MMP-2, VCAM-1 and NCAM-1 expression in the brain of rats with experimental autoimmune encephalomyelitis as a trigger mechanism for synaptic plasticity and pathology

Jovanova-Nešić, Katica; Shoenfeld, Yehuda

doi:10.1016/j.jneuroim.2006.08.013

Cited by 20 publications

(23 citation statements)

References 51 publications

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“…As to the wide distribution of VCAM-1 in human tissues and organs, this molecule is implicated in a plenty of pathophysiological situations, which include autoimmune diseases [31], cardiovascular disease [32], or infections [33]. Recently, its function in tumor progression and metastasis has drawn increasing attentions.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-181a-5p Impedes IL-17-Induced Nonsmall Cell Lung Cancer Proliferation and Migration through Targeting VCAM-1

Cao

Zhao

et al. 2017

Cell Physiol Biochem

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Aim: The contribution of the inflammatory mediator interleukin-17 (IL-17) in nonsmall cell lung cancer (NSCLC) malignancy has been reported in the literature. MicroRNA-181a-5p (miR-181a-5p) acts as a tumor suppressor which can regulate target gene at the posttranscriptional level. Our study aimed to investigate the interaction between IL-17 and miR-181a-5p in NSCLC. Methods: 35 patients with NSCLC and 24 COPD controls were selected and examined in our study. In vitro, H226 and H460 cell lines were exposed to different doses (20, 40, 60, and 80 ng/mL) of IL-17 to examine the effect of IL-17 on miR-181a-5p and vascular cell adhesion molecule 1 (VCAM-1) expression. MiR-181 mimic and miR-181a-5p inhibitor were transfected to explore the regulation of VCAM-1 as well as tumor cell proliferation and migration. Results: miR-181a-5p expression was downregulated, and IL-17 and VCAM-1 expression was upregulated in NSCLC tissues. Furthermore, IL-17 decreased miR-181a-5p expression but increased VCAM-1 expression in H226 and H460 cells. MiR-181 regulated VCAM-1 expression through binding to 3’-UTR sequence. MiR-181 attenuated tumor cell proliferation and migration. IL-17 modulated miR-181a-5p expression through activating NF-κB but not Stat3. Conclusion: Taken together, our data show the regulation of VCAM-1 expression by miR-181a-5p under IL-17 exposure, predicting a potential way for counteracting cancer metastasis.

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Section: Discussionmentioning

confidence: 99%

MicroRNA-181a-5p Impedes IL-17-Induced Nonsmall Cell Lung Cancer Proliferation and Migration through Targeting VCAM-1

Cao

Zhao

et al. 2017

Cell Physiol Biochem

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“…MMP levels are increased in MS (Anthony et al, 1997;Cossins et al, 1997;Gijbels et al, 1992;Maeda and Sobel, 1996;Ozenci et al, 2000;Ozenci et al, 1999;Rosenberg et al, 1996;Sellebjerg et al, 2000;Trojano et al, 1999;Waubant et al, 1999) and in animal models of MS including experimental allergic encephalomyelitis (EAE) Gijbels et al, 1993;Graesser et al, 1998;Graesser et al, 2000;Jovanova-Nesic and Shoenfeld, 2006;Kieseier et al, 1998;Teesalu et al, 2001), and are very closely linked to pathogenesis and disease progression. Elevated serum MMP activity is detectable extremely early in the disease course, being present even in prodromal phases prior to development of clinically diagnosed MS (Correale and Bassani Molinas Mde, 2003).…”

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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“…In contrast to non-CNS barriers that constitutively express high levels of both adhesion molecules VCAM-1 and ICAM-1 (Steffen, Breier, Butecher, Schultz, & Engelhardt, 1996;Hofman et al, 2002), we and others have shown that brain-derived endothelial cells (Brown, McFarlin, & Raine, 1991;Jovanova-Nesic, & Shoenfeld, 2006) have reduced levels of expression of these molecules under basal conditions (Wolburg, Gerhardt, Schulz, Wolburg, & Engelhardt, 2004), and represent a less permissive barrier to cell migration comparing to that high endothelial venules (HUVECs) in the periphery (Wong, Prameya, & Dorovini-Zis, 1999).…”

Section: Introductionmentioning

confidence: 60%

“…The mechanisms of CSF secretion by CP (Speake et al, 2001), and the role of CP in CSF homeostasis and brain viability becomes more evident when the system fails (Johanson, Silverberg, Donahue, & Stopa, 2005). Thus, limited number of endothelial cells and increased expression of VCAM-1 + immunoreactivity in the choroids plexus in acute EAE (Jovanova-Nesic, & Shoenfeld, 2006) shows emerging importance of the choroids plexus epithelial system in EAE induction. Detailed analysis of epithelial cell expression of adhesive molecules and matrix metalloproteinases (MMPs) are necessary to evaluate how diminished choroidal functions affect the surrounding brain in the face of EAE, and multiple sclerosis (Sobel, 1998).…”

Section: Introductionmentioning

confidence: 99%

Magnetic Brain Stimulation Upregulates Adhesion and Prevents Eae: MMP-2, ICAM-1, and VCAM-1 in the Choroid Plexus as a Target

Jovanova-Nešić¹,

Jovičić²,

Sovilj³

et al. 2009

International Journal of Neuroscience

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Clinical signs appearance and significant increases of ICAM-1 and MMP-2 expressions with the clusters of VCAM-1(+) immunoreactivity in the choroids plexus epithelium to transferred anti-myelin oligodendroglial antibodies into the third brain ventricle, indicate important role of choroids plexus in the induction of acute experimental autoimmune encephalomyelitis (EAE). Magnetic brain stimulation with AKMA micro-magnet flux density of 60 miliTesla, 5 mm in diameter, implanted upon the pineal gland (PG), immediately after antibody injection, significantly decreases the expression of MMP-2 and ICAM-1 in the choroids plexus of the rat brain and abruptly suppresses the induction of acute EAE.

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MMP-2, VCAM-1 and NCAM-1 expression in the brain of rats with experimental autoimmune encephalomyelitis as a trigger mechanism for synaptic plasticity and pathology

Cited by 20 publications

References 51 publications

MicroRNA-181a-5p Impedes IL-17-Induced Nonsmall Cell Lung Cancer Proliferation and Migration through Targeting VCAM-1

MicroRNA-181a-5p Impedes IL-17-Induced Nonsmall Cell Lung Cancer Proliferation and Migration through Targeting VCAM-1

Cleavage of myelin associated glycoprotein by matrix metalloproteinases

Magnetic Brain Stimulation Upregulates Adhesion and Prevents Eae: MMP-2, ICAM-1, and VCAM-1 in the Choroid Plexus as a Target

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