Vascular endothelial growth factor correlates with matrix metalloproteinase-9 in the pleural effusion

Jin, Heung Yong; Lee, K.S; Jin, Sun; Lee, Y.C

doi:10.1016/j.rmed.2003.09.002

Cited by 25 publications

(24 citation statements)

References 17 publications

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“…Mice lacking integrin β 3 have been reported to support effective angiogenesis [30], [31] whereas pharmacological inhibition of α V β 3 reduces angiogenesis in certain models [32]. The present data are consistent with reports showing that integrin α V β 3 is not needed for tumor angiogenesis in that β 3 -deficiency had no significant effects on vessel density or morphology.…”

Section: Discussionsupporting

confidence: 91%

Increased Fibrosis and Interstitial Fluid Pressure in Two Different Types of Syngeneic Murine Carcinoma Grown in Integrin β3-Subunit Deficient Mice

et al. 2012

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Stroma properties affect carcinoma physiology and direct malignant cell development. Here we present data showing that αVβ3 expressed by stromal cells is involved in the control of interstitial fluid pressure (IFP), extracellular volume (ECV) and collagen scaffold architecture in experimental murine carcinoma. IFP was elevated and ECV lowered in syngeneic CT26 colon and LM3 mammary carcinomas grown in integrin β3-deficient compared to wild-type BALB/c mice. Integrin β3-deficiency had no effect on carcinoma growth rate or on vascular morphology and function. Analyses by electron microscopy of carcinomas from integrin β3-deficient mice revealed a coarser and denser collagen network compared to carcinomas in wild-type littermates. Collagen fibers were built from heterogeneous and thicker collagen fibrils in carcinomas from integrin β3-deficient mice. The fibrotic extracellular matrix (ECM) did not correlate with increased macrophage infiltration in integrin β3-deficient mice bearing CT26 tumors, indicating that the fibrotic phenotype was not mediated by increased inflammation. In conclusion, we report that integrin β3-deficiency in tumor stroma led to an elevated IFP and lowered ECV that correlated with a more fibrotic ECM, underlining the role of the collagen network for carcinoma physiology.

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Section: Discussionsupporting

confidence: 91%

Increased Fibrosis and Interstitial Fluid Pressure in Two Different Types of Syngeneic Murine Carcinoma Grown in Integrin β3-Subunit Deficient Mice

et al. 2012

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“…The fact that VEGF, which is a known potent inducer of capillary permeability [11], acts in part via actions upon MMP production further supports a role for MMP expression in abnormal vascular permeability in IPF [12,13].…”

mentioning

confidence: 88%

MMP expression and abnormal lung permeability are important determinants of outcome in IPF

McKeown¹,

Richter²,

O'Kane³

et al. 2009

European Respiratory Journal

156

113

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Matrix metalloproteinases (MMPs) degrade all of the extracellular matrix components of the intersititium and may play a role in abnormal alveolar permeability, which is a feature of idiopathic pulmonary fibrosis (IPF). The aims of the present study were to evaluate MMP protein levels in patients with IPF and determine any relationship to treatment and markers of permeability.In total, 20 patients with IPF and eight normal controls underwent bronchoalveolar lavage. MMP, tissue inhibitor of metalloproteinase, and vascular endothelial growth factor (VEGF) levels were related to clinical outcome and protein permeability index.MMP-3, -7, -8 and -9 were elevated in IPF lavage fluid and levels remained high despite treatment. Levels of MMP-3, -7, -8 and -9, VEGF and protein permeability index were higher in those who died early during follow-up. VEGF, and MMP-8 and -9 levels were higher in those with a rapidly declining lung function over 1 yr. Levels of MMP-3, -7, -8 and -9 correlated with an increased permeability index.Matrix metalloproteinase levels were elevated in idiopathic pulmonary fibrosis patients and were not modulated by current standard treatment. Matrix metalloproteinase production through an interaction with the known vascular permogen, vascular endothelial growth factor, was potentially associated with abnormal capillary permeability and may have potentiated the neoangiogenesis seen in idiopathic pulmonary fibrosis. The changes were greatest in those who died or progressed during follow-up, suggesting that drugs targeting vascular endothelial growth factor or matrix metalloproteinase activity warrant assessment as novel therapy for idiopathic pulmonary fibrosis.

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“…Several studies have shown that MMPs, in particular MMP-9, are expressed during the various manifestations of tuberculosis, including active cavitary tuberculosis (2,16,35), meningitis (20,22,34,41), and pleuritis (15,16,18). Thus, there are emerging data to suggest a strong role for MMP activity with the various pathological states associated with tuberculosis.…”

mentioning

confidence: 99%

Role for Matrix Metalloproteinase 9 in Granuloma Formation during PulmonaryMycobacterium tuberculosisInfection

et al. 2006

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Recent studies have shown that matrix metalloproteinases (MMPs) are induced by Mycobacterium tuberculosis during pulmonary infection. Here, expression of MMP-9 during pulmonary M. tuberculosis infection was characterized to determine whether its production correlated with disease resistance in vivo and to determine what role, if any, MMP-9 might have in granuloma formation. Following aerosol infection with M. tuberculosis, dissemination of bacilli occurred earlier in the C57BL/6 resistant mouse strain than in the susceptible CBA/J strain, as was evident from an increased number of bacteria in the blood, spleen, and liver at day 14 after infection. In addition, early dissemination of the bacilli was associated with early induction of protective immunity as assessed from gamma interferon levels. Nonspecific blocking of MMPs in C57BL/6 mice early during infection reduced hematogenous spread of the bacilli, suggesting that MMPs indeed play a role in facilitating dissemination, likely via extracellular matrix degradation. The concentration of active MMP-9, specifically, was greater in the lungs of C57BL/6 mice than in those of the CBA/J mice at day 28, thereby suggesting that MMP-9 is not one of the MMPs directly involved in promoting early dissemination of M. tuberculosis. Instead, however, histological lung sections and flow cytometric analysis of lung cells from MMP-9-knockout mice showed that MMP-9 is involved in macrophage recruitment and granuloma development. These combined data support the idea that early MMP activity is an essential component of resistance to pulmonary mycobacterial infection and that MMP-9, specifically, is required for recruitment of macrophages and tissue remodeling to allow for the formation of tight, well-organized granulomas.

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Vascular endothelial growth factor correlates with matrix metalloproteinase-9 in the pleural effusion

Cited by 25 publications

References 17 publications

Increased Fibrosis and Interstitial Fluid Pressure in Two Different Types of Syngeneic Murine Carcinoma Grown in Integrin β3-Subunit Deficient Mice

Increased Fibrosis and Interstitial Fluid Pressure in Two Different Types of Syngeneic Murine Carcinoma Grown in Integrin β3-Subunit Deficient Mice

MMP expression and abnormal lung permeability are important determinants of outcome in IPF

Role for Matrix Metalloproteinase 9 in Granuloma Formation during PulmonaryMycobacterium tuberculosisInfection

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