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Interplay between mesenchymal stem cells and macrophages:Promoting bone tissue repair

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World Journal of Stem Cells 2024年第4期16卷 375-388页

作者： Fei-Fan Zhang Yang Hao Kuai-Xiang Zhang Jiang-Jia Yang Zhi-Qiang Zhao Hong-Jian Liu Ji-Tian Li Molecular Biology Lab Henan Luoyang Orthopedic Hospital(Henan Provincial Orthopedic Hospital)Zhengzhou 450000Henan ProvinceChina Graduate School Hunan University of Chinese MedicineChangsha 410208Hunan ProvinceChina Graduate School Henan University of Chinese MedicineZhengzhou 450046Henan ProvinceChina Department of Orthopaedics The First Affiliated Hospital of Zhengzhou UniversityZhengzhou 450052Henan ProvinceChina

The repair of bone tissue damage is a complex process that is well-orchestrated in time and space,a focus and difficulty in orthopedic treatment.In recent years,the success of mesenchymal stem cells(MSCs)-mediated bone repair in clinical trials of large-area bone defects and bone necrosis has made it a candidate in bone tissue repair engineering and regenerative medicine.MSCs are closely related to macrophages.On one hand,MSCs regulate the immune regulatory function by influencing macrophages proliferation,infiltration,and phenotype polarization,while also affecting the osteoclasts differentiation of macrophages.On the other hand,macrophages activate MSCs and mediate the multilineage differentiation of MSCs by regulating the immune microenvironment.The cross-talk between MSCs and macrophages plays a crucial role in regulating the immune system and in promoting tissue regeneration.Making full use of the relationship between MSCs and macrophages will enhance the efficacy of MSCs therapy in bone tissue repair,and will also provide a reference for further application of MSCs in other diseases.

关键词： Bone tissue damage Inflammation macrophages Mesenchymal stem cells Tissue regeneration

Pre-incubated with BSA-complexed free fatty acids alters ER stress/autophagic gene expression by carboxylated multi-walled carbon nanotube exposure in THP-1 macrophages

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Chinese Chemical Letters 2019年第6期30卷 1224-1228页

作者： Qianyu Yang Maolin Wang Yongbing Sun Shengming Peng Yanhuai Ding Yi Cao Key Laboratory of Environment-Friendly Chemistry and Application of Ministry of Education Lab of Biochemistry College of Chemistry Xiangtan University Xiangtan 411105 China National Engineering Research Center for Solid Preparation Technology of Chinese Medicines Jiangxi University of Traditional Chinese Medicines Nanchang 330006 China

Recently we found that multi-walled carbon nanotube (MWCNT) exposure alters the mRNA levels of endoplasmic reticulum (ER) stress/autophagic genes, but the impact of biological molecules on this response is unclear. Herein, we compared the different actions of carboxylated MWCNTs (c-MWCNTs) pre-incubated with bovine serum albumin (BSA) or BSA-complexed free fatty acid (denoted as FFA) on macrophages derived from THP-1 monocytes (denoted as THP-1 macrophages). C-MWCNTs exhibited increased diameter and hydrodynamic size as well as decreased absolute zeta potential value after pre-incubation with BSA or FFA, which suggested a coating effect. Cytotoxicity or oxidative stress were not significantly induced after exposure to BSA-or FFA-coated c-MWCNTs. BSA-pre-incubated c-MWCNTs significantly enhanced the expression of the ER stress gene, DDIT3 and the autophagic genes, ATG5, BECN1, and PLIN2, but the mRNA levels of these genes was significantly decreased by FFA-pre-incubated c-MWCNTs. FFA-pre-incubated c-MWCNTs induced significantly higher lipid accumulation and interleukin-6 (IL-6) protein level compared with BSA-pre-incubated c-MWCNTs, which suggested that FFA-pre-incubated c-MWCNTs may more effectively induce the formation of macrophage foam cells. Collectively, our data indicated that pre-incubation with FFA may influence c-MWCNT-induced ER stress/autophagic gene expression and foam cell formation in THP-1 macrophages.

