JOURNAL OF HEPATOLOGY
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2019
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IF 18.946
Shaoping She,Xiaoning Wu,Danfeng Zheng,Xiaolei Pei,Jing Ma,Yameng Sun,Jialing Zhou,Lin Nong,Changyuan Guo,Ping Lv,Quansheng Song,Can Zheng,Weiwei Liang,Shiyang Huang,Qingqing Li,Zhongtian Liu,Zhanming Song,Yuzi Li,Yu Zhang,Wei Kong,Hong You,Jianzhong Xi,Ying Wang
Background & Aims C-C motif chemokine receptor 2 (CCR2) has been recognized as a promising target for the treatment of liver fibrosis. PC3-secreted microprotein (PSMP)/microseminoprotein (MSMP) is a novel chemotactic cytokine and its receptor is CCR2. In the present study we investigated the expression and role of PSMP in liver fibrosis/cirrhosis. Methods PSMP expression was studied in patients with fibrosis/cirrhosis and in 3 murine models of liver fibrosis, including mice treated with carbon tetrachloride (CCl 4 ), bile-duct ligation, or a 5-diethoxycarbonyl-1,4-dihydrocollidine diet. The role of PSMP was evaluated in Psmp -/- mice and after treatment with a PSMP antibody in wild-type mice. The direct effects of PSMP on macrophages and hepatic stellate cells were studied in vitro . Results In this study, we found that PSMP was highly expressed in fibrotic/cirrhotic tissues from patients with different etiologies of liver disease and in the 3 experimental mouse models of fibrosis. Damage-associated molecular pattern molecules HMGB-1 and IL-33 induced hepatocytes to produce PSMP. PSMP deficiency resulted in a marked amelioration of hepatic injury and fibrosis. In CCl 4 -induced hepatic injury, the infiltration of macrophages and CCR2 + monocytes into the liver was significantly decreased in Psmp -/- mice. Consistent with the decreased levels of intrahepatic macrophages, proinflammatory cytokines were significantly reduced. Moreover, adeno-associated virus-8 vectors successfully overexpressing human PSMP in Psmp -/- mouse livers could reverse the attenuation of liver injury and fibrosis induced by CCl 4 in a CCR2-dependent manner. Treatment with a specific PSMP-neutralizing antibody, 3D5, prevented liver injury and fibrosis induced by CCl 4 in mice. At the cellular level, PSMP directly promoted M1 polarization of macrophages and activation of LX-2 cells. Conclusion PSMP enhances liver fibrosis through its receptor, CCR2. PSMP is a potentially attractive therapeutic target for the treatment of patients with liver fibrosis. Lay summary Our present study identifies the essential role of the protein PSMP for the development and progression of liver fibrosis in humans and mice. PSMP promotes liver fibrosis through inflammatory macrophage infiltration, polarization and production of proinflammatory cytokines, as well as direct activation of hepatic stellate cells via its receptor CCR2. A PSMP antibody can significantly reduce liver fibrosis development in vivo . These findings indicate that PSMP is a potential therapeutic target and its antibody is a potential therapeutic agent for the treatment of liver fibrosis.
研究领域:
肝病学
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免疫学
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分子生物学
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药理学
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DOI
PubMed
高影响因子
MOLECULAR PHARMACEUTICS
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2018
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IF 4.556
Song Shen,Yue Zhang,Kai-Ge Chen,Ying-Li Luo,Jun Wang
Accumulating evidence has confirmed that malignant tumors have a complex microenvironment, which consists of a heterogeneous collection of tumor cells and other cell subsets (including the full gamut of immune cells). Tumor-associated macrophages (TAMs), derived from circulating Ly6Chi monocytes, constitute the most substantial fraction of tumor-infiltrating immune cells in nearly all cancer types and contribute to tumor progression, vascularization, metastasis, immunosuppression, and therapeutic resistance. Interrupting monocyte recruitment to tumor tissues by disturbing pivotal signaling pathways (such as CCL2-CCR2) is viewed as one of the most promising avenues for tumor microenvironment manipulation and cancer therapy. One critical issue for monocyte-based therapy is to deliver therapeutic agents into monocytes efficiently. In the present study, we systematically investigated the relationship between the surface potential and the biodistribution of polymeric nanoparticles in monocytes in vivo, aiming to screen and identify an appropriate delivery system for monocyte targeting, and we found that cationic nanoparticles have a higher propensity to accumulate in monocytes compared with their neutral counterparts. We further demonstrated that siCCR2-encapsulated cationic nanoparticle (CNP/siCCR2) could modify immunosuppressive tumor microenvironment more efficiently and exhibit superior antitumor effect in an orthotopic murine breast cancer model.
