Secretions of MMP‐9 by soluble glucocorticoid‐induced tumor necrosis factor receptor (sGITR) mediated by protein kinase C (PKC)δ and phospholipase D (PLD) in murine macrophage

Lee, Hee-Sook; Park, So-Yun; Lee, Hyeon Woo; Choi, Hye-Seon

doi:10.1002/jcb.20099

Cited by 20 publications

(13 citation statements)

References 28 publications

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“…8,10,20,43 The high phosphatidic acid levels in the VM-M2 and VM-M3 cells are intriguing since phosphatidic acid participates in key macrophage functions to include invasion, phagocytosis, inflammation and the respiratory burst. 9,41,[44][45][46] Furthermore, phosphatidic acid and related lipid phosphate messengers may enhance tumor metastasis through receptor driven cellular processes as previously described. 9,47 The VM-M2 and VM-M3 cells will serve as an important new cell system for evaluating the role of lipids in metastatic disease.…”

Section: Discussionmentioning

confidence: 83%

Metastatic cancer cells with macrophage properties: Evidence from a new murine tumor model

Huysentruyt

Mukherjee

Banerjee

et al. 2008

Intl Journal of Cancer

154

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Metastasis is the process by which cancer cells disseminate from the primary neoplasm and invade surrounding tissue and distant organs, and is the primary cause of morbidity and mortality for cancer patients. Most conventional cancer therapies are ineffective in managing tumor metastasis. This has been due in large part to the absence of in vivo metastatic models that represent the full spectrum of metastatic disease. Here we identify 3 new spontaneously arising tumors in the inbred VM mouse strain, which has a relatively high incidence of CNS tumors. Two of the tumors (VM-M2 and VM-M3) reliably expressed all of the major biological processes of metastasis to include local invasion, intravasation, immune system survival, extravasation and secondary tumor formation involving liver, kidney, spleen, lung and brain. Metastasis was assessed through visual organ inspection, histology, immunohistochemistry and bioluminescence imaging. The metastatic VM tumor cells also expressed multiple properties of macrophages including morphological appearance, surface adhesion, phagocytosis, total lipid composition (glycosphingolipids and phospholipids) and gene expression (CD11b, Iba1, F4/80, CD68, CD45 and CXCR4). The third tumor (VM-NM1) grew rapidly and expressed properties of neural stem/progenitor cells, but was neither invasive nor metastatic. Our data indicate that spontaneous brain tumors can arise from different cell types in VM mice and that metastatic cancer can represent a disease of macrophage-like cells similar to those described in several human metastatic cancers.The new VM tumor model will be useful for defining the biological processes of cancer metastasis and for evaluating potential therapies for tumor management. ' 2008 Wiley-Liss, Inc.Key words: metastasis; microglia; gangliosides; neural stem cell; glioblastoma Metastasis is the process by which cancer cells disseminate from the primary neoplasm and invade surrounding tissue and distant organs and is the primary cause of morbidity and mortality for cancer patients. This process involves cancer cell detachment from the primary tumor, intravasation into the circulation, evasion of immune attack, extravasation at distant capillary beds and invasion and proliferation in distant organs. [1][2][3] In addition, the metastatic cells establish a microenvironment facilitating colonization (angiogenesis and further proliferation), resulting in macroscopic malignant secondary tumors.1-4 Metastatic cells preferentially invade those organs (lymph nodes, lung, liver, brain, bone, pleura and peritoneum) that promote tumor cell growth and survival consistent with the ''seed and soil'' hypothesis. 1,5,6 The metastatic and invasive potential of cancer cells is often correlated with abnormalities in phospholipids and in cell-surface glycolipids, which contribute to tumor progression.7-10 Hence, aberrant cellular migration and proliferation characterize the metastatic phenomenon.In this study, we analyzed the morphological, behavioral, biochemical and genetic properties of 3 n...

