Classical Macrophage Activation Up-Regulates Several Matrix Metalloproteinases through Mitogen Activated Protein Kinases and Nuclear Factor-κB

Huang, Wei-Chun; Sala-Newby, Graciela B.; Susana, Angela; Johnson, Jason L.; Newby, Andrew C.

doi:10.1371/journal.pone.0042507

Cited by 144 publications

(153 citation statements)

References 40 publications

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“…In vitro data support the fact that macrophages can efficiently produce MMPs and degrade the cartilage matrix, 59,60 with MMP production being a forte of M1 macrophages. 61 Interestingly, F4/80 þ macrophages were shown to be present in invading vascular canals during the formation of the primary and secondary ossification centers in mouse long bone development. 62 Overall, macrophage contributions to the early stages of cartilage remodeling should not be ruled out.…”

Section: Macrophage Participation In Hard Callus Formation and Remodementioning

confidence: 99%

Unraveling macrophage contributions to bone repair

et al. 2013

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Macrophages have reemerged to prominence with widened understanding of their pleiotropic contributions to many biologies and pathologies. This includes clear advances in revealing their importance in wound healing. Here we have focused on the current state of knowledge with respect to bone repair, which has received relatively little scientific attention compared with its soft-tissue counterparts. Our detailed characterization of resident tissue macrophages residing in bone-lining tissues (osteomacs), including their pro-anabolic function, exposed a more prominent role for these cells in bone biology than previously anticipated. Recent studies have confirmed the importance of macrophages in early inflammatory processes that establish the healing cascade after bone fracture. Emerging data support that macrophage influence extends into both anabolic and catabolic phases of repair, suggesting that these cells have prolonged and diverse functions during fracture healing. More research is needed to clarify macrophage phase-specific contributions, temporospatial subpopulation variance and macrophage specific-molecular mediators. There is also clear motivation for determining whether macrophage alterations underlie compromised fracture healing. Overall, there is strong justification to pursue strategies targeting macrophages and/or their products for improving normal bone healing and overcoming failed repair.

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Section: Macrophage Participation In Hard Callus Formation and Remodementioning

confidence: 99%

Unraveling macrophage contributions to bone repair

et al. 2013

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“…Mast cell numbers and the extent of mast cell degranulation were assessed manually. Cryosections of the aortic root (10 mm) were collected and stained with COX-2 or arginase-1 to detect M1 and M2 macrophages as described previously (21). Additionally, the aortic arch and its main branch points were excised (4 mm), fixed, and embedded in paraffin.…”

Section: Histological Analysis and Morphometrymentioning

confidence: 99%

Interruption of the OX40–OX40 Ligand Pathway in LDL Receptor–Deficient Mice Causes Regression of Atherosclerosis

Foks

Puijvelde

Bot

et al. 2013

The Journal of Immunology

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Patients suffering from cardiovascular disease have well-established atherosclerotic lesions, rendering lesion regression of therapeutic interest. The OX40 (TNFRSF4)–OX40 ligand (OX40L; TNFSF4) pathway is important for the proliferation and survival of T cells, stimulates B cells, and is associated with cardiovascular disease. We hypothesized that interference with the OX40–OX40L pathway, in combination with decreases in cholesterol, may induce regression of atherosclerosis. LDLr−/− mice were fed a Western-type diet for 10 wk, after which they received chow diet and were treated with anti-OX40L or PBS for 10 wk. A significant regression of lesions was observed in the aorta and aortic arch of anti-OX40L–treated mice compared with control mice. Interference of the OX40–OX40L pathway reduced Th2 responses, as shown by decreases in GATA-3 and IL-4 levels. Also, IgE levels were decreased, as demonstrated by reduced mast cell presence and activation. Notably, IL-5 production by T and B1 cells was increased, thus enhancing atheroprotective oxidized low-density lipoprotein–specific IgM production. The increase in IL-5 production and IgM was mediated by IL-33 production by APCs upon OX40L blockade. We conclude that interruption of the OX40–OX40L signaling pathway, combined with decreases in dietary cholesterol, induces the regression of atherosclerosis through induction of IL-5–producing T cells and oxidized low-density lipoprotein–specific IgM and reductions in Th2 and mast cells.

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“…Signal-transduction pathways, such as MAPKs (eg, ERK1 and ERK2) can inhibit or stimulate the transcription of MMPs. 26 The ETS family, 27 NFκB, 28 STATs, 11 CIZ, and p53 29 serve as positive modulators, while TGFβ-inhibitory elements or AG-rich elements serve as negative modulators of MMP transcription.…”

mentioning

confidence: 99%

Matrix metalloproteinases in head and neck cancer: current perspectives

Gkouveris¹,

Nikitakis²,

Aseervatham³

et al. 2017

MNM

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Matrix metalloproteinases (MMPs) are zinc-dependent endopeptidases encoded by 24 distinct genes. Their functions have been implicated in numerous normal and pathologic processes, including uterine involution and organogenesis, inflammation and wound healing, vascular and autoimmune disease progression. Pertinent to this review, the role of MMPs in cancer biology is fairly well researched and documented, and remains a subject of continuing intense investigation. Not only are several MMPs overexpressed in head and neck squamous cell carcinomas (HNSCCs), expression has been correlated with salient tumorigenic hallmarks, such as cell proliferation, angiogenesis, invasion, and metastasis. The utility of changes in the expression profile, as well as various MMP polymorphisms as potential prognostic markers in oral cancers and oral premalignant lesions, have been investigated. Furthermore, the potential therapeutic utility of targeting MMPs in cancer remains attractive, although outcomes in this respect appear so far to be less encouraging with respect to HNSCCs. Because of the disappointing results observed in clinical trials where MMP-targeting regimens for HNSCCs utilized broad-spectrum small MMP catalytic site inhibitors, investigators now envision new strategies for MMP-specific targeting based on the recognition of new noncatalytic MMP domains with distinct functions. This review provides an overview of MMP activities in general and in cancers, and an update of their activities in HNSCC. Specifically, their role in the development and progression of HNSCC and their function as signaling molecules is discussed. Finally, their role as potential prognostic biomarkers and therapeutic targets in HNSCC is revisited.

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Classical Macrophage Activation Up-Regulates Several Matrix Metalloproteinases through Mitogen Activated Protein Kinases and Nuclear Factor-κB

Cited by 144 publications

References 40 publications

Unraveling macrophage contributions to bone repair

Unraveling macrophage contributions to bone repair

Interruption of the OX40–OX40 Ligand Pathway in LDL Receptor–Deficient Mice Causes Regression of Atherosclerosis

Matrix metalloproteinases in head and neck cancer: current perspectives

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