关键词： Multi-walled carbon nanotubes (MWCNTs) THP-1 macrophages Endoplasmic reticulum (ER) stress Autophagy Foam cells

Tumor-associated macrophages (TAMs) as biomarkers for gastric cancer:A review

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Chronic Diseases and Translational Medicine 2018年第3期4卷 156-163页

作者： Meri R.Raiha Pauli A.Puolakkainen Department of Surgery Helsinki University Hospital and University of HelsinkiHelsinki 00014Finland

Gastric adenocarcinoma is one of the most common types of cancer worldwide, with an incidence of a million new cases annually. In addition to having a high mortality rate due to often delayed detection and its poor response to cancer therapy, it also spreads aggressively. Inflammation has been shown to play a role in carcinogenesis. Consequently, macrophages are important in phagocytosis, antigen presenting and producing cytokines and growth factors. As a response to microenvironmental signals, they may polarize into tumor resisting M1 or tumor promoting M2 macrophages. Recently, studies have indicated that M2-type macrophage resembling tumor-associated macrophages (TAMs) might be used as an independent prognostic factor for gastric cancer. This review will discuss the possible use of TAMs as prognostic tools for gastric cancer and whether they are suitable for use in clinical environment.

关键词： Gastric cancer Tumor-associated macrophages Biomarkers Prognosis Diagnosis

Reprogramming cholesterol metabolism in macrophages and its role in host defense against cholesterol-dependent cytolysins

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Cellular & Molecular Immunology 2022年第3期19卷 327-336页

作者： Min-Sub Lee Steven J.Bensinger Department of Molecular and Medical Pharmacology University of CaliforniaLos AngelesCA90095USA Department of Microbiology Immunology and Molecular GeneticsUniversity of CaliforniaLos AngelesCA90095USA

Cholesterol is a critical lipid for all mammalian cells,ensuring proper membrane integrity,fluidity,and biochemical function.Accumulating evidence indicates that macrophages rapidly and profoundly reprogram their cholesterol metabolism in response to activation signals to support host defense processes.However,our understanding of the molecular details underlying how and why cholesterol homeostasis is specifically reshaped during immune responses remains less well understood.This review discusses our current knowledge of cellular cholesterol homeostatic machinery and introduces emerging concepts regarding how plasma membrane cholesterol is partitioned into distinct pools.We then discuss how proinflammatory signals can markedly reshape the cholesterol metabolism of macrophages,with a focus on the differences between MyD88-dependent pattern recognition receptors and the interferon signaling pathway.We also discuss recent work investigating the capacity of these proinflammatory signals to selectively reshape plasma membrane cholesterol homeostasis.We examine how these changes in plasma membrane cholesterol metabolism influence sensitivity to a set of microbial pore-forming toxins known as cholesterol-dependent cytolysins that specifically target cholesterol for their effector functions.We also discuss whether lipid metabolic reprogramming can be leveraged for therapy to mitigate tissue damage mediated by cholesterol-dependent cytolysins in necrotizing fasciitis and other related infections.We expect that advancing our understanding of the crosstalk between metabolism and innate immunity will help explain how inflammation underlies metabolic diseases and highlight pathways that could be targeted to normalize metabolic homeostasis in disease states.

