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C-X3-C motif chemokine ligand 1/receptor 1 regulates the M1 polarization and chemotaxis of macrophages after hypoxia/reoxygenation injury

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Chronic Diseases and Translational Medicine 2021年第4期7卷 254-265页

作者： Shuiming Guo Lei Dong Junhua Li Yuetao Chen Ying Yao Rui Zeng Nelli Shushakova Hermann Haller Gang Xu Song Rong Department of Nephrology Division of Internal MedicineTongji HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhanHubei 430030China Department of Respiratory Division of Internal MedicineTongji HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhanHubei 430030China Department of Nephrology Hannover Medical SchoolHannover 30625Germany

Background:macrophages play an important role in renal ischemia reperfusion injury,but the functional changes of macrophages under hypoxia/reoxygenation and the related mechanism are unclear and need to be further clarified.Methods:The effects of hypoxia/reoxygenation on functional characteristics of RAW264.7 macrophages were analyzed through the protein expression detection of pro-inflammatory factors TNF-αand CD80,anti-inflammatory factors ARG-1 and CD206.The functional implications of C-X3-C motif chemokine receptor 1(CX3CR1)down-regulation in hypoxic macrophages were explored using small interfering RNA technology.Significance was assessed by the parametrict-test or nonparametric Mann-Whitney test for two group comparisons,and a one-way ANOVA or the Kruskal-Wallis test for multiple group comparisons.Results:Hypoxia/reoxygenation significantly increased the protein expression of M1-related pro-inflammatory factors TNF-α,CD80 and chemokine C-X3-C motif chemokine ligand 1(CX3CL1)/CX3CR1 and inhibited the protein expression of M2-related anti-inflammatory factors ARG-1 and CD206 in a time-dependent manner in RAW264.7 cells.However,the silencing of CX3CR1 in RAW264.7 cells using specific CX3CR1-siRNA,significantly attenuated the increase in protein expression of TNF-α(Pmacrophages compared with the control group,and CX3CR1-siRNA had an inhibitory role(40%and 20%reduction,respectively).For elucidating the mechanism,we showed that the phosphorylation levels of ERK(P<0.01)and the p65 subunit of NF-κB(P<0.01)of the RAW264.7 cells in the hypoxic/reoxygenation group were significantly increased,which could be attenuated by down-regulation of CX3CR1 expression(P<0.01,both).ERK inhibitors also significantly blocked the effects of hypoxic/reoxygenation on the

关键词： macrophages Hypoxia/Reoxygenation C-X3-C motif chemokine ligand 1/receptor 1 Phenotypic polarization

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Androgen receptor deficiency in monocytes/ macrophages does not alter adiposity or glucose homeostasis in male mice

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Asian Journal of Andrology 2018年第3期20卷 276-283页

作者： Katya B Rubinow Barbara Houston Shari Wang Leela Goodspeed Kayoko Ogimoto Gregory J Morton Christopher McCarty Robert E Braun Stephanie T Page Division of Metabolism Endocrinology and Nutrition Department of Medicine University of Washington School of Medicine Seattle WA 98195 USA Jackson Laboratory Bar Harbor ME 04609 USA

Androgen deprivation in men leads to increased adiposity, but the mechanisms underlying androgen regulation of fat mass have not been fully defined. Androgen receptor （AR） is expressed in monocytes/macrophages, which are resident in key metabolic tissues and influence energy metabolism in surrounding cells. Male mice bearing a cell-specific knockout of the AR in monocytes/macrophages （M-ARKO） were generated to determine whether selective loss of androgen signaling in these cells would lead to altered body composition. Wild-type （WT） and M-ARKO mice （12-22 weeks of age, n = 12 per group） were maintained on a regular chow diet for 8 weeks and then switched to a high-fat diet for 8 additional weeks. At baseline and on both the regular chow and high-fat diets, no differences in lean mass or fat mass were observed between groups. Consistent with the absence of differential body weight or adiposity, no differences in food intake （3.0 ± 0.5 g per day for WT mice vs 2.8 ± 0.4 g per day for M-ARKO mice） or total energy expenditure （0.6 ± 0.1 Kcal h-1 for WT mice vs 0.5 ± 0.1 Kcal h-1 for M-ARKO mice） were evident between groups during high-fat feeding. Liver weight was greater in M-ARKO than that in WT mice （1.5 ± 0.1 g vs 1.3 ± 0.0 g, respectively, P = 0.02）. Finally, M-ARKO mice did not exhibit impairments in glucose tolerance or insulin sensitivity relative to WT mice at any study time point. In aggregate, these findings suggest that AR signaling specifically in monocytes/macrophages does not contribute to the regulation of systemic energy balance, adiposity, or insulin sensitivity in male mice.