研究领域:
纳米技术
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肿瘤学
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免疫疗法
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分子生物学
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产品关联
DOI
PubMed
高影响因子
PHYTOMEDICINE
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2024
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IF 6.7
Heung Lam MOK,Ka Wing CHENG,Yiqi XU,Chunhua HUANG,Cheng LYU,Jiaruo XU,Die HU,Lin ZHU,Chengyuan LIN,Hor-Yue TAN,Zhaoxiang BIAN
Background Ulcerative colitis (UC) is associated with intestinal macrophage infiltration due to disruption of the mucosal barrier and bacterial invasion. Therefore, it is crucial to identify therapeutic agents capable of attenuating the macrophage-induced inflammatory response to preserve mucosal homeostasis and immune tolerance. The modified Zhenwu decoction (CDD-2103) is a novel herbal formulation developed based on the principles of Traditional Chinese medicine. To date, there are no clinically approved herbal formulations for UC with a well-known mechanism of action on macrophages. Purpose The objective of this study was to systematically investigate the inhibitory effect of the active fraction of CDD-2103 in a mouse model of chronic colitis and delineate the mechanisms underlying its inhibitory action. Methods CDD-2103 was extracted into four fractions using organic solvents with increasing polarity. A chronic 49-day dextran sulfate sodium (DSS)-induced colitis mice model, closely resembling human clinical conditions, was used to examine the effect of CDD-2103 on chronic colitis. To confirm the effect of CDD-2103 on macrophages in this chronic colitis model, adoptive macrophage transfer and CCL2 supplementation were conducted. The mechanisms of action of CDD-2103 were further elucidated utilizing bone marrow-derived macrophages (BMDMs). Transcriptome analysis was conducted to gain insights into the underlying mechanism of action of CDD-2103 in BMDMs. Results Our in vitro and in vivo findings demonstrated that the ethanol-enriched fraction of CDD-2103 exhibited significant anti-inflammatory effects, leading to the suppression of colitis severity. This effect was associated with diminished accumulation of colonic macrophages in the lamina propria of CDD-2103-intervened colitis mice. Specifically, CDD-2103 inhibited CCR2/L2-mediated proinflammatory macrophage infiltration into the colon without affecting macrophage proliferation. Mechanistically, CDD-2103 inhibited Fyn expression-mediated p38 MAPK activation and subsequently suppressed CCR2 expression in BMDMs. Conclusions Collectively, our study supports the potential use of CDD-2103 to limit macrophage infiltration, thereby reducing inflammation during UC treatment. CDD-2103 and the components in the ethanolic fraction are promising candidates for the development of novel drugs for UC management. Additionally, our study underscores Fyn-mediated CCR2 expression as a potential therapeutic target for the management of UC.
研究领域:
药理学
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免疫学
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中医药
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炎症性肠病
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分子生物学
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DOI
PubMed
高影响因子
Advanced Healthcare Materials
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2025
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IF 9.6
Meng Yan,Yuan Zhong,Sheng Ni,Shirong Zhang,Yingying Jiang,Li Zhu,Kun Zhang,Kaiyong Cai,Kai Qu,Chuanwei Li,Wei Wu
Atherosclerosis (AS) is a prevalent chronic inflammatory disease characterized by excessive accumulation of reactive oxygen species (ROS) and persistent inflammation. Polyphenolic natural antioxidants possess strong ROS-scavenging properties. However, the poor targeting ability and rapid metabolism greatly limit their further clinical applications. To this end, a multifunctional biomimetic nanoplatform (CCR2@NPs) is developed by engineering macrophage membranes with the overexpressed C-C chemokine receptor 2 (CCR2) and subsequently enhances the target delivery to inflammatory lesions of AS via the C-C motif ligand 2 (CCL2)/CCR2 chemotactic signaling pathway for significantly improving drug bioavailability. In pathological local lesions, CCR2@NPs can effectively scavenge the excessive ROS, alleviate vascular injury, and finally inhibit AS progression. This strategy enables precise, synergistic therapy and offers new insights into the potential treatment approaches for AS.
