Matrix metalloproteinase-9 (MMP-9) and tissue inhibitor of matrix metalloproteinase (TIMP-1) in patients with relapsing–remitting multiple sclerosis treated with interferon beta

Boz, Cavit; Özmenoğlu, Mehmet; Velioğlu, Sibel; Kilinç, Kağan; Örem, Asım; Alioğlu, Zekeriya; Altunayoglu, Vildan

doi:10.1016/j.clineuro.2005.01.005

Cited by 65 publications

(41 citation statements)

References 39 publications

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“…There is also evidence implicating TIMPs in MS, with alterations in MS serum (Waubant et al, 2001;Waubant et al, 1999) and CSF (Boz et al, 2006). In TIMP-1 knockout mice, EAE is more severe, suggesting TIMP-1 may have protective effects (Crocker et al, 2006), so the balance between MMPs and TIMPs may also be important.…”

Section: Introductionmentioning

confidence: 99%

Cleavage of myelin associated glycoprotein by matrix metalloproteinases

Milward

Kim

Szklarczyk

et al. 2008

Journal of Neuroimmunology

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Derivative myelin associated glycoprotein (dMAG) results from proteolysis of transmembrane MAG and can inhibit axonal growth. We have tested the ability of certain matrix metalloproteinases Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public Access

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Section: Introductionmentioning

confidence: 99%

Cleavage of myelin associated glycoprotein by matrix metalloproteinases

Milward

Kim

Szklarczyk

et al. 2008

Journal of Neuroimmunology

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“…Increased MMPs activity might be one of the factors that cause progression of MS disease (5). Imbalance in the level of these enzymes has been detected in the serum and cerebrospinal fluid (CSF) of MS patients (6)(7)(8). These enzymes have a key role in the destruction of the blood-brain barrier (BBB) and central nervous system (7)(8)(9).…”

Section: Introductionmentioning

confidence: 99%

“…Imbalance in the level of these enzymes has been detected in the serum and cerebrospinal fluid (CSF) of MS patients (6)(7)(8). These enzymes have a key role in the destruction of the blood-brain barrier (BBB) and central nervous system (7)(8)(9). Matrix methalloproteinase-7 (MMP-7) is an important member of MMPs family that af-fects many ECM and non-ECM substrates, and has a role in tumor metastasis and angiogenesis (10).…”

Section: Introductionmentioning

confidence: 99%

The Association Between Matrix Metalloproteinase-7 A-181G Polymorphism and the Risk of Relapsing-Remitting Multiple Sclerosis in Iranian Kurdish Patients from Kermanshah

Mohammadi¹,

Rahimi²,

Rahimi³

2015

Avicenna J Med Biochem

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Background: Multiple sclerosis (MS) is a common chronic genetic disease of the central nervous system. The relapsing-remitting-MS (RR-MS) is the most common form of this disease. Matrix metalloproteinase-7 (MMP-7) is an important member of the MMP family, which degrades many extracellular matrix components. The common polymorphism of MMP-7 A-181G is associated with some diseases. Objectives: The aim of the present study was to determine the influence of this polymorphism on the risk of RR-MS. Materials and Methods: Eighty RR-MS patients and 80 healthy individuals as controls from the Kermanshah province were studied for MMP-7 A-181G polymorphism by using the PCR-RFLP method. Data were analyzed using the SPSS statistical software package version 16.0. Results: In RR-MS patients the frequency of MMP-7 GG genotype was significantly (P = 0.028) higher compared to that of the controls. The presence of GG genotype increased the risk of RR-MS by 1.69 times [OR = 1.69 and 95% CI = 1.05-2.72, P = 0.03]. The frequency of MMP-7 G allele in RR-MS patients was significantly higher (51.2%, P = 0.043) than that of the controls (40%). The presence of this allele increased the risk of RR-MS by 1.58 folds (P = 0.044). Conclusions: Our findings indicate that the presence of G allele of MMP-7 A-181G polymorphism might increase the risk of RR-MS in our population.

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“…44 -46 In contrast, and in parallel to our findings in TIMP-1 Ϫ/Ϫ mice, increased expression of MMPs by macrophages has been reported in the active lesions from human cases of MS. 47 Many studies therefore have relied on the ratio of TIMP-1 levels relative to MMP expression as an indicator of net proteolytic activity. 45,48,49 Although this approach may reflect the overall function of MMPs, it reveals little of the contribution of TIMP-1 to this disease. Given the general lack of increased TIMP-1 expression in human cases of MS, the dramatic increase in TIMP-1 during EAE models of demyelination represent a primary difference between MS in humans and autoimmune-induced myelin damage in WT animals.…”

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confidence: 99%

Persistent Macrophage/Microglial Activation and Myelin Disruption after Experimental Autoimmune Encephalomyelitis in Tissue Inhibitor of Metalloproteinase-1-Deficient Mice

Crocker

Whitmire

Frausto

et al. 2006

The American Journal of Pathology

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Increased leukocyte trafficking into the parenchyma during inflammatory responses in the central nervous system (CNS) isMultiple sclerosis (MS) is a demyelinating disease of the central nervous system (CNS). The etiology of MS is not known but inflammation and autoimmunity are central components of this disease. Many of the key features of MS can be modeled in rodents or nonhuman primates by immunization with myelin or myelin peptides that produce a condition called experimental autoimmune encephalomyelitis (EAE). In EAE, the development of myelin-specific T-cell responses and the infiltration of activated lymphocytes into the CNS parenchyma result in inflammation-mediated myelin injury. The infiltration of activated leukocytes into the CNS is required for immune-mediated myelin injury in both MS and EAE.1 Extravasation of immune cells into the CNS is facilitated by matrix metalloproteinases (MMPs). This large and diverse family of extracellular proteases are important regulators of tissue homeostasis and also are associated with cellular injury and pathology in a wide variety of CNS diseases, including MS. [2][3][4] In EAE, increased expression and activity of MMPs has been reported. 5 MMPs are produced predominantly by activated immune cells, 6,7 and MMPs facilitate the transmigration of these cells across the blood brain barrier by the proteolytic cleavage of substrates within the extracellular matrix.8 Deletion of MMP genes and pharmacological inhibition of MMP proteins lead to reduced immune cell trafficking into the CNS and attenuated demyelination during EAE.2,9 These findings indicate that elevated MMP expression and activity reported in the cerebrospinal fluid of MS patients likely reflects inadequate endogenous regulation

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Matrix metalloproteinase-9 (MMP-9) and tissue inhibitor of matrix metalloproteinase (TIMP-1) in patients with relapsing–remitting multiple sclerosis treated with interferon beta

Cited by 65 publications

References 39 publications

Cleavage of myelin associated glycoprotein by matrix metalloproteinases

Cleavage of myelin associated glycoprotein by matrix metalloproteinases

The Association Between Matrix Metalloproteinase-7 A-181G Polymorphism and the Risk of Relapsing-Remitting Multiple Sclerosis in Iranian Kurdish Patients from Kermanshah

Persistent Macrophage/Microglial Activation and Myelin Disruption after Experimental Autoimmune Encephalomyelitis in Tissue Inhibitor of Metalloproteinase-1-Deficient Mice

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