Immunohistochemical analysis of MMP-9, MMP-2 and TIMP-1, TIMP-2 expression in the central nervous system following infection with viral and bacterial meningitis.

Sulik, Artur; Chyczewski, L

doi:10.2478/v10042-008-0058-8

Cited by 19 publications

(16 citation statements)

References 22 publications

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“…Endothelial permeability changes are also associated with the activation of MMPs and the spatial redistribution of surface cadherin and occludin (Alexander & Elrod 2002). MMP9, secreted by endothelial cells, disrupted the blood-brain barrier and made leukocyte recruitment because it was able to degrade components of the basal membrane of cerebral vessels (Sulik & Chyczewski 2008). Endothelial MMP2, which is activated by breast cancer cell adhesion to VE cells, could degrade interendothelial junctional protein VE-cadherin and promote cancer cell transendothelial migration (Shen et al 2010).…”

Section: Discussionmentioning

confidence: 99%

Melatonin inhibits IL1β-induced MMP9 expression and activity in human umbilical vein endothelial cells by suppressing NF-κB activation

Qin

Lu²,

Li³

et al. 2012

Journal of Endocrinology

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Matrix metalloproteinases (MMPs) have been involved in inflammatory and degradative processes in pathologic conditions. The purpose of this study was to investigate the protective effect of melatonin in human umbilical vein endothelial cell (HUVEC) monolayer permeability and the regulation of MMP9 induced by interleukin 1b (IL1b (IL1B)) in HUVECs. Protection studies were carried out with melatonin, a well-known antioxidant and antiinflammatory molecule. MMP9 expression was increased with IL1b induction in HUVECs. Melatonin showed a barrier-protective role by downregulation of MMP9 and upregulation of tissue inhibitor of metalloproteinase-1 expression in HUVECs. Meanwhile, melatonin also decreased sodium fluorescein permeability and counteracted the downregulation of vascular endothelial cadherin and occludin expression in HUVECs. During inflammatory stimulus, nuclear factor-kB (NF-kB) plays a significant role in regulating MMP genes expression, thus the function of NF-kB in HUVECs' barrier disruption was investigated. IL1b induced nuclear translocation of NF-kB in HUVECs and regulated MMP9 expression. However, NF-kB translocation into the nucleus was inhibited significantly by melatonin. Our results show that melatonin decreases the permeability of monolayer endothelial cell induced by IL1b. At the same time, melatonin decreased the expression and activity of MMP9 by a NF-kB-dependent pathway in HUVECs induced by IL1b.

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Section: Discussionmentioning

confidence: 99%

Melatonin inhibits IL1β-induced MMP9 expression and activity in human umbilical vein endothelial cells by suppressing NF-κB activation

Qin

Lu²,

Li³

et al. 2012

Journal of Endocrinology

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“…() found that MMP‐9 is elevated in cerebrospinal fluid (CSF) in patients with bacterial meningitis. Furthermore, Sulik and Chyczewski () reported a higher proportion of MMP‐9‐positive endothelial cells in postmortem brains in patients with bacterial and viral meningitis. Giraudon et al .…”

Section: Pathologies: Predisposition Diagnosis and Therapy (Animal mentioning

confidence: 99%

MMP‐9 in translation: from molecule to brain physiology, pathology, and therapy

Vafadari

Salamian

Kaczmarek

2016

Journal of Neurochemistry

311

257

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Matrix metalloproteinase-9 (MMP-9) is a member of the metzincin family of mostly extracellularly operating proteases. Despite the fact that all of these enzymes might be target promiscuous, with largely overlapping catalogs of potential substrates, MMP-9 has recently emerged as a major and apparently unique player in brain physiology and pathology. The specificity of MMP-9 may arise from its very local and time-restricted actions, even when released in the brain from cells of various types, including neurons, glia, and leukocytes. In fact, the quantity of MMP-9 is very low in the naive brain, but it is markedly activated at the levels of enzymatic activity, protein abundance, and gene expression following various physiological stimuli and pathological insults. Neuronal MMP-9 participates in synaptic plasticity by controlling the shape of dendritic spines and function of excitatory synapses, thus playing a pivotal role in learning, memory, and cortical plasticity. When improperly unleashed, MMP-9 contributes to a large variety of brain disorders, including epilepsy, schizophrenia, autism spectrum disorder, brain injury, stroke, neurodegeneration, pain, brain tumors, etc. The foremost mechanism of action of MMP-9 in brain disorders appears to be its involvement in immune/inflammation responses that are related to the enzyme's ability to process and activate various cytokines and chemokines, as well as its contribution to bloodbrain barrier disruption, facilitating the extravasation of leukocytes into brain parenchyma. However, another emerging possibility (i.e., the control of MMP-9 over synaptic plasticity) should not be neglected. The translational potential of MMP-9 has already been recognized in both the diagnosis and treatment domains. The most striking translational aspect may be the discovery of MMP-9 up-regulation in a mouse model of Fragile X syndrome, quickly followed by human studies and promising clinical trials that have sought to inhibit MMP-9. With regard to diagnosis, suggestions have been made to use MMP-9 alone or combined with tissue inhibitor of matrix metalloproteinase-1 or brain-derived neurotrophic factor as disease biomarkers.

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“…MMPs are produced mainly by activated neutrophils and, to a lesser extent, also by macrophages, monocytes, and possibly TNF-␣-stimulated endothelial cells (194,233). Furthermore, constitutive MMP expression is found on microglial cells and astrocytes and may be modulated during neuroinflammation and meningitis (102,173,464).…”

Section: Mmpsmentioning

confidence: 99%

Pathogenesis and Pathophysiology of Pneumococcal Meningitis

et al. 2011

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SUMMARY Pneumococcal meningitis continues to be associated with high rates of mortality and long-term neurological sequelae. The most common route of infection starts by nasopharyngeal colonization by Streptococcus pneumoniae , which must avoid mucosal entrapment and evade the host immune system after local activation. During invasive disease, pneumococcal epithelial adhesion is followed by bloodstream invasion and activation of the complement and coagulation systems. The release of inflammatory mediators facilitates pneumococcal crossing of the blood-brain barrier into the brain, where the bacteria multiply freely and trigger activation of circulating antigen-presenting cells and resident microglial cells. The resulting massive inflammation leads to further neutrophil recruitment and inflammation, resulting in the well-known features of bacterial meningitis, including cerebrospinal fluid pleocytosis, cochlear damage, cerebral edema, hydrocephalus, and cerebrovascular complications. Experimental animal models continue to further our understanding of the pathophysiology of pneumococcal meningitis and provide the platform for the development of new adjuvant treatments and antimicrobial therapy. This review discusses the most recent views on the pathophysiology of pneumococcal meningitis, as well as potential targets for (adjunctive) therapy.

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Immunohistochemical analysis of MMP-9, MMP-2 and TIMP-1, TIMP-2 expression in the central nervous system following infection with viral and bacterial meningitis.

Cited by 19 publications

References 22 publications

Melatonin inhibits IL1β-induced MMP9 expression and activity in human umbilical vein endothelial cells by suppressing NF-κB activation

Melatonin inhibits IL1β-induced MMP9 expression and activity in human umbilical vein endothelial cells by suppressing NF-κB activation

MMP‐9 in translation: from molecule to brain physiology, pathology, and therapy

Pathogenesis and Pathophysiology of Pneumococcal Meningitis

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