关键词： androgen receptor knockout mice macrophages male hypogonadism metabolic syndrome

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Quercetin modulates iron homeostasis and iNOS expression of splenic macrophages in a rat model of iron deficiency anemia

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Chinese Journal of Natural Medicines 2018年第8期16卷 580-589页

作者： Maryam Mazhar Nurul Kabir Shabana U Simjee Dr. Panjwani Center for Molecular Medicine and Drug Research International Centerjbr Chemical and Biological SciencesUniversity of Karachi Karachi 75270 Pakistan H.E.J. Research Institute. for Chemistry International CenterJor Chemical and Biological Sciences University of Karachi Karachi 75270 Pakistan

Iron deficiency anemia is one of the most common micronutrient deficient conditions around the globe with various consequences,including the weakened immune system.Quercetin is widely distributed bioflavonoid;it has been debated for its dual roles in iron regulation.Quercetin-iron interaction in the body is a complex mechanism which has not been completely understood.The present study aimed to investigate the effect of quercetin on iron supplementation in iron deficiency anemia and on i NOS expression in splenic macrophages.The rat model of iron deficiency anemia was induced by feeding low iron diet to weanling rats for 20 days.The animals were then administered with ferrous sulfate,quercetin,and their combination for 30 days.Blood parameters,histopathological analysis,iron storage,CD68,i NOS and SLC40 expression in rat spleen were investigated.Our results showed that quercetin regulated iron absorption,despite SLC40 down-expression,indicating possible alternate route of iron transport,and that quercetin modulated i NOS production in splenic macrophages..

关键词： Iron deficiency anemia Inducible nitric oxide synthase macrophages Spleen Quercetin

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TLE4 acts as a corepressor of Hes1 to inhibit inflammatory responses in macrophages

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Protein & Cell 2019年第4期10卷 300-305页

作者： Zhang Xiang Li Xiaoyu Ning Fei Shang Yingli Hu Xiaoyu Institute for Immunology and School of Medicine Tsinghua University Beijing 100084 China.

macrophages play a key role in maintaining homeostasis and in mounti ng compete nt immune responses.Upon stimulation,one of the key effector functions of activated macrophages is production of inflammatory cytokines including interleukin 6(IL-6)and interleukin 12(IL-12).IL-6 and IL-12 are important for transition from innate to adaptive immunity,and thus essential for host defense against multiple pathogens(Kishimoto,2005;Trinchieri,2003).

关键词： macrophages key role compete

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RhoB regulates the function of macrophages in the hypoxia-induced inflammatory response

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Cellular & Molecular Immunology 2017年第3期14卷 265-275页

作者： Gaoxiang Huang Jie Su Mingzhuo Zhang Yiduo Jin Yan Wang Peng Zhou Jian Lu Department of Pathophysiology Second Military Medical University Shanghai 200433 People's Republic of China

Immune cells, particularly macrophages, play critical roles in the hypoxia-induced inflammatory response. The small GTPase RhoB is usually rapidly induced by a variety of stimuli and has been described as an important regulator of cytoskeletal organization and vesicle and membrane receptor trafficking. However, it is unknown whether RhoB is involved in the hypoxia-induced inflammatory response. Here, we investigated the effect of hypoxia on the expression of RhoB and the mechanism and significance of RhoB expression in macrophages. We found that hypoxia significantly upregulated the expression of RhoB in RAW264.7 cells, mouse peritoneal macrophages, and the spleen of rats. Hypoxia-induced expression of RhoB was significantly blocked by a specific inhibitor of hypoxia-inducible factor-1α （HIF-1α）, c-Jun N-terminal kinase （JNK）, or extracellular-signal regulated protein kinase （ERK）, indicating that hypoxia-activated HIF-1α, JNK, and ERK are involved in the upregulation of RhoB by hypoxia. Knockdown of RhoB expression not only significantly suppressed basal production of interleukin-1 beta （IL-1β）, interleukin 6 （IL-6）, and tumor necrosis factor alpha （TNF-α） in normoxia but also more markedly decreased the hypoxia-stimulated production of these cytokines. Furthermore, we showed that RhoB increased nuclear factor-kappa B （NF-κB） activity, and the inhibition of NF-κB transcriptional activity significantly decreased the RhoB-increased mRNA levels of IL-1β, IL-6, and TNF-α. Finally, we demonstrated that RhoB enhanced cell adhesion and inhibited cell migration in normoxia and hypoxia. Taken together, these results suggest that RhoB plays an important role in the hypoxia-induced activation of macrophages and the inflammatory response.

