1 stimulation enhanced migration, but not proliferation, of ID8 cells. Cx3cr1 deficiency significantly suppressed intraperitoneal tumor growth, reduced ascitic fluid volume, and prolonged survival. This was accompanied by reduced CX3CR1 TAM accumulation and decreased MMP-2 and TGF-β expression, which were predominantly produced by infiltrating macrophages. The CX3CL1-CX3CR1 axis promotes ovarian cancer progression by recruiting MMP-2- and TGF-β-producing macrophages. Targeting CX3CR1-dependent TAM functions may represent a therapeutic strategy for limiting peritoneal dissemination in ovarian cancer. - Source: PubMed
Publication date: 2026/06/05
Tanizaki-Horiuchi YukoIshida YukoKobayashi AyaYahata TamakiKuninaka YumiToujima SaoriNosaka MizuhoMatsuki ReikoKimura AkihikoMizoguchi MikaMukaida NaofumiIno KazuhikoKondo Toshikazu - Schizophrenia pathogenesis may involve aberrant synaptic pruning mediated by excessive complement system activity (CSA) and altered microglial function. Microglia and CSA are tightly regulated by neuro-immune regulators (NIREGs) which regulate adverse innate response and play a critical role in the regulation of the synaptic pruning process. This study investigated transcriptional alterations of NIREGs in the brain and blood tissues of individuals living with schizophrenia (SZ individuals) vs. healthy controls (HC). - Source: PubMed
Publication date: 2026/06/11
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Toor FatimaSargsyan ManeAkselrod AbigailZhao ChunfangSen NamitaNasim MansoorStroustrup AnnemariePerveen Shahana - Vascular cognitive impairment (VCI) is a syndrome of cognitive dysfunction attributable to vascular risk factors and cerebrovascular diseases, representing a major component of global dementia burden. Dysglycemia, encompassing diabetes mellitus and impaired glucose regulation, is increasingly recognized as a modifiable risk factor for cognitive decline, particularly VCI. Chronic low-grade inflammation mediates the association between metabolic dysfunction and neurodegeneration. The lack of validated diagnostic tools for early VCI detection in high-risk dysglycemic populations highlights the urgent need for robust diagnostic models based on molecular signatures. - Source: PubMed
Publication date: 2026/05/22
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