Dopamine induces growth inhibition and vascular normalization through reprogramming M2-polarized macrophages in rat C6 glioma

Qin, Tian; Wang, Chenlong; Chen, Xuewei; Duan, Chenfan; Zhang, Xiaoyan; Zhang, Jing; Chai, Hongyan; Tang, Tian; Chen, Honglei; Yue, Jiang; Liu, Ying; Yang, Jing

doi:10.1016/j.taap.2015.03.021

Cited by 54 publications

(37 citation statements)

References 45 publications

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“…56) inhibition shifts to the M1 phenotype. Similar anti-tumor effects have been shown by dopamine or targeting miR-142-3p, which affects the M2-polarization of TAMs 58,59 . On the basis of these studies, the identification of targeting approaches that convert M2 macrophages to M1 macrophages has been suggested as a potential therapeutic strategy to reduce glioma growth.…”

Section: Tams and High-grade (Malignant) Gliomasupporting

confidence: 69%

The role of microglia and macrophages in glioma maintenance and progression

2015

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There is a growing recognition that gliomas are complex tumors composed of neoplastic and non-neoplastic cells, which each individually contribute to cancer formation, progression and response to treatment. The majority of the non-neoplastic cells are tumor-associated macrophages (TAMs), either of peripheral origin or representing brain-intrinsic microglia, that create a supportive stroma for neoplastic cell expansion and invasion. TAMs are recruited to the glioma environment, have immune functions, and can release a wide array of growth factors and cytokines in response to those factors produced by cancer cells. In this manner, TAMs facilitate tumor proliferation, survival and migration. Through such iterative interactions, a unique tumor ecosystem is established, which offers new opportunities for therapeutic targeting.

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Section: Tams and High-grade (Malignant) Gliomasupporting

confidence: 69%

The role of microglia and macrophages in glioma maintenance and progression

2015

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“…In another experiment, ZA (100 μg/kg) liposomes were injected intravenously. Sal (80 mg/kg) was intragastrically administered once daily for 6 d. Clod and ZA doses were based on the literature and the efficiency of macrophage depletion was assessed by flow cytometry analysis of CD11b + cells in peripheral blood and immunohistochemical analysis of synovial tissue sections for F4/80.…”

Section: Methodsmentioning

confidence: 99%

Frontline Science: Reprogramming COX-2, 5-LOX, and CYP4A-mediated arachidonic acid metabolism in macrophages by salidroside alleviates gouty arthritis

