3P-0857 The vasoactivity of tissue type plasminogen activator (tPA) and TNK-tPA

Nassar, Hanan R.; Nassar, Taher; Haj‐Yehia, Abdullah; Akkawi, Sa’ed; Bdeir, Khalil; Higazi, Abd-Al Roof

doi:10.1016/s1567-5688(03)91075-0

Cited by 2 publications

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“…38 Other reports have shown that a-defensins are able to enter the cells 40 possibly by binding to the low-density lipoprotein receptor-related protein/a2-macroglobulin receptor and inhibit PKCa/b by direct binding to this kinase. 41 In agreement with these observations, HNP-1 is among the most potent inhibitory peptides of PKC. 42 Therefore, one of the possible mechanisms by which defensins inhibit the replication of viruses involves interference with the PKCmediated inhibition of viral entry.…”

Section: View Article Onlinesupporting

confidence: 68%

Virucidal activity of human α- and β-defensins against hepatitis C virus genotype 4

et al. 2016

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Hepatitis C virus (HCV) is the major etiological agent of human non-A and non-B hepatitis affecting about 180 million people worldwide. The goal of the current study was to find effective anti-HCV proteins. As a result, defensins were selected as promising candidates due to their well-known anti-viral potential and small size. We conducted in vitro evaluation of two kinds of defensins (human α- and β-defensins and synthetic linear avian α-defensins) using tissue culture combined with reverse transcription nested PCR (RT-nested-PCR) and real-time PCR. Human α- and β-defensins showed strong anti-HCV activity in experiments on cellular protection, neutralization, and treatment at all concentrations used (10, 20 and 50 μg). The synthetic linear defensins could reach similar anti-HCV potential only at a noticeably higher concentration (250 μg) and do not show noticeable activity at 10 and 20 μg. This study suggests that defensins are potent anti-HCV agents.

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Section: View Article Onlinesupporting

confidence: 68%

Virucidal activity of human α- and β-defensins against hepatitis C virus genotype 4

et al. 2016

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“…Subsequently, Lipton and colleagues showed that tPA knockout mice were similarly resistant to brain infarction after focal cerebral ischemia [20]. At the level of the neurovascular unit, tPA can cause direct vasoactivity [21] and bind to the NR1 subunit of the N-methyl-D-aspartate receptor, resulting in cleavage of the NR1 subunit and amplification of intracellular Ca++ conductance [7,22,23]. Furthermore, tPA (and possibly plasmin) may also target non-fibrin substrates in brain extracellular matrix [3,4,24].…”

Section: Pleiotropic Actions Of Tpa In the Brainmentioning

confidence: 99%

Targeting Extracellular Matrix Proteolysis for Hemorrhagic Complications of tPA Stroke Therapy

Wang¹,

Rosell²,

Lo³

2008

CNSNDDT

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To date, tPA-based thrombolytic therapy is the only FDA-approved treatment for achieving vascular reperfusion and clinical benefit, but this agent is given to only about 2-5% of stroke patients in the United States of America. This may be related, in part, to the elevated risks of symptomatic intracranial hemorrhage, and the consequently reduced therapeutic time window. Recent efforts have aimed at identifying new combination strategies that might increase thrombolytic efficacy of tPA to benefit reperfusion, while reducing its associated neurotoxicity and hemorrhagic complications. Emerging experimental studies demonstrate that the breakdown of neurovascular matrix initiates blood-brain barrier disruption with edema and/or hemorrhage. Perturbation of extracellular homeostasis triggered by dysregulated extracellular proteases may underlie processes responsible for the hemorrhagic complications of thrombolytic stroke therapy. This short review summarizes experimental investigations of this field in pre-clinical stroke models. The data strongly suggest that targeting the extracellular matrix proteolytic imbalance within the neurovascular unit may provide new approaches for improving the safety and efficacy of thrombolytic reperfusion therapy of stroke.

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3P-0857 The vasoactivity of tissue type plasminogen activator (tPA) and TNK-tPA

Cited by 2 publications

References 0 publications

Virucidal activity of human α- and β-defensins against hepatitis C virus genotype 4

Virucidal activity of human α- and β-defensins against hepatitis C virus genotype 4

Targeting Extracellular Matrix Proteolysis for Hemorrhagic Complications of tPA Stroke Therapy

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