研究领域:
心血管病学
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纳米医学
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炎症生物学
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氧化应激
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药物递送系统
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生物材料
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转化医学
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DOI
PubMed
高影响因子
Science Advances
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2025
·Vol. 11
·期 30
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IF 12.5
Weichen Xu,Shaoyue Li,Xuexia Shan,Qiao Wang,Xinhua Chen,Shengbo Wu,Yincheng Gao,Dandan Shan,Shisi Ding,Weiwei Ren,Xiaodong Hou,Shuo Liu,Taixia Wang,Yuting Shen,Zhiyuan Niu,Huixiong Xu,Liping Sun,Wenwen Yue
Pancreatic ductal adenocarcinoma (PDAC) is a highly lethal malignancy with pronounced resistance to conventional therapies. Irreversible electroporation (IRE) is a promising therapy for PDAC; however, its clinical efficacy is limited by a high recurrence rate. Here, using a preclinical PDAC model, we characterized the tumor immune microenvironment following insufficient IRE (iIRE) through single-cell RNA sequencing. We found that iIRE induces a CCR2 + tumor-associated macrophage (CCR2 + TAM)–mediated immunosuppressive microenvironment in residual tumors. Consequently, we developed a macrophage-based proteolipid vesicle (mPLV) coencapsulating the CCR2 antagonist PF-4136309 (PF) and gemcitabine (GEM), named PF/GEM@mPLV. Our findings suggest that PF/GEM@mPLV achieves high drug accumulation within tumors through iIRE-induced inflammation. Reduction of CCR2 + TAMs enhances antitumor immunity and improves chemotherapeutic response. PF/GEM@mPLV markedly inhibits tumor recurrence following iIRE, diminishes hepatic metastases, and prolongs survival in preclinical PDAC models. These findings uncover the role of CCR2 + TAMs in iIRE-induced immunosuppression, offering a promising strategy to enhance the clinical potential of IRE in PDAC.
研究领域:
肿瘤学
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免疫学
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生物工程
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分子生物学
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医学研究
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产品关联
DOI
PubMed
高影响因子
Acta Biomaterialia
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2023
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IF 9.7
Xinyu Zhang,Xueli Xu,Huimin Liu,Nengyi Ni,Shuangqing Liu,Yufang Gong,Guiqi Ma,Linlin Song,Qingwei Meng,Qing Fan,Xiao Sun
Ferroptosis-based nanoplatforms have shown great potential in cancer therapy. However, they also face issues such as degradation and metabolism. Carrier-free nanoplatforms consisting of active drugs can effectively avoid the security issues associated with additional carrier ingredients. Herein, a biomimetic carrier-free nanoplatform ( [email protected] ) was designed to treat cancer by modulating cascade metabolic pathways of ferroptosis. CCR2-overexpressing macrophage membrane-modified HESN can target cancer cells via the CCR2-CCL2 axis. The acidic tumor microenvironment (TME) can disrupt the supramolecular interaction of HESN, releasing hemin and erastin. Then, erastin could induce cancer cells ferroptosis by inhibiting system X C − pathways, while hemin, a vital component of blood to transport oxygen, could be broken down by heme oxygenase-1 (HO-1), increasing the intracellular Fe 2+ concentration to induce cancer cells' ferroptosis further. Meanwhile, erastin could enhance the activity of HO-1, further promoting the release of Fe 2+ from hemin. As a result, [email protected] demonstrated superior therapeutic efficacy in both primary and metastatic tumors in vitro and in vivo . The carrier-free [email protected] provided cascade ferroptosis tumor therapy strategies for potential clinical application. Statement of significance CCR2-overexpressing biomimetic carrier-free nanoplatform ( [email protected] ) was designed for cancer treatment by modulating metabolic pathways of ferroptosis. HESN modified with CCR2-overexpressing macrophage membrane can target tumor cells via the CCR2-CCL2 axis. HESN was composed of hemin and erastin without additional vectors. Erastin could directly induce ferroptosis, while hemin could be broken down by heme oxygenase-1 (HO-1), increasing the intracellular Fe 2+ concentration to enhance ferroptosis further. Meanwhile, erastin could improve the activity of HO-1, promoting the release of Fe 2+ from hemin. Therefore, [email protected] with good bioavailability, stability, and simple preparation can realize cascade ferroptosis tumor therapy and have the potential prospect of clinical translation.