Liu

Tang

Liu

et al. 2018

Journal of Leukocyte Biology

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Cyclooxygenase-2 (COX-2), 5-lipoxygenase (5-LOX), and cytochrome P450 (CYP) 4A-mediated arachidonic acid (AA) metabolism play an essential role in human inflammatory disorders. Blocking COX-2 pathway would shunt AA metabolism to the other pathway, thereby decreasing the efficacy and exacerbating adverse effects. Here we demonstrated that reprogramming COX-2, 5-LOX, and CYP4A-mediated AA metabolism in macrophages by salidroside (Sal) ameliorates monosodium urate (MSU) crystal-induced inflammation. Compared with COX-2 inhibitor celecoxib, Sal (80 mg/kg) presented a superior anti-arthritic profile in MSU crystal-treated rats, accompanied with the decreased expression of COX-2, 5-LOX, and CYP4A and production of prostaglandin E2 (PGE 2 ), leukotriene B4 (LTB 4 ), and 20-hydroxyeicosatetraenoic acid in the synovial fluid macrophages. Sal decreased representative M1 marker (iNOS and CD86, etc.) expression and M1 cytokine (TNF-and IL-1 ) production, whereas it increased M2 marker (CD206 and Arg-1) expression and M2 cytokine (TGF-and IL-10) production. The injection of conditioned medium from MSU crystal-treated macrophages into the ankle joint of rats reproduced the gouty inflammation, which was attenuated by Sal. Mechanistically, down-regulation of COX-2, 5-LOX, and CYP4A in the RAW264.7 and NR8383 macrophages by Sal skewed macrophage polarization away from the M1 phenotype, and thereby prevented neutrophil migration and chondrocyte degradation with STAT1 and NF-B inactivation. Conversely, overexpression of COX-2, 5-LOX, CYP4A or STAT1, or exogenous addition of IL-1 or TNF-partially abolished these effects. Together, inhibition of COX-2, 5-LOX, and CYP4A in macrophages by Sal ameliorates MSU crystal-induced inflammation through decreasing TNF-and IL-1 production, and may serve as a novel therapeutic strategy. K E Y W O R D Sarachidonic acid, gouty inflammation, macrophage, metabolism, salidroside INTRODUCTIONGout is the most common inflammatory arthritis in men older than 40 years. 1 Nonsteroidal anti-inflammatory drugs (NSAIDs) are used as Abbreviations: 20-HETE, 20-hydroxyeicosatetraenoic acid; 5-LOX, 5-lipoxygenase; ADAMTS-5, a disintegrin and metalloproteinase with thrombospondin motif 5; Clod, clodronate liposome; COX-2, cyclooxygenase-2; CYP4A, cytochrome P450 4A; LTB 4 , leukotriene B 4 ; MMP-13, Matrix metalloproteinase-13; MSU, monosodium urate; NF-B, nuclear transcription factor kappa B; PGE 2 , prostaglandin E 2 ; Sal, salidroside; STAT1, signal transducers and activators of transcription 1; ZA, zoledronic acid first-line therapy to manage gouty arthritis, whereas the inevitable gastrointestinal or cardiovascular side effects restrict their utilization. 2 Newly developed anti-IL-1 drugs appear to be highly effective, but present limitations such as high cost and hematopoietic disorders. 3 Therefore, there is an urgent need to identify novel agents for gouty arthritis treatment.Gout is triggered by monosodium urate (MSU) crystal deposition in and around joints. Macrophages play a pivotal role in the initiati...

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“…In human tumors, microglial/macrophage density was increased with a corresponding increase in tumorigenic neovascularization (Nishie et al, 1999;Brandenburg et al, 2016) and macrophages were increasingly associated with blood vessels (Leek et al, 1996;Brandenburg et al, 2016). Since microglia are the macrophages of the CNS, the implication that macrophages induce angiogenesis in tumor environments (Kobayashi et al, 1994;Sunderkotter et al, 1994;Polverini, 1997;Wang et al, 2013;Qin et al, 2015) could also apply to microglia (Wyckoff et al, 2004). Interestingly, despite the fact that it is difficult to distinguish brain resident microglia from infiltrated macrophages molecularly, recent evidence suggest that the pro-angiogenic function is predominantly carried out by microglia rather than macrophages in brain tumors (Brandenburg et al, 2016).…”

Section: Microglia and Blood Vessels In Brain Tumorsmentioning

confidence: 99%

Microglial interactions with the neurovascular system in physiology and pathology

Zhao

Eyo

Murugan

et al. 2018

Developmental Neurobiology

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Microglia as immune cells of the central nervous system (CNS) play significant roles not only in pathology but also in physiology, such as shaping of the CNS during development and its proper maintenance in maturity. Emerging research is showing a close association between microglia and the neurovasculature that is critical for brain energy supply. In this review, we summarize the current literature on microglial interaction with the vascular system in the normal and diseased brain. First, we highlight data that indicate interesting potential involvement of microglia in developmental angiogenesis. Then we discuss the evidence for microglial participation with the vasculature in neuropathologies from brain tumors to acute injuries such as ischemic stroke to chronic neurodegenerative conditions. We conclude by suggesting future areas of research to advance the field in light of current technical progress and outstanding questions. © 2018 Wiley Periodicals, Inc. Develop Neurobiol 78: 604-617, 2018.

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Dopamine induces growth inhibition and vascular normalization through reprogramming M2-polarized macrophages in rat C6 glioma

Cited by 54 publications

References 45 publications

The role of microglia and macrophages in glioma maintenance and progression

The role of microglia and macrophages in glioma maintenance and progression

Frontline Science: Reprogramming COX-2, 5-LOX, and CYP4A-mediated arachidonic acid metabolism in macrophages by salidroside alleviates gouty arthritis

Microglial interactions with the neurovascular system in physiology and pathology

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