Macrophages and angiogenesis in rheumatic diseases

Maruotti, Nicola; Annese, Tiziana; Cantatore, Francesco Paolo; Ribatti, Doménico

doi:10.1186/2045-824x-5-11

Cited by 46 publications

(34 citation statements)

References 93 publications

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“…Actually, classically activated M1 macrophages, driven by TNF-a secreted is thought to be the primary trigger for the recruitment. 26,27 Besides, MCP-1, IL-6, and adiponectin play important roles through other pathways than the paracrine loop. 28,29 The increase in the expression of MCP-1 will lead an influx of monocytes and macrophages.…”

Section: Discussionmentioning

confidence: 99%

TNF-a mediated inflammatory macrophage polarization contributes to the pathogenesis of steroid-induced osteonecrosis in mice

Feng

et al. 2015

Int J Immunopathol Pharmacol

100

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The phenotypic polarization of macrophages are involved in steroid-induced osteonecrosis (ON). This study tried to investigate the detrimental and beneficial roles of M1/M2 macrophages associated with TNF-a in ON. Mice ON model was induced by the injection of methylprednisolone. After that, flow cytometry technique, immunohistochemistry, immunofluorescence, ELISA, and RT-PCR methods were used to investigate the expression pattern of macrophages and the expression of inflammatory cytokines. During the progression of ON, massive chronic inflammatory cells infiltrated into the necrotic zone, represented by the infiltration of macrophages. In the early stage of ON, there was high TNF-a activity; and a large population of M1 macrophages infiltrated into the necrotic zone. On the contrary, the expression of TNF-a gradually decreased; simultaneously, a larger M2 cell population presented in the necrotic zone in the late stage of ON. The increased M2 macrophages could be beneficial for resolving inflammation and promoting tissue repair, confirmed by the histologic findings of appositional new bone formation around the necrotic bone. Thus, it showed that TNF-a-mediated alteration of M1/M2 macrophage polarization contributed to the pathogenesis of steroid-induced osteonecrosis. M1-polarized macrophages appeared to be disruptive in the early stage of ON, while M2-polarized macrophages played an important role in the late stage during the pathogenesis of ON.

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Section: Discussionmentioning

confidence: 99%

TNF-a mediated inflammatory macrophage polarization contributes to the pathogenesis of steroid-induced osteonecrosis in mice

Feng

et al. 2015

Int J Immunopathol Pharmacol

100

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“…34,35 Macrophages subsequently become "activated macrophages" displaying different phenotypes depending on the nature of the recruiting stimulus and the location. 36 Activated macrophages may release cytokines (IL-1, IL-6, TNF-α), chemokines (eg, monocyte chemotactic protein-1, MCP-1/CCL2), digestive enzymes (eg, collagenases), prostaglandins, and reactive oxygen species (ROS), which can aggravate or accelerate damage to the normal tissues. 37 Further, activated macrophages are known to participate in antigen presentation, and thereby they are thought to contribute to the activation and proliferation of antigen specific T-cells and their consequent destructive effects.…”

Section: Macrophagesmentioning

confidence: 99%

Folate-targeted nanoparticles for rheumatoid arthritis therapy

Nogueira

Gomes

Preto

et al. 2016

Nanomedicine: Nanotechnology, Biology and Medicine

125

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Rheumatoid arthritis is a debilitating autoimmune disease of the joints which affects many people worldwide. Up till now, there is a lack of optimal therapy against this disease. In this review article, the authors outlined in depth the current mechanism of disease for rheumatoid arthritis and described the latest research in using folic acid-targeted nanoparticles to target synovial macrophages in the fight against rheumatoid arthritis.

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“…The number of neutrophils peaks 24 h after MI, whereas that of Mos/Mps peaks approximately 3 days after MI and drops to normal after 16 days. In addition, activated Mos/Mps, which participate in phagocytosis and the clearance of necrotic debris, release several pro‐inflammatory cytokines, such as TNFα, IL‐1β and IL‐6 (Maruotti et al, ). Following the acute inflammatory response, the infarcted myocardium is subjected to structural remodelling processes, including collagen deposition, angiogenesis and scar formation (Hofmann and Frantz, ).…”

Section: Introductionmentioning

confidence: 99%