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Section: Discussionmentioning

confidence: 83%

Metastatic cancer cells with macrophage properties: Evidence from a new murine tumor model

Huysentruyt

Mukherjee

Banerjee

et al. 2008

Intl Journal of Cancer

154

View full text Add to dashboard Cite

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“…In addition, ROS have been implicated in zymogen activation through sulfenic acid production with the cysteine in the MMP pro-peptide, thereby allowing conformational change and autocatalysis (Nelson et al, 2004). Furthermore, prior studies have shown that the secretion of MMPs was dependent upon various PKC isoforms (Chakrabarti et al, 2006; Hussain et al, 2002; Lee et al, 2004; O’Toole et al, 2008; Park et al, 2003). Given that the activity of the conventional PKCs (α,β,γ) is calcium-dependent, it is conceivable that the acrolein-induced increase in intracellular calcium, observed in this study, could result in MMP release through the stimulated activity of one of these PKC isoforms.…”

Section: Discussionmentioning

confidence: 99%

Acrolein activates matrix metalloproteinases by increasing reactive oxygen species in macrophages

O’Toole

Zheng

Hellmann

et al. 2009

Toxicology and Applied Pharmacology

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Acrolein is a ubiquitous component of environmental pollutants such as automobile exhaust, cigarette, wood, and coal smoke. It is also a natural constituent of several foods and is generated endogenously during inflammation or oxidation of unsaturated lipids. Because increased inflammation and episodic exposure to acrolein-rich pollutants such as traffic emissions or cigarette smoke have been linked to acute myocardial infarction, we examined the effects of acrolein on matrix metalloproteinases (MMPs), which destabilize atherosclerotic plaques. Our studies show that exposure to acrolein resulted in the secretion of MMP-9 from differentiated THP-1 macrophages. Acrolein-treatment of macrophages also led to an increase in reactive oxygen species (ROS), free intracellular calcium ([Ca 2+ ] i ), and xanthine oxidase (XO) activity. ROS production was prevented by allopurinol, but not by rotenone or apocynin and by buffering changes in [Ca 2+ ] I with BAPTA-AM. The increase in MMP production was abolished by pre-treatment with the antioxidants Tiron and N-acetyl cysteine (NAC) or with the xanthine oxidase inhibitors allopurinol or oxypurinol. Finally, MMP activity was significantly stimulated in aortic sections from apoE-null mice containing advanced atherosclerotic lesions after exposure to acrolein ex vivo. These observations suggest that acrolein exposure results in MMP secretion from macrophages via a mechanism that involves an increase in [Ca 2+ ] I , leading to xanthine oxidase activation and an increase in ROS production. ROSdependent activation of MMPs by acrolein could destabilize atherosclerotic lesions during brief episodes of inflammation or pollutant exposure.

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“…40–44 For example, α and βIPKC increase the activity of MMP-9, but not MMP-2, primarily through the JNK-dependent pathway. 44 Other PKCs, such as θ and ζPKC, increase both MMP-2 and MMP-9 via ERK and NFκB pathways in adult rat cardiac fibroblasts.…”

Section: Cardiac Fibrosismentioning

confidence: 99%

Protein kinase C in heart failure: a therapeutic target?

Palaniyandi

Sun

Ferreira

et al. 2008

Cardiovascular Research

170

130

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Heart failure (HF) afflicts about 5 million people and causes 300 000 deaths a year in the United States alone. An integral part of the pathogenesis of HF is cardiac remodelling, and the signalling events that regulate it are a subject of intense research. Cardiac remodelling is the sum of responses of the heart to causes of HF, such as ischaemia, myocardial infarction, volume and pressure overload, infection, inflammation, and mechanical injury. These responses, including cardiomyocyte hypertrophy, myocardial fibrosis, and inflammation, involve numerous cellular and structural changes and ultimately result in a progressive decline in cardiac performance. Pharmacological and genetic manipulation of cultured heart cells and animal models of HF and the analysis of cardiac samples from patients with HF are all used to identify the molecular and cellular mechanisms leading to the disease. Protein kinase C (PKC) isozymes, a family of serine–threonine protein kinase enzymes, were found to regulate a number of cardiac responses, including those associated with HF. In this review, we describe the PKC isozymes that play critical roles in specific aspects of cardiac remodelling and dysfunction in HF.

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Secretions of MMP‐9 by soluble glucocorticoid‐induced tumor necrosis factor receptor (sGITR) mediated by protein kinase C (PKC)δ and phospholipase D (PLD) in murine macrophage

Cited by 20 publications

References 28 publications

Metastatic cancer cells with macrophage properties: Evidence from a new murine tumor model

Metastatic cancer cells with macrophage properties: Evidence from a new murine tumor model

Acrolein activates matrix metalloproteinases by increasing reactive oxygen species in macrophages

Protein kinase C in heart failure: a therapeutic target?

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