关键词： Cholesterol macrophages Innate Immunity Metabolism

Function of microglia and macrophages in secondary damage after spinal cord injury

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Neural Regeneration Research 2014年第20期9卷 1787-1795页

作者： Xiang Zhou Xijing He Yi Ren Department of Orthopedic Surgery the Second Hospital of Xi’an Jiaotong University Department of Biomedical Sciences Florida State University College of MedicineTallahasseeFLUSA

Spinal cord injury （SCI） is a devastating type of neurological trauma with limited therapeutic op- portunities. The pathophysiology of SCI involves primary and secondary mechanisms of injury. Among all the secondary injury mechanisms, the inflammatory response is the major contrib- utor and results in expansion of the lesion and further loss of neurologic function. Meanwhile, the inflammation directly and indirectly dominates the outcomes of SCI, including not only pain and motor dysfunction, but also preventingneuronal regeneration. Microglia and macrophages play very important roles in secondary injury. Microglia reside in spinal parenchyma and survey the microenvironment through the signals of injury or infection. macrophages are derived from monocytes recruited to injured sites from the peripheral circulation. Activated resident microglia and monocyte-derived macrophages induce and magnify immune and inflammatory responses not only by means of their secretory moleculesand phagocytosis, but also through their influence on astrocytes, oligodendrocytes and demyelination. In this review, we focus on the roles of mi- croglia and macrophages in secondary injury and how they contribute to the sequelae of SCI.

关键词： astrocytes cytokines chemokines demyelination inflammation oligodendrocytes MI/M2 activation macrophages microglia secondary damage spinal cord injury

Fumarate hydratase:a new checkpoint of metabolic regulation in inflammatory macrophages

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Signal Transduction and Targeted Therapy 2023年第10期8卷 4421-4423页

作者： Aicha Jeridi Theodore S.Kapellos Ali Onder Yildirim Comprehensive Pneumology Center(CPC) Institute of Lung Health and Immunity(LHI)Member of the German Center for Lung Research(DZL)Helmholtz MunichMunichGermany Institute of Experimental Pneumology University HospitalLudwig-Maximilians UniversityMünchenGermany

A recent article published by Hooftman et al.1 in Nature identified a crucial function for fumarate hydratase(FH)in bone marrow-derived macrophages(BMDMs).Pharmacological inhibition or genetic ablation of FH led to increased fumarate levels and downstream suppression of mitochondrial respiration implying the importance of cellular metabolic states and cytokine balance shift in innate immunity.

关键词： al. macrophages respiration

Direct regulation of interleukin-6 expression by Notch signaling in macrophages

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Cellular & Molecular Immunology 2012年第2期9卷 155-162页

作者： Wipawee Wongchana Tanapat Palaga Graduate Program in Biotechnology Faculty of Science Chulalongkorn University Bangkok Thailand Department of Microbiology Faculty of Science Chulalongkorn University Bangkok Thailand

Interleukin-6 （IL-6） is a pleiotropic, pro-inflammatory cytokine produced by various types of cells, including macrophages. Within the IL-6 gene promoter region, the signature binding motif of CBFI/Su（H）/Lag-1 （CSL）, a key DNA-binding protein in the Notch signaling pathway, was identified and found to overlap with a consensus nuclear factor （NF）-κB-binding site. Notch signaling is highly conserved and is involved in the regulation of biological functions in immune cells. In this study, we investigated the role of Notch signaling in the regulation of the IL-6transcript in murine macrophages. The upregulation of Notch1 protein levels and the appearance of cleaved Notch1 （Va11744） correlated well with the increased IL-6 mRNA expression levels in murine primary bone marrow-derived macrophages （BMMφ） after activation by lipopolysaccharide （LPS） together with interferon-gamma （IFN-γ）. Treatment of BMMφ with the γ-secretase inhibitor IL-CHO to suppress the transduction of Notch signaling resulted in a partial decrease in the level of IL-6mRNA and the amount of I L-6 protein produced. In contrast, the overexpression of a constitutively activated intracellular Notch I protein （N^IC） in the RAW264.7 macrophage-like cell line resulted in significantly higher IL-6transcript expression levels than in cells transfected with the empty vector control. The NF-κB inhibitor completely abrogated IL-6 mRNA expression induced by the overexpression of N^IC. Chromatin immunoprecipitation （CHIP） using an anti-Notch1 antibody demonstrated that Notch 1 is associated with the IL-6promoter in RAW264.7 cells activated by LPS/IFN-γ but not in unstimulated cells. Taken together, these results strongly suggest that Notch 1 positively regulates IL-6 expression via NF-κB in activated macrophages.