研究领域:
癌症治疗
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纳米技术
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药学
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生物医学工程
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细胞生物学
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产品关联
DOI
PubMed
高影响因子
Cell Reports Medicine
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2025
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IF 10.6
Chengbin Ding,Guofeng Tang,Yan Sun,Xiaodong Fu,Ye Tian,Jiamian Zhan,Songtao Zhang,Xianglong Xing,Jianing Liu,Xiaozhong Qiu,Leyu Wang
C-C chemokine receptor type 2 (CCR2 − ) cardiac-resident macrophages (CCR2 − cRMs) are known to promote cardiac repair after myocardial infarction (MI). However, the substantial depletion and slow recovery of CCR2 − cRMs pose significant barriers in cardiac recovery. Here, we construct a functional conductive cardiac patch (CCP) that can provide exogenously elastic conductive microenvironment and induce endogenously reparative microenvironment mediated by CCR2 − cRMs for MI repair. This CCP exhibits suitable mechanical properties, conductivity, and high water retention, reminiscent of natural myocardium, which can actively engage in modulating CCR2 − cRM renewal and their cell crosstalk. The functional CCP can promote the expression of Connexin43 between CCR2 − cRMs and cardiomyocytes (CMs) and regulate paracrine signaling to activate epicardial cell epithelial-to-mesenchymal transition (EMT) toward endothelial cells using rat and Wt1 CreERT2 transgenic lineage tracing mice. Overall, this study provides a promising strategy to construct a synergistic reparative microenvironment for MI repair.
研究领域:
心血管研究
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组织工程
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免疫学
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细胞生物学
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产品关联
DOI
PubMed
高影响因子
EXPERIMENTAL ANIMALS
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2024
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IF 2.2
Xinpeng WANG,Linguo XIE,Chunyu LIU
CCR2 (C-C chemokine receptor type 2) is a monocyte chemokine associated with oxidative stress and inflammation. Kidney stones (KS) are composed of calcium oxalate (CaOx), which trigger renal oxidative stress and inflammatory. This study aims to evaluate the effects of CCR2 on KS in vivo and in vitro. Eight-week-old male C57BL/6J mice were intraperitoneally injected with glyoxylate (GOX) daily to establish a KS model, and along with CCR2 antagonist (INCB3344) treatment on days 2, 4, and 6. The results showed that CCR2 antagonist reduced renal injury markers (blood urea nitrogen and serum creatinine), alleviated renal tubular injury and CaOx crystal deposition. CCR2 antagonist also decreased CCR2 expression induced by GOX treatment and increased Nrf2 expression. GOX treatment promoted malondialdehyde (MDA) production, decreased glutathione (GSH) content, and inhibited catalase (CAT) and superoxide dismutase (SOD) activity, however, CCR2 antagonist attenuated the above effects of GOX. CCR2 antagonist had inhibitory effects on GOX-induced inflammatory cytokine expression (IL1B, IL6 and MCP1), and inhibited apoptosis by increasing Bcl-2 expression and decreasing Bax and cleaved-caspase 3 expression. In vitro experiments were performed by co-culture model of CaOx-induced damaged HK-2 cells and macrophage-like THP-1 cells. CCR2 antagonist inhibited CaOx-induced THP-1 cell M1 polarization by decreasing the TNF-α, IL6 and iNOS levels, and further alleviated CaOx-induced oxidative stress damage, inflammatory response and apoptosis of HK-2 cells. The study suggests that CCR2 antagonist may be resistant to CaOx crystals-induced oxidative stress and inflammation by inhibiting macrophage M1 polarization.
