Ask about this productRelated genes to: MCP3 antibody
- Gene:
- CCL7 NIH gene
- Name:
- C-C motif chemokine ligand 7
- Previous symbol:
- SCYA6, SCYA7
- Synonyms:
- MCP-3, NC28, FIC, MARC, MCP3
- Chromosome:
- 17q12
- Locus Type:
- gene with protein product
- Date approved:
- 1993-11-04
- Date modifiied:
- 2016-10-05
Related products to: MCP3 antibody
Related articles to: MCP3 antibody
- Interstitial cystitis/bladder pain syndrome (IC/BPS) is a chronic inflammatory condition with limited treatments. Although macrophages are implicated in its pathogenesis, the mechanisms driving their phenotypic switching remain unclear. This study identifies CCR1's role in IC/BPS and evaluates CCR1 inhibition as a therapeutic strategy. Integrated bulk and single-cell RNA sequencing reveal enrichment of pro-inflammatory CCR1⁺ macrophages in bladder tissue from patients with IC/BPS. In a lipopolysaccharide-induced rat model, pharmacological inhibition of CCR1 suppresses M1 polarization, promotes M2 polarization, and improves pain thresholds, urinary symptoms as well as bladder inflammation. Mechanistically, CCR1 knockdown enhances FOXO1 phosphorylation and degradation, reduces its nuclear translocation, and activates PPARγ signaling to promote M2 polarization. Analysis of clinical samples shows increased CCL7 levels in bladder tissue and urine, with urinary levels correlating with symptom severity. These findings identify CCR1 as a candidate target for further therapeutic evaluation in IC/BPS. - Source: PubMed
Publication date: 2026/05/09
Luo RuixiangLi WenshuangLiu BolongHuang JunlongDing HongluZhang ChiLi XiaoyangWang ZiqiaoLiu ZhengZhou XiangfuChen Jialiang - Radiofrequency microneedling (RFMN) is an emerging therapeutic approach that enhances skin rejuvenation by delivering targeted thermal injury to the dermal and subdermal layers while sparing the epidermis. However, the molecular mechanisms underlying its biological effects especially in comparison to medical microneedling remain poorly understood. In this study, we aimed to investigate, for the first time, the molecular and histological responses to RFMN using a standardized three-dimensional (3D) human skin model. As a secondary objective, we assessed the modulatory effects of RFMN aftercare treatment with a dexpanthenol-containing ointment. - Source: PubMed
Publication date: 2026/04/22
Huth SebastianMarquardt YvonneHuth LauraDjahed SinaBaron Jens Malte - Platelet-rich fibrin (PRF) is extensively utilized to enhance localized tissue healing, a process that critically depends on the transient polarization of macrophages toward a pro-inflammatory phenotype. Given that PRF, like other blood clot derivatives, may intrinsically modulate macrophage behavior, we conducted a comprehensive screening assay to characterize the global macrophage response to PRF exposure. To this end, we employed two widely used monocytic cell lines-U937 (histiocytic lymphoma) and THP-1 (acute monocytic leukemia)-as models to investigate macrophage responses. Cells were exposed to lysates derived from PRF, and transcriptomic alterations were profiled using bulk RNA sequencing. Differential gene expression analysis was performed, with significance determined by an adjusted p-value threshold of <0.05. In U937-derived macrophages, gene expression profiling revealed a transcriptional signature consistent with inflammatory activation. Clustering of upregulated genes highlighted pathways associated with chemokine activity (e.g., CCL2, CCL3, CCL4, CCL5, CCL7, CCL8, CCL20, CCL23, CCL26, CXCL5, CXCL6, CXCL8, CXCL16, and PPBP), RAGE receptor binding (FPR1, S100A8, S100A9, and S100A12), IgG binding (FCGR1A, FCGR2A, FCGR2B, and FCGR3A), prostaglandin biosynthesis (CBR1, CD74, EDN1, FABP5, IL1B, MIF, PTGES, and PTGS1), and collagen catabolism (CTSL, FAP, MMP3, MMP7, MMP9, MMP12, MMP14, MMP19, and MRC2). In contrast, PRF exposure in THP-1 cells primarily enriched genes involved in steroid biosynthesis, suggesting a more limited or distinct response. These findings underscore U937 cells as a more responsive and appropriate bioassay for modeling inflammatory macrophage polarization in response to PRF. Moreover, the identified gene signatures recapitulate key aspects of early wound healing, providing a relevant platform for studying macrophage reactivation in chronic wound environments. - Source: PubMed
Publication date: 2026/04/22
Panahipour LaylaHuang XiaoyuZampino FrancescaMiron Richard JGruber Reinhard - Ovarian cancer (OC) remains a malignancy characterized by obscure risk factors and unfavorable prognosis. While 3-tert-butyl-4-hydroxyanisole (3-BHA) is suspected of exerting toxic effects on ovarian health, the precise molecular mechanisms underlying its impact remain elucidated. This study aims to systematically investigate the potential pathogenic mechanisms of 3-BHA in the progression of OC.Integrated transcriptomic data from the GEO database (GSE18520 and GSE40595) were analyzed. A synergistic computational framework was employed, incorporating Differentially Expressed Genes (DEGs) identification, Weighted Gene Co-expression Network Analysis (WGCNA), multiple machine learning algorithms, and SHapley Additive exPlanations (SHAP) analysis to achieve high-interpretability feature selection.Five hub genes-CXCR4, CCL7, CXCL8, CXCR2, and CX3CL1-were identified, all demonstrating robust diagnostic efficacy with AUC values of 0.911, 0.882, 0.823, 0.772, and 0.837, respectively. Prognostic profiling via GEPIA3 highlighted CXCR2 overexpression as a potential critical biomarker driving poor clinical outcomes in OC. Furthermore, molecular docking validated the strong binding affinity of 3-BHA with CX3CL1 and CXCR2. Subsequent 100 ns molecular dynamics simulations and thermodynamic stability assessments confirmed the structural stability of the 3-BHA-CXCR2 complex.By integrating bioinformatics and computational toxicology, this study deciphers the potential mechanistic landscape through which 3-BHA influences OC. These findings not only refine the toxicological understanding of 3-BHA but also provide novel candidates for early diagnosis and prognostic risk stratification in OC. - Source: PubMed
Publication date: 2026/05/03
Shi YifeiNiu DongJin Chunhui - Urinary tract infections (UTIs) caused by uropathogenic (UPEC) are prevalent among women. UPEC infection can lead to kidney injury, and currently, there are no effective methods to mitigate this damage. Previous studies have shown that macrophage infiltration is closely associated with kidney injury induced by UTIs. However, the mechanisms underlying macrophage recruitment to the kidneys remain unclear. In this study, IL-17B may play a critical role in protecting against UPEC-induced kidney injury by modulating macrophage infiltration and bacterial colonization. Compared with wild-type (WT) mice, IL-17B mice exhibited significantly higher mortality and more M1-type macrophage infiltration, which was associated with renal injury. rIL-17B treatment significantly reduced macrophage infiltration in the kidneys of CFT073-infected mice. Additionally, analysis of chemokines indicated that IL-17B is a key regulator of macrophage recruitment by influencing the expression of CCL2, CCL3, and CCL7. Overall, IL-17B can serve as a crucial cytokine for treating urinary tract infections and mitigating kidney damage. - Source: PubMed
Publication date: 2026/05/01
Wang ChangyingLiu MinWang LuyueZhang YixinNiu ZihanLiu XueXiong Huabao