Goat Anti-Human CD192, N-terminus
- Known as:
- Goat Antibody toHuman CD192, N-terminus
- Catalog number:
- 129-10110
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Ray Biotech
- Gene target:
- Goat Anti-Human CD192 N-terminus
Related genes to: Goat Anti-Human CD192, N-terminus
- Gene:
- CCR2 NIH gene
- Name:
- C-C motif chemokine receptor 2
- Previous symbol:
- CMKBR2
- Synonyms:
- CC-CKR-2, CKR2, MCP-1-R, CD192, FLJ78302
- Chromosome:
- 3p21.31
- Locus Type:
- gene with protein product
- Date approved:
- 1995-05-30
- Date modifiied:
- 2016-10-05
Related products to: Goat Anti-Human CD192, N-terminus
Related articles to: Goat Anti-Human CD192, N-terminus
- Subarachnoid hemorrhage (SAH) causes long-term cognitive dysfunction due to early brain injury, but effective therapies are limited. Remote ischemic post-conditioning (RIPostC) confers neuroprotection, but its mechanisms remain incompletely understood. Here we show that RIPostC preserves the neurovascular unit by modulating monocyte-derived macrophages (MDMs) via the Gas6/Axl/Vimentin axis. In 405 SAH patients, elevated cerebrospinal fluid leukocyte counts correlate positively with Hunt-Hess and 3-month mRS scores. In a rat SAH model, RIPostC suppresses periventricular CCR2 cell infiltration, reduces MDMs, shifts their polarization from M1-like to M2-like, preserves blood-brain barrier integrity, and improves cognitive function. Mechanistically, RIPostC downregulates Vimentin. However, the Vimentin inhibitor Withaferin A mimics anti-infiltration but does not promote M2-like polarization. RIPostC upregulates neuronal Gas6, which engages MDM Axl. Besides, Gas6 knockdown abolishes RIPostC's protective effects. Additionally, RIPostC selectively expands a reparative Stab1Clec10a MDM subset. In human THP-1 cells, recombinant Gas6 suppresses Vimentin and induces M2-like polarization via Axl, and the Axl inhibitor R428 blocks this effect. Thus, RIPostC enhances neuronal Gas6 to activate MDM Axl and downregulate Vimentin, limiting infiltration and driving reparative polarization, which preserves neurovascular unit integrity and improves cognition after SAH. - Source: PubMed
Publication date: 2026/09/27
Zhu YajunHuang ZichaoRong XiLei XingweiLiang FumingLi XiaoguoZhou JiruWang YuHuang YifanTang ShuangZhong JianjunYan JinDeng HongjiZeng ChunGuo Zongduo - Postoperative peritoneal adhesions arise from a dysregulated wound-healing response in which macrophages may have context-dependent effects. We investigated the contribution of macrophage-rich peritoneal and mesenteric compartments, the origin of macrophage-like cells in ischemic lesions, and the association between CCR2-dependent recruitment and postoperative inflammatory and reparative gene expression. Using a murine ischemic-button model, we assessed the effects of clodronate liposome treatment, bone marrow chimerism, and global CCR2 deficiency. Adhesion formation, F4/80+ cell accumulation, donor-marker expression, and selected inflammatory and wound-healing-associated transcripts were analyzed at predefined postoperative time points. Clodronate liposome treatment was associated with reduced adhesion formation and substantial depletion of F4/80+ cells in peritoneal lavage and mesenteric tissue. However, F4/80+ cell numbers within ischemic buttons at postoperative day 3 were not significantly reduced, indicating that the depletion experiment does not establish selective depletion of all lesional macrophages. Bone marrow chimera experiments identified donor-marker-positive, F4/80+ cells within ischemic buttons, supporting recruitment of hematopoietic cells with a macrophage-like phenotype. CCR2 deficiency reduced F4/80+ cell accumulation in ischemic buttons and was associated with increased adhesion scores and altered expression of inflammatory and wound-healing-associated genes. These findings identify differential associations of clodronate-sensitive macrophage-rich compartments and CCR2-dependent hematopoietic recruitment with postoperative adhesion formation. Depletion of macrophage-rich peritoneal and mesenteric compartments was associated with reduced adhesion formation, whereas global CCR2 deficiency was associated with fewer lesional F4/80+ cells and greater adhesion severity. Because clodronate depletion, F4/80 staining, bone marrow chimerism, and global CCR2 deficiency do not provide cell-specific or fate-mapped resolution, these data do not establish distinct resident versus infiltrating macrophage functions or a reparative phenotype of CCR2-dependent cells. Cell-specific and temporally resolved validation is required to define the contributions and temporal relationships of individual macrophage subsets. - Source: PubMed
Publication date: 2026/09/08