研究领域:
药理学
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肾病学
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炎症
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氧化应激
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细胞生物学
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产品关联
DOI
PubMed
高影响因子
Evidence-based Complementary and Alternative Medicine
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2021
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IF 2.63
Xubin Bao,Cai Chen,Liyong Yuan
Triptolide (T10) is a common anti-inflammatory and analgesic drug. However, the activation of microglia and elimination of the corresponding inflammatory response are new targets for the treatment of neuropathic pain. Chemokine CCL (CCL2) is a key mediator for activating microglia. In this study, the effects of triptolide on the activation and polarization of microglia cells and CCL2 and its corresponding receptor, chemokine receptor 2 (CCR2), were mainly discussed. Microglia were stimulated with 1 μg/mL lipopolysaccharide (LPS) and pretreated with 10, 20, and 40 nM T10 and CCR2 antagonist (RS102895), respectively. The quantitative polymerase chain reaction (QPCR) and western blot results showed that T10 could obviously inhibit the upregulation of CCL2 and CCR2 induced by LPS stimulation in microglia cells, inhibit the fluorescence intensity of glial fibrillary acidic protein (GFAP) and inducible nitric oxide synthase (iNOS) antibody immunostaining in cells, and upregulate the fluorescence intensity of arginase 1 antibody in cells. The expression of interleukin-6 (IL-6), interleukin-1β (IL-1β), and tumor necrosis factor-α (TNF-α) was inhibited in a dose-dependent manner. RS102895 can significantly reverse the activation and M2 polarization of microglia pretreated with 40 nM T10 and weaken the anti-inflammatory effect of T10. The addition of CCL2 did not extremely affect the function of RS102895. T10 may inhibit microglia activation and M1 polarization by inhibiting the expression of CCL2 and CCR2, promoting M2 polarization, reducing the level of inflammatory factors in cells, and exerting its analgesic effect, which is worthy of clinical promotion as a drug for neuropathic pain.
研究领域:
药理学
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神经科学
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免疫学
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DOI
PubMed
高影响因子
JOURNAL OF NANOBIOTECHNOLOGY
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2026
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IF 15
Yang Hang,Jinghan Yang,Xiaoquan Wei,Xiaojing Li,Min Xu,Yuxuan Chen,Weiwei Chen,Genhong Yao,Xiaojun Tang,Xiaojuan Han,Min Nie,Lingyun Sun
Lupus nephritis (LN) is a common renal complication of systemic lupus erythematosus, and its severity is closely correlated with disease prognosis. Conventional therapy for LN faces challenges including multiple side-effects caused by systemic administration and low drug delivery efficiency due to lack of organ targeting. Herein, we designed a renal-targeted delivery platform based on C-C Motif Chemokine Receptor 2 (CCR2)-C-C Motif Chemokine ligand 2 chemotaxis, constructed by engineering CCR2-overexpressing mesenchymal stromal cell-derived EVs loaded with mycophenolic acid (MPA)-encapsulated MSNs (MPA@CMSNs). In LN models, MPA@CMSNs enabled efficient delivery of MPA into renal region and significantly alleviated kidney inflammation. Mechanistically, MPA@CMSNs effectively inhibited the proliferation and differentiation of proinflammatory immune cells, while concurrently suppressing the Dectin3/NF-κB signaling pathway in macrophages to remodel and optimize the renal immune microenvironment. Collectively, our findings present an efficient renal-targeted strategy with profound therapeutic efficacy against LN, offering a promising approach for targeted disease treatment.