关键词： CSL interleukin-6 macrophages NF-κB Notch signaling

Expression and preliminary functional analysis of Siglec-F on mouse macrophages

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Journal of Zhejiang University-Science B(Biomedicine & Biotechnology) 2012年第5期13卷 386-394页

作者： Yin-he FENG Hui MAO Department of Respiratory Medicine West China HospitalSichuan UniversityChengdu 610041China

Sialic acid-binding immunoglobulin-like lectin (Siglec)-F is a mouse functional paralog of human Siglec-8 that induces apoptosis in human eosinophils, and therefore may be useful as the basis of treatments for a variety of disorders associated with eosinophil hyperactivity, such as asthma. The expression pattern and functions of this protein in various cell types remain to be elucidated. The aim of this study was to determine the expression of Siglec-F on mouse macrophages by immunocytochemical staining, and also to investigate the effects of Siglec-F engagement by a Siglec-F antibody on phagocytic activity of macrophages. The results showed that Siglec-F expression was detected on mouse alveolar macrophages, but not on peritoneal macrophages. Furthermore, Siglec-F engagement did not affect the phagocytic activity of alveolar macrophages in the resting state or in the activated state following stimulation by the proinflammatory mediator tumor necrosis factor alpha (TNF-α) or lipopolysaccharide (LPS). Siglec-F expression on alveolar macrophages may be a result of adaptation. macrophages actively regulate immune responses via production of cytokines. Therefore, further investigation of the effects of Siglec-F engagement on immune mediators or cytokines released by alveolar macrophages is required.

关键词： Siglec-F Expression macrophages Phagocytosis Eosinophil

Corticosterone rapidly promotes respiratory burst of mouse peritoneal macrophages via non-genomic mechanism

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Chinese Medical Journal 2011年第19期124卷 3127-3132页

作者： SHI Wen-lei MA Qian ZHANG Lu-ding HUANG Jun-long ZHOU Jian LIU Lei SHEN Xing-hua JIANG Chun-lei Laboratory of Stress Medicine Department of Nautical Medicine Second Military Medical University Shanghai 200433 China Department of Pediatrics Chang-Zheng Hospital Shanghai 200003 China

Background The immunomodulatory effects of glucocorticoids （GCs） have been described as bimodal. High concentration of GCs exerts immunosuppressive effects and low levels of GCs are immunopermissive. While the immunosuppressive mechanisms of GCs have been investigated intensely, the immunopermissive effects of GCs remain unclear. A lot of studies showed GCs could exert rapid non-genomic actions. We herein studied the rapid immunopromoting effects of GCs.Methods We observed the rapid （within 30 minutes） effects of corticosterone on respiratory burst of mouse peritoneal macrophages and studied their mechanisms. The superoxide anions were measured by cytochrome C reduction assay.Protein kinase C phosphorylation was measured by Western blotting and membrane fluidity was evaluated by fluorescence polarization measurement.Results The 10-8 mol/L and 10-7 mol/L corticosterone rapidly increased the superoxide anions production by macrophages, which were insensitive to GC-receptor antagonist, mifepristone, and protein-synthesis inhibitor,cycloheximide. Corticosterone coupled to bovine serum albumin was able to mimic the effects of corticosterone. The effects were independent of protein kinase C pathway and the change in membrane fluidity.Conclusions The results indicate that corticosterone rapidly promote the superoxide anions production by mouse peritoneal macrophages may through non-genomic mechanisms. This study may contribute to understanding the effects of GCs under stress condition and the physiological significance of nongenomic effects of GCs.

关键词： glucocorticoids macrophages superoxide anions respiratory burst neuroimmunomodulation