Interleukin-18 induces EMMPRIN expression in primary cardiomyocytes via JNK/Sp1 signaling and MMP-9 in part via EMMPRIN and through AP-1 and NF-κB activation

Reddy, V. Seenu; Prabhu, Sumanth D.; Mummidi, Srinivas; Valente, Anthony J.; Venkatesan, Balachandar; Shanmugam, Prakashsrinivasan; Delafontaine, Patrick; Chandrasekar, Bysani

doi:10.1152/ajpheart.00451.2010

Cited by 72 publications

(81 citation statements)

References 52 publications

(73 reference statements)

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“…Mechanisms of regulation of endogenous CD147 expression are not well established, although several growth factors and cytokines have been shown to increase CD147 levels in a variety of contexts (Hagemann et al, 2005;Menashi et al, 2003;Reddy et al, 2010;Rucci et al, 2010). Previous studies have shown that Src is a crucial regulator of invadopodia formation (Murphy and Courtneidge, 2011), and a recent study showed that the Src family kinase, Fyn kinase, induces emmprin expression (Ramos and Dang, 2011).…”

Section: Discussionmentioning

confidence: 99%

Regulation of invadopodia formation and activity by CD147

Grass

Bratoeva

Toole

2012

Journal of Cell Science

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SummaryA defining feature of malignant tumor progression is cellular penetration through the basement membrane and interstitial matrices that separate various cellular compartments. Accumulating evidence supports the notion that invasive cells employ specialized structures termed invadopodia to breach these structural barriers. Invadopodia are actin-based, lipid-raft-enriched membrane protrusions containing membrane-type-1 matrix metalloproteinase (MT1-MMP; also known as matrix metalloproteinase 14; MMP14) and several signaling proteins. CD147 (emmprin, basigin), an immunoglobulin superfamily protein that is associated with tumor invasion and metastasis, induces the synthesis of various matrix metalloproteinases in many systems. In this study we show that upregulation of CD147 is sufficient to induce MT1-MMP expression, invasiveness and formation of invadopodia-like structures in non-transformed, non-invasive, breast epithelial cells. We also demonstrate that CD147 and MT1-MMP are in close proximity within these invadopodialike structures and co-fractionate in membrane compartments with the properties of lipid rafts. Moreover, manipulation of CD147 levels in invasive breast carcinoma cells causes corresponding changes in MT1-MMP expression, invasiveness and invadopodia formation and activity. These findings indicate that CD147 regulates invadopodia formation and activity, probably through assembly of MT1-MMPcontaining complexes within lipid-raft domains of the invadopodia.

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Section: Discussionmentioning

confidence: 99%

Regulation of invadopodia formation and activity by CD147

Grass

Bratoeva

Toole

2012

Journal of Cell Science

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“…Tumor necrosis factor-a increases MMP-9 promoter activity in plasmids, likely through activator protein-1, nuclear factor k-light-chain-enhancer of activated B cells, or specificity protein-1 (Sato et al, 1993). Likewise, interleukins such as interleukin-17 and -18 induce MMP-9 expression via nuclear factor k-light-chain-enhancer of activated B cells and activator protein-1 pathways (Reddy et al, 2010).…”

Section: Inflammation and Mmps In Vvsmentioning

confidence: 99%

Matrix Metalloproteinases as Regulators of Vein Structure and Function: Implications in Chronic Venous Disease

MacColl

Khalil

2015

J Pharmacol Exp Ther

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Lower-extremity veins have efficient wall structure and function and competent valves that permit upward movement of deoxygenated blood toward the heart against hydrostatic venous pressure. Matrix metalloproteinases (MMPs) play an important role in maintaining vein wall structure and function. MMPs are zinc-binding endopeptidases secreted as inactive pro-MMPs by fibroblasts, vascular smooth muscle (VSM), and leukocytes. ProMMPs are activated by various activators including other MMPs and proteinases. MMPs cause degradation of extracellular matrix (ECM) proteins such as collagen and elastin, and could have additional effects on the endothelium, as well as VSM cell migration, proliferation, Ca 21 signaling, and contraction. Increased lower-extremity hydrostatic venous pressure is thought to induce hypoxia-inducible factors and other MMP inducers/ activators such as extracellular matrix metalloproteinase inducer, prostanoids, chymase, and hormones, leading to increased MMP expression/activity, ECM degradation, VSM relaxation, and venous dilation. Leukocyte infiltration and inflammation of the vein wall cause further increases in MMPs, vein wall dilation, valve degradation, and different clinical stages of chronic venous disease (CVD), including varicose veins (VVs). VVs are characterized by ECM imbalance, incompetent valves, venous reflux, wall dilation, and tortuosity. VVs often show increased MMP levels, but may show no change or decreased levels, depending on the VV region (atrophic regions with little ECM versus hypertrophic regions with abundant ECM) and MMP form (inactive pro-MMP versus active MMP). Management of VVs includes compression stockings, venotonics, and surgical obliteration or removal. Because these approaches do not treat the causes of VVs, alternative methods are being developed. In addition to endogenous tissue inhibitors of MMPs, synthetic MMP inhibitors have been developed, and their effects in the treatment of VVs need to be examined.

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“…41,42 Overexpression of IL-18 in cardiomyocytes also induced activation of multiple transcription factors, including NF-B and IFN regulatory factor-1. 43 Data increasingly support an important role of IL-18 in mediating aspects of adverse cardiac remodeling.…”

Section: Cytokinesmentioning

confidence: 99%

The Fire Within: Cardiac Inflammatory Signaling in Health and Disease

Coggins

Rosenzweig

2012

Circulation Research

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Inflammatory mediators are operative in the pathogenesis of the most common forms of heart disease.Although in most cases the induction of these pathways is maladaptive and deleterious, there are notable exceptions when inflammatory pathways participate in healing or limiting the extent of injury. The appreciation of the role of these mechanisms in myocardial homeostasis and pathophysiology has led to increased efforts to elucidate the specific signaling pathways most relevant to the heart. Our goal in this introductory overview is to provide context for the five detailed reviews that follow by introducing the major relevant stimuli, the receptors, and pathways that mediate inflammatory signaling in the heart. We try to impart a sense of the scope and complexity of these pathways, as well as their interactions with signaling pathways regulating cell survival and metabolism. These complexities underscore the potential challenges of therapeutically targeting inflammatory mechanisms in heart disease and may help explain the mostly disappointing results of this approach to date. (Circ Res. 2012;110:116-125.)

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Interleukin-18 induces EMMPRIN expression in primary cardiomyocytes via JNK/Sp1 signaling and MMP-9 in part via EMMPRIN and through AP-1 and NF-κB activation

Cited by 72 publications

References 52 publications

Regulation of invadopodia formation and activity by CD147

Regulation of invadopodia formation and activity by CD147

Matrix Metalloproteinases as Regulators of Vein Structure and Function: Implications in Chronic Venous Disease

The Fire Within: Cardiac Inflammatory Signaling in Health and Disease

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