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PubMed
高影响因子
LIFE SCIENCES
·
2026
·
IF 6.4
Jun Zhou,Haojie Jin,Yifan Zheng,Kunying Ding,Yu Long,Chenjie Yu,Yueran Zhang,Fen Zhuge,Minhua Chen,Zhengwei Fu,Yinhua Ni
Cyclo(Val-Pro) and cyclo(Phe-Phe) ameliorate metabolic disorders and inflammation. • Cyclo(Val-Pro) and cyclo(Phe-Phe) target chemokine signaling in the liver. • Cyclo(Val-Pro) and cyclo(Phe-Phe) regulate macrophage infiltration/polarization. • Cyclo(Val-Pro) targets CCR2 and cyclo(Phe-Phe) targets ADCY7 in macrophages. Metabolic dysfunction-associated steatotic liver disease (MASLD), hallmarked by hepatic metabolic disorders and chronic inflammation, is a growing global public health threat with limited approved pharmacological options. Natural cyclodipeptides exhibit favorable metabolic stability and bioactivity profiles, making them ideal molecules for drug discovery in metabolic diseases; however, their roles and mechanisms in MASLD remain poorly defined. Here, we investigated the protective effects of cyclo(Val-Pro) and cyclo(Phe-Phe), two bioactive cyclodipeptides previously identified in hydrolyzed chicken meat extract (HCE), against MASLD. Administration of both cyclodipeptides effectively ameliorated metabolic disturbance and hepatic inflammation in high-fat diet-induced MASLD mice, and mitigated lipopolysaccharide-triggered acute inflammation in a complementary in vivo model. Liver transcriptomic analysis revealed that the two cyclodipeptides significantly modulated the hepatic chemokine signaling pathway in MASLD mice. Mechanistically, both cyclodipeptides reduced hepatic CD11b- and F4/80-associated signals and modulated macrophage-associated pro-inflammatory and anti-inflammatory marker expression in vivo and in vitro. Further validation using molecular docking, target inhibitor intervention, drug affinity responsive target stability, cellular thermal shift assay, site-directed mutagenesis, and gene knockout approaches supported that cyclo(Val-Pro) regulated the expression of macrophage C C chemokine receptor type 2 (CCR2), while cyclo(Phe-Phe) modulated adenylyl cyclase 7 (ADCY7), an upstream chemokine signaling regulator, to block downstream inflammatory cascades. Collectively, our findings support further investigation of these two cyclodipeptides and suggest that CCR2- and ADCY7-associated pathways may contribute to their effects in MASLD. Cyclo(Val-Pro) and cyclo(Phe-Phe) ameliorated metabolic dysfunction, hepatic steatosis, and inflammation in HFD-induced MASLD mice, accompanied by attenuation of hepatic macrophage-associated inflammatory signals. These effects may be associated with distinct CCR2- and ADCY7-associated signaling pathways and reduced chemokine-related responses. Download: Download high-res image (145KB) Download: Download full-size image
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DOI
高影响因子
Theranostics
·
2026
·Vol. 16
·期 13
·7388
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IF 14.9
Yuqi Zhao,Tao Xie,Yanming Ma,Yuhao Wang,Shenghang Liu,Hui Li,Youjun Liu,Renfeng Liu,Hailiang Xu,Cheng Ju,Weidong Wu,Yifan Wang,Siyuan He,Rongjin Luo,Dageng Huang,Shuaijun Jia,Chunping Hu,Liang Yan,Zhiyuan Wang,Lei Zhu
Rationale Spinal cord injury (SCI) triggers a complex secondary injury process characterized by inflammation, neuronal loss, extracellular matrix (ECM) disruption, and limited endogenous repair. Although cell-based therapies hold potential for SCI treatment, their efficacy is often constrained by poor lesion targeting, inadequate persistence after delivery, and limited temporal control over therapeutic factor release. Methods To address these limitations, we developed a macrophage-based mRNA delivery platform by electroporating CCR2 positive (CCR2 + ) macrophages with ANXA1, GDNF, and CTGF mRNAs. In vitro , we assessed transfection efficiency, cell viability, secretion kinetics of therapeutic proteins, anti-inflammatory activity, and neuroprotective and regenerative effects. In vivo , using a mouse SCI model, we evaluated lesion-site accumulation, inflammatory regulation, tissue repair, electrophysiological recovery, transcriptomic alterations, and behavioral outcomes. Results Following electroporation, CCR2⁺ macrophages efficiently expressed ANXA1, GDNF, and CTGF while maintaining high viability, with no marked shift toward CD86- or CD206-associated phenotypes. These engineered macrophages showed enhanced accumulation at the lesion site and sustained therapeutic protein secretion for up to 14 days. In vitro , they protected neuronal cells against oxidative stress-induced injury and promoted neurite outgrowth. In vivo , they attenuated inflammation, improved the local repair microenvironment, and promoted axonal regeneration, remyelination, and ECM remodeling, accompanied by partial recovery of electrophysiological and motor function after SCI. RNA-seq analysis further supported broad changes in pathways related to immune regulation, neural repair, myelination, and matrix remodeling. Conclusions CCR2-enriched macrophages engineered with reparative mRNAs may represent a promising treatment strategy for SCI. By linking CCR2-associated lesion accumulation with multimodal reparative activity, this cell-based platform provides a potential approach for coordinated microenvironmental regulation and tissue repair.
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DOI
PubMed
高影响因子
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