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
- The clinical outcomes of trabeculectomy, a standard glaucoma filtration surgery (GFS), have dramatically improved with the introduction of mitomycin C (MMC), an antimetabolite widely used to inhibit postoperative scarring. MMC exerts anti-scarring effects primarily by promoting apoptosis and suppressing fibroblast proliferation at the surgical site. However, despite these beneficial effects, MMC also induces the production of inflammatory cytokines, and its full mechanism of action remains incompletely understood. Moreover, a subset of patients continues to experience poor surgical outcomes even after MMC application, highlighting the need for complementary therapeutic strategies. Comprehensive transcriptomic analysis of postoperative GFS tissues revealed that MMC promoted the expression of genes associated with cellular senescence and inflammatory responses. Supporting this, in vitro experiments suggested that the transcriptional changes were associated with MMC-induced senescence-associated secretory phenotype (SASP)-like changes in the fibroblasts. Single-cell RNA sequencing (scRNA-Seq) analyses of postoperative GFS tissues also revealed that fibroblasts after GFS with MMC secrete SASP factors. Furthermore, Cell-Cell communication analysis identified CCL7 as one of the key molecules involved in inflammatory cell migration and the promotion of fibrosis. Importantly, we demonstrated that fibroblasts exhibiting SASP-like features can be selectively eliminated by a specific senolytic agent, suggesting a novel and promising therapeutic approach that may improve long-term surgical outcomes after GFS. - Source: PubMed
Kimura AkitoshiFujimoto TomokazuIraha SatoshiYasunaga Kei-IchiroInoue-Mochita MiyukiFunagura NaofumiTanigawa ShunsukeKurotaki DaisukeKoga TomoakiWatanabe-Kitamura FumikaTsutsumi-Kuroda UtakoNakao MitsuyoshiInoue Toshihiro - Alveolar microenvironment-driven macrophage polarization critically influences chronic obstructive pulmonary disease (COPD) progression. Nuclear factor erythroid 2-related factor 2 (NRF2), a key transcription factor, regulates macrophage polarization, suppresses inflammation, and promotes cellular repair. However, its role in macrophage-mediated inflammation and metabolic regulation, particularly hyaluronic acid (HA)-related remodeling, remains incompletely defined. This study investigates a novel dimension of NRF2 in COPD pathogenesis through macrophage-specific modulation, aiming to uncover its previously unrecognized mechanism. - Source: PubMed
Publication date: 2026/08/14
Bai GeWang JiaqiWen QianmeiHuang YuningLi HaiqingXu YanhuiLiu YiyiYi ErkangWu FanCui JiedaMei XinyueZhang YuxiaZhou YuminSun RuitingRan Pixin - Intrahepatic cholangiocarcinoma (ICC) presents significant therapeutic challenges due to its late-stage diagnosis and inherent treatment resistance, resulting in dismal prognosis. While ferroptosis induction has emerged as a promising antitumor strategy, its clinical implementation in ICC has been impeded by poorly defined resistance mechanisms. Here, we systematically investigated the immunomodulatory role of the CXCL5/CXCR2 axis in governing ferroptosis susceptibility through dual mechanistical pathways. In vitro studies revealed that CXCL5/CXCR2 signaling confers ferroptosis resistance by transcriptional upregulation of prostaglandin-endoperoxide synthase 2 (PTGS2), which can serve as a functional regulatory factor for ferroptosis. Utilizing a tumor-immune co-culture platform, we further demonstrated that CXCL5/CXCR2 axis-driven recruitment of N2 tumor-associated neutrophils (TANs) orchestrates a protective microenvironment against ferroptosis. Intriguingly, PTGS2 enhances N2 TANs chemotaxis via CCL2 and CCL7, and the recruited N2 TANs subsequently activate the NF-κB/PTGS2 pathway, thereby establishing a synergistic positive feedback loop. Notably, combinatorial treatment with the CXCR2 antagonist SB225002 and ferroptosis inducer Erastin exhibited synergistic antitumor activity in preclinical ICC models. This study provides mechanistic insights into the ferroptosis-immune crosstalk and proposes a novel combinatorial therapeutic paradigm for overcoming treatment resistance in ICC. - Source: PubMed
Publication date: 2026/08/17
Ye ChanqiLin KefengYang ShuyaoZhang YanGao WenliChen JiaqiDong YingBai RuiTian YangWang MinghaoYuan ZhijunMa YuxiaoHe YuqinChen RuyinFu WenguangJiang QiLi QiongRuan Jian - Atrophic non-union is a significant clinical challenge associated with impaired early inflammation resolution and delayed osteogenesis. Although the osteoimmune microenvironment is critical for bone healing, the specific molecular mechanisms regulating this process require further elucidation. - Source: PubMed
Publication date: 2026/07/20
Zhong KaiShao YufeiZhou YuHuang ZengyiLiu Xing - Immune-resistant colorectal cancer (irCRC), represented by microsatellite stable/proficient mismatch repair (MSS/pMMR) tumors, responds poorly to immune checkpoint blockade (ICB). Here, we developed an ultrasound-targeted nanodroplet destruction (UTND) strategy combined with surface anti-PD-L1-decorated nanodroplets (PPP@P@map) to enhance ICB responsiveness in MSS colorectal cancer. In CT26 and CMT93 murine subcutaneous MSS colorectal cancer models, PPP@P@map combined with UTND markedly suppressed tumor growth compared with control treatments. Single-cell RNA sequencing identified CAF_Pi16 as a candidate therapy-associated cancer-associated fibroblast subset that showed a treatment-related increase after PPP@P@map + UTND, which was further supported by flow cytometry and multiplex immunofluorescence validation. Mechanistically, UTND induced oxidative stress in tumor cells and promoted the generation of advanced glycation end products (AGEs), which activated the AGE-RAGE/PKCα/NF-κB pathway in CAF_Pi16 and increased CCL7 secretion. CAF_Pi16-derived CCL7 provided a CCR2-dependent functional cue to CD8 T cells. In purified CD8 T cells, CCL7 activated NF-κB-related signalling, enhanced activation and cytotoxic effector features, and promoted NKG2D expression; these effects were attenuated by CCR2 blockade or NF-κB inhibition. Functionally, CCL7 enhanced CD8 T cell-mediated tumor-cell killing, whereas NKG2D blockade reduced this effect and weakened the antitumor efficacy of PPP@P@map + UTND in vivo. Together, these findings reveal a UTND-induced tumor cell-CAF_Pi16-CCL7-CD8+ T-cell signalling axis that enhances NKG2D-associated antitumor immunity and provides a mechanistic basis for further investigation of UTND-based strategies to improve ICB responsiveness in MSS/pMMR colorectal cancer. - Source: PubMed
Publication date: 2026/07/29
Tuo BaojingLi NaLiu SenboGao ShuochenLiu HangPei LipingGao XueyanLi KaiboXu YanxinSun ZhenqiangZhang YanLiu LinWang Chengzeng