关键词： hypoxia macrophages NF-KB proinflammatory cytokines RhoB

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Promotion of Sema4D expression by tumor-associated macrophages: Significance in gastric carcinoma

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World Journal of Gastroenterology 2018年第5期24卷 593-601页

作者： Han Li Jin-Shen Wang Lin-Jun Mu Ke-Shu Shan Le-Ping Li Yan-Bing Zhou Department of General Surgery Affiliated Hospital of Qingdao University Department of Gastrointestinal Surgery Shandong Provincial Hospital Affiliated to Shandong University Department of Emergency Surgery Weifang People’s Hospital

AIM To study the role of semaphorin 4 D(Sema4 D) expression promoted by tumor-associated macrophages(TAMs) in gastric carcinoma cells and its clinical significance in the invasion and metastasis of gastric carcinoma.METHODS CD68 and Sema4 D expression was analyzed in gastric carcinoma and adjacent normal tissues from 290 patients using the immunohistochemical streptavidinperoxidase method, and their relationships with clinicopathological features were evaluated. Human M2 macrophages were induced in vitro and co-cultured in non-contact with gastric carcinoma SGC-7901 cells. Changes in the secretory Sema4 D level in the SGC-7901 cell supernatant were measured using an enzymelinked immunosorbent assay. The effects of TAMs on SGC-7901 cell invasion and migration were assessed with invasion and migration assays, respectively.RESULTS CD68 and Sema4 D protein expression was significantly higher in gastric carcinoma tissues than in adjacent normal tissues(71.7% vs 33.8% and 74.5% vs 42.8%, respectively; P < 0.01). CD68 and Sema4 D protein expression was significantly associated with histological differentiation, TNM stage, and lymph node metastasis(P < 0.05), and their expression levels were positively correlated with one another(r = 0.467, P < 0.01). In the in vitro experiment, secretory Sema4 D protein expression was significantly increased in the supernatant of SGC-7901 cells co-cultured with TAMs compared with the blank control(1224.13 ± 29.43 vs 637.15 ± 33.84, P < 0.01). Cell invasion and metastasis were enhanced in the Transwell invasion and migration assays(P < 0.01).CONCLUSION TAMs promote the invasion and metastasis of gastric carcinoma cells possibly through upregulated secretory Sema4 D protein expression. Combined detection of TAM markers, CD68 and Sema4 D, in gastric carcinoma tissue shows potential to predict the trend of gastric carcinoma progression.

关键词： Gastric carcinoma CD68 Semaphorin 4D Tumor-associated macrophages

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Functional macrophages and gastrointestinal disorders

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World Journal of Gastroenterology 2018年第11期24卷 1181-1195页

作者： Yue-Hong Liu Yue Ding Chen-Chen Gao Li-Sheng Li Yue-Xiu Wang Jing-Dong Xu School of Basic Medical Science Beijing Capital Medical University Department of Physiology and Pathophysiology School of Basic Medical ScienceCapital Medical University Function Platform Center School of Basic Medical ScienceCapital Medical University Beijing Institute for Brain Disorders Capital Medical University

macrophages(MΦ) differe ntiate from blood monocytes and participate in innate and adaptive immunity.Because of their abilities to recognize pathogens and activate bactericidal activities,MΦ are always discovered at the site of immune defense.MΦ in the intestine are unique,such that in the healthy intestine,they possess complex mechanisms to protect the gut from inflammation.In these complex mechanisms,they produce anti-inflammatory cytokines,such as interleukin-10 and transforming growth factor-β,and inhibit the inflammatory pathways mediated by Toll-like receptors.It has been demonstrated that resident MΦ play a crucial role in maintaining intestinal homeostasis,and they can be recognized by their unique markers.Nonetheless,in the inflamed intestine,the function of MΦ will change because of environmental variation,which may be one of the mechanisms of inflammatory bowel disease(IBD).We provide further explanation about these mechanisms in our review.In addition,we review recent discoveries that MΦ may be involved in the development of gastrointestinal tumors.We will highlight the possible therapeutic targets for the management of IBD and gastrointestinal tumors,and we also discuss why more details are needed to fully understand all other effects of intestinal MΦ.