Woestemeier AnnaLysson MariolaBraun LaraJafari AzinLingohr PhilippWehner SvenKalff Jörg CHong Gun-Soo - Lung cancer remains the leading cause of cancer-related mortality worldwide, with metastasis, therapeutic resistance, and an immunosuppressive TME representing major barriers to successful treatment. Among the chemokine signaling networks implicated in these processes, the CCL2-CCR2 axis has emerged as an important regulator of tumor progression. By orchestrating the recruitment of monocytes, tumor-associated macrophages, myeloid-derived suppressor cells, and other stromal components, this pathway can establish an immune-permissive niche that supports angiogenesis, epithelial-mesenchymal transition, extracellular-matrix remodeling, metastatic dissemination, and resistance to chemotherapy, targeted therapies, and immunotherapy. Mechanistically, CCL2-CCR2 signaling interacts with key oncogenic pathways, including PI3K/Akt/mTOR, STAT3, NF-κB, Toll-like receptor signaling, and non-coding RNA-mediated networks, thereby amplifying pro-tumor inflammatory circuits within the lung TME. Although accumulating evidence indicates that the axis can exert context-dependent tumor-suppressive effects under specific biological conditions, such as promoting M1 macrophage recruitment or enhancing antitumor immunity in selected settings, its overall contribution in lung cancer appears predominantly tumor-promoting. This review comprehensively summarizes the molecular mechanisms governing CCL2-CCR2 signaling in primary lung cancer and in lung metastases. We further discuss emerging therapeutic strategies directed at this axis, including CCR2 antagonists, CCL2-neutralizing agents, engineered immune-cell approaches, and rational combinations with immune-checkpoint inhibitors and targeted therapies. Collectively, the current evidence provides a strong biological rationale and preliminary translational support for further investigation of the CCL2-CCR2 axis as a potential therapeutic target and exploratory biomarker in advanced lung cancer. However, clinical validation remains limited, and additional well-designed studies are required to determine whether modulation of this pathway can meaningfully improve patient outcomes. - Source: PubMed
Publication date: 2026/09/10
Huang YujieMa JiaBi JianPingPi GuoliangLi YingPeng YiXiao ChuangyingTuo XiulinHan Guang - Atherosclerotic plaques contain vascular smooth muscle cell (VSMC)-derived populations that no longer fit a simple contractile-versus-synthetic model. Lineage tracing, single-cell transcriptomics, spatial profiling and multimodal surface-protein measurements now show that VSMC-derived cells occupy heterogeneous lesional states with pathogenic, reversible or plaque-stabilizing properties. This diversity creates a translational bottleneck. Intracellular markers and transcriptomic clusters can define state transitions, but they do not by themselves provide handles for live-cell isolation, molecular imaging, targeted delivery or selective intervention. This narrative review examines how VSMC state discovery can be translated into cell-surface signatures and surface-accessible intervention interfaces. We distinguish state/lineage markers, surface identification and sorting signatures, functional surface interfaces, causally supported candidate targets, and intervention-supported surface targets. Current evidence positions CD29, CD90, CD142, and CD200 primarily as tools for live-cell identification, whereas fibroblast activation protein (FAP) represents the most advanced example of an intervention-supported surface target for the depletion of a disease-associated modulated VSMC state. We propose a state-matched framework in which pathogenic states are selectively depleted, plastic or reversible states are modulated or reprogrammed, and matrix-supportive plaque-stabilizing states are preserved. C-C chemokine receptor type 2 (CCR2), guanylyl cyclase-B/natriuretic peptide receptor 2 (GC-B/NPR2), matrix metalloproteinase 14 (S14), and CD47 span different intermediate levels of therapeutic evidence, from targeted delivery to functional surface modulation and causal intervention, whereas CD36, triggering receptor expressed on myeloid cells 2 (TREM2), and integrins remain constrained by incomplete cell-state or lineage specificity. Major barriers include human protein-level and surface validation, state specificity, spatial accessibility and direct therapeutic testing. - Source: PubMed
Publication date: 2026/09/20
Xu YinfeiWang YiWu HuiLi PengfeiZhuang JiaqiShen ZheanLu ZiyiZhang ChengChen Yan - The mechanisms that cause hypertension remain elusive despite more than a century of investigation. Some of its triggers include aging, sex, salt, diet, stress, experience with adversity, socio-cultural-economic disparities, and poor-quality sleep. The renin-angiotensin-aldosterone and the endothelin systems and other hormones contribute to varying degrees to the rise in BP and target organ damage. It has become increasingly recognized that inflammation and the innate and adaptive immune systems play a role in the etiopathogenesis of hypertension. We review here the participation of different cellular and molecular (genetic and epigenetic) mechanisms that play a role in hypertension via the immune system, including neutrophil extracellular traps, memory T cells, and aldosterone-modulated trained immunity mediated by monocytes/macrophages. Molecular mechanisms, including the effects of neutrophil gelatinase-associated lipocalin as an immunomodulator, and the role of isolevoglandins in mediating oxidative stress-induced activation of the adaptive immune system are analysed. We conclude by summarizing potential therapeutic avenues to address inflammation in hypertension. - Source: PubMed
Publication date: 2026/09/18
Fields EviatarBerillo OlgaSchiffrin Ernesto L