Effect of interferon �-1a on serum matrix metalloproteinase?9 (MMP-9) and tissue inhibitor of matrix metalloproteinase (TIMP-1) in relapsing remitting multiple sclerosis patients

Karabudak, Rana; Kurne, Aslı; Güç, Dicle; Şengelen, Meltem; Canpınar, Hande; Kansu, Emin

doi:10.1007/s00415-004-0285-7

Cited by 32 publications

(18 citation statements)

References 23 publications

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“…MMP release as a consequence of Erk1/2 signaling has recently been demonstrated in several cell types including microvascular endothelial cells and HUVECs [25][26][27][28][29][30][31]. MMP9 activity has been associated with increased BBB permeability in models of stroke [33,34] and trauma [35] and its role in immune cell BBB transmigration to the brain is well characterized [36][37][38][39][40]. Macrophages in MS lesions, and in some reports leukocytes, express several MMPs including MMP9 and CSF concentration of MMP9 may reflect disease activity in MS [41].…”

Section: Discussionmentioning

confidence: 99%

Death receptor expression and function at the human blood brain barrier

Wosik¹,

Biernacki²,

Khouzam³

et al. 2007

Journal of the Neurological Sciences

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Section: Discussionmentioning

confidence: 99%

Death receptor expression and function at the human blood brain barrier

Wosik¹,

Biernacki²,

Khouzam³

et al. 2007

Journal of the Neurological Sciences

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“…Moreover the serum MMP-9:TIMP-1 ratio was a good predictor of the number of gadolinium-enhancing lesions [53]. In yet another study, Karabudak et al [54] reported that while MMP-9 levels did not change during a 1 year period with interferon-beta therapy, levels of TIMP-1 increased.…”

Section: Mmpmentioning

confidence: 96%

Elevation of matrix metalloproteinases (MMPs) in multiple sclerosis and impact of immunomodulators

Yong

Zabad

Agrawal

et al. 2007

Journal of the Neurological Sciences

150

127

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“…It was demonstrated that matrix metalloproteinase type 9 (MMP-9) activity can be decreased by IFNβ-1b treatment in vitro 16 , which could difficult the migration of lymphocytes across the fibronectin of cerebral endothelium. Another study did not find any difference in the MMP-9 levels during the treatment with IFNβ 17 . Besides the role of the metalloproteinases, IFNβ can modulate the expression and traffic of other molecules like cytokines, chemokines, adhesion molecules and integrins [16][17][18] , improving endothelial barrier function and prevent the transmigration of leukocytes and other neurotoxic mediators across the BBB to sites of CNS inflammation 10 .…”

Section: Effects On Bbbmentioning

confidence: 99%

Classical immunomodulatory therapy in multiple sclerosis: how it acts, how it works

Mendes

Sá

2011

Arq. Neuro-Psiquiatr.

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Interferon beta (IFNβ) and glatiramer acetate (GA) were the first immunomodulators approved to the treatment of relapsing-remitting multiple sclerosis (MS) and clinically isolated syndromes. Despite the enlargement of the therapeutic armamentarium, IFNβ and GA remain the most widely drugs and the therapeutic mainstay of MS. Objective: To review the mechanisms of action of IFNβ and GA and main clinical results in MS. Results: IFNβ modulates T and B-cell activity and has effects on the blood-brain barrier. The well proved mechanism of GA is an immune deviation by inducing expression of anti-inflammatory cytokines. Some authors favor the neuroprotective role of both molecules. Clinical trials showed a 30% reduction on the annualized relapse rate and of T2 lesions on magnetic resonance. Conclusion: Although the precise mechanisms how IFNβ and GA achieve their therapeutics effects remain unclear, these drugs have recognized beneficial effects and possess good safety and tolerability profiles. The large clinical experience in treating MS patients with these drugs along almost two decades deserves to be emphasized, at a time where the appearance of drugs with more selective mechanisms of action, but potentially less safer, pave the way to a better selection of the most appropriate individualized treatment. Key words: multiple sclerosis, interferon beta, glatiramer acetate, immunomodulatory therapy.Terapêutica imunomoduladora clássica na esclerose múltipla: como atua, como funciona RESUMO O interferão beta (IFNβ) e o acetato de glatirâmero (GA) foram os primeiros imunomoduladores aprovados para o tratamento da esclerose múltipla (EM) surtoremissão e doentes com síndromes clinicamente isoladas. Apesar do alargamento do armamentário terapêutico, o IFNβ e o GA continuam a ser os medicamentos mais usados na EM. Objetivo: Rever os mecanismos de acção do IFNβ e do GA e os principais resultados na clínica. Resultados: O IFNβ modula a actividade das células T e B e tem efeitos sobre a barreira hemato-encefálica. O mecanismo melhor comprovado do GA é o desvio imune através da indução da expressão de citocinas. Alguns autores favorecem ainda um papel neuroprotetor para ambos. Os ensaios clínicos mostraram diminuição da taxa anualizada de surtos de 30% e das lesões em T2 na ressonância magnética. Conclusão: Embora os mecanismos pelos quais o IFNβ e o GA atingem os seus efeitos terapêuticos continuem a ser pouco claros, estes fármacos possuem efeitos benéficos reconhecidos e bons perfis de segurança e tolerabilidade. A grande experiência clínica no tratamento da EM com estes fármacos ao longo de quase duas décadas merece ser destacada, numa altura em que o aparecimento de novos fármacos com mecanismos de acção mais seletivos, mas potencialmente menos seguros, possibilitarão melhor seleção e individualização do tratamento. Palavras-chave: esclerose múltipla, interferão beta, acetato de glatirâmero, terapêutica imunomoduladora.

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Effect of interferon �-1a on serum matrix metalloproteinase?9 (MMP-9) and tissue inhibitor of matrix metalloproteinase (TIMP-1) in relapsing remitting multiple sclerosis patients

Cited by 32 publications

References 23 publications

Death receptor expression and function at the human blood brain barrier

Death receptor expression and function at the human blood brain barrier

Elevation of matrix metalloproteinases (MMPs) in multiple sclerosis and impact of immunomodulators

Classical immunomodulatory therapy in multiple sclerosis: how it acts, how it works

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