关键词： macrophages Homeostasis Inflammatory bowel disease Gastrointestinal tumors Therapeutic targets

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TSC1 controls IL-1β expression in macrophages via mTORCl-dependent C/EBPβ pathway

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Cellular & Molecular Immunology 2016年第5期13卷 640-650页

作者： Tao Yang Linnan Zhu Yanhua Zhai Qingjie Zhao Jianxia Peng Hongbing Zhang Zhongzhou Yang Lianfeng Zhang Wenjun Ding Yong Zhao State Key Laboratory of Biomembrane and Membrane Biotechnology Institute of Zoology Chinese Academy of Sciences Beijing China Division of Molecular Embryonic Development State Key Laboratory of Reproductive Biology Institute of Zoology Chinese Academy of Sciences Beijing China School of Life Science University of Chinese Academy of Sciences Beijing China Department of Physiology and Pathophysiology National Laboratory of Medical Molecular Biology Institute of Basic Medical Sciences and School of Basic Medicine Chinese Academy of Medical Sciences and Peking Union Medical College Beijing China MOE Key Laboratory of Model Animal for Disease Study Model Animal Research Center Nanjing University Nanjing China Key Laboratory of Human Diseases Comparative Medicine Ministry of Health Institute of Laboratory Animal Science CAMS & PUMC Beijing China

The tuberous sclerosis complex I （TSC1） is a tumor suppressor that inhibits the mammalian target of rapamycin （mTOR）, which serves as a key regulator of inflammatory responses after bacterial stimulation in monocytes, macrophages, and primary dendritic cells. Previous studies have shown that TSC1 knockout （KO） macrophages produced increased inflammatory responses including tumor necrosis factor-a （TNF-a） and IL-12 to pro-inflammatory stimuli, but whether and how TSC1 regulates pro-lL-lJ~ expression remains unclear. Here using a mouse model in which myeloid lineage-specific deletion of TSC1 leads to constitutive mTORC1 activation, we found that TSC1 deficiency resulted in impaired expression of pro-I L-1β in macrophages following l ipopolysaccharide stimulation. Such decreased pro-I L-1β expression in TSC1 KO macrophages was rescued by reducing mTORC1 activity with rapamycin or deletion of mTOR. Rictor deficiency has no detectable effect on pro-lL-1β synthesis, suggesting that TSC1 positively controls pro-1L-1β expression through mTORC 1 pathway. Moreover, mechanism studies suggest that mTORC 1-mediated downregulation of the CCAAT enhancer-binding protein （C/EBPβ） critically contributes to the defective pro-lL-1β expression. Overall, these findings highlight a critical role of TSC1 in regulating innate immunity by control of the mTOR1-C/EBPβ pathway.

关键词： IL-1 inflammation innate immunity macrophages mTOR, TSC1

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macrophages play a role in inflammatory transformation of colorectal cancer

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World Journal of Gastrointestinal Oncology 2021年第12期13卷 2013-2028页

作者： Lu Lu Yu-Jing Liu Pei-Qiu Cheng Hu Dan Han-Chen Xu Guang Ji Institute of Digestive Diseases Longhua HospitalShanghai University of Traditional Chinese MedicineShanghai 200032China Shanghai Pudong New Area Hospital of Traditional Chinese Medicine Shanghai 200120China

Colorectal cancer(CRC)is one of the most common and fatal cancers worldwide,and it is also a typical inflammatory cancer.The function of macrophages is very important in the tissue immune microenvironment during inflammatory and carcinogenic transformation.Here,we evaluated the function and mechanism of macrophages in intestinal physiology and in different pathological stages.Furthermore,the role of macrophages in the immune microenvironment of CRC and the influence of the intestinal population and hypoxic environment on macrophage function are summarized.In addition,in the era of tumor immunotherapy,CRC currently has a limited response rate to immune checkpoint inhibitors,and we summarize potential therapeutic strategies for targeting tumorassociated macrophages.

关键词： Colorectal cancer macrophages Inflammatory transformation Tumor microenvironment

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Ratiometric sensing lysosomal pH in inflammatory macrophages by a BODIPY-rhodamine dyad with restrained FRET

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Chinese Chemical Letters 2020年第5期31卷 1091-1094页

作者： Yu Yan Xiaodong Zhang Xinfu Zhang Ning Li Huizi Man Lingcheng Chen Yi Xiao State Key Laboratory of Fine Chemicals Dalian University of TechnologyDalian 116024China

Inflammation,as the pathophysiological response of body to harmful stimuli,leads to changes in cellular microenvironment.To research pH changes in lysosomes of macrophages during inflammation,we designed a FRET(F(o|")rster resonance energy transfer)based probe,BDP-RhB.The probe showed good lysosome targeting ability,wide response range of pH from 8.0 to 4.0 with significant ratio(I582/I518)change from 0.6 to 3.4,and good reversibility and sustainability.By applying BDP-RhB,we found a decrease of lysosomal pH of macrophages during inflammation.

关键词： pH probe Inflammation Lysosome FRET macrophages

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