A

2020 ◽  
pp. 55-126
Author(s):  
Sean Ainsworth
Keyword(s):  
Growth Factors ◽  
Adverse Effects ◽  
Acetylsalicylic Acid ◽  
Plasminogen Activator ◽  
Tissue Type ◽  
Vascular Endothelial Growth Factors ◽  
Vascular Endothelial ◽  
Tissue Type Plasminogen Activator ◽  
Type Plasminogen Activator ◽  
Endothelial Growth Factors

This chapter presents information on neonatal drugs that begin with A, including use, pharmacology, adverse effects, fetal and infant implications of maternal treatment, treatment, and supply of Abacavir, Acetylcysteine (N-acetylcysteine), Aciclovir = Acyclovir (USAN), Adenosine, Adrenaline = Epinephrine (rINN), Albendazole, Alginate compounds (Gaviscon®), Alimemazine (trimeprazine— former BAN and USAN), Alteplase (tissue-type plasminogen activator [rt-PA]), Amikacin, Amiodarone, Amlodipine, Amodiaquine with artesunate, Amoxicillin = Amoxycillin (former BAN), Amphotericin B, Ampicillin, Anti-vascular endothelial growth factors (for ROP), Arginine (L-arginine), Artemether with lumefantrine, Aspirin = acetylsalicylic acid (INN), Atosiban, Atracurium, Atropine, and Azithromycin

scholarly journals Arsenite Inhibits Tissue-Type Plasminogen Activator Synthesis through NRF2 Activation in Cultured Human Vascular Endothelial EA.hy926 Cells

2021 ◽  
Vol 22 (2) ◽  
pp. 739
Author(s):  
Tsuyoshi Nakano ◽  
Tsutomu Takahashi ◽  
Chika Yamamoto ◽  
Eiko Yoshida ◽  
Toshiyuki Kaji ◽  
...  
Keyword(s):  
Plasminogen Activator ◽  
Fibrinolytic Activity ◽  
Vascular Endothelial Cells ◽  
Tissue Type ◽  
Vascular Endothelial ◽  
Tissue Type Plasminogen Activator ◽  
Nrf2 Pathway ◽  
Type Plasminogen Activator ◽  
Ea.Hy926 Cells ◽  
Pai 1

Chronic arsenic exposure is known to be related to the progression of atherosclerosis. However, the pathogenic mechanisms of arsenic-induced atherosclerosis have not been fully elucidated. Because disruption of the blood coagulation/fibrinolytic system is involved in the development of arteriosclerosis, we investigated the effect of arsenite on fibrinolytic activity in human vascular endothelial EA.hy926 cells in the present study. Fibrinolysis depends on the balance between tissue-type plasminogen activator (t-PA) and plasminogen activator inhibitor 1 (PAI-1) secreted from vascular endothelial cells. We found that arsenite reduced fibrinolytic t-PA activity by inhibiting its synthesis without affecting PAI-1 production. The inhibitory effect of arsenite on t-PA expression was partially recovered by the reactive oxygen species (ROS) scavenger Trolox. The nuclear factor erythroid 2 related factor 2 (NRF2) pathway is known to be activated by arsenite via ROS production. We confirmed that arsenite activated the NRF2 pathway, and arsenite-induced inhibition of fibrinolytic t-PA activity was abrogated in NRF2-knockdown EA.hy926 cells. These results suggest that arsenite inhibits the fibrinolytic activity of t-PA by selectively suppressing its synthesis via activation of the NRF2 pathway in vascular endothelial cells.

Effects of IL-1β and IL-6 on tissue-type plasminogen activator expression in vascular endothelial cells

2008 ◽  
Vol 123 (2) ◽  
pp. 342-351 ◽  
Author(s):  
Pia Larsson ◽  
Erik Ulfhammer ◽  
Lena Karlsson ◽  
Maria Bokarewa ◽  
Karin Wåhlander ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Plasminogen Activator ◽  
Vascular Endothelial Cells ◽  
Tissue Type ◽  
Vascular Endothelial ◽  
Tissue Type Plasminogen Activator ◽  
Type Plasminogen Activator

scholarly journals Tissue-type plasminogen activator (t-PA) is stored in Weibel-Palade bodies in human endothelial cells both in vitro and in vivo

Blood ◽  
2002 ◽  
Vol 99 (10) ◽  
pp. 3637-3645 ◽  
Author(s):  
Denise Huber ◽  
Elisabeth M. Cramer ◽  
Jocelyne E. Kaufmann ◽  
Paolo Meda ◽  
Jean-Marc Massé ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Plasminogen Activator ◽  
Immunoelectron Microscopy ◽  
Tissue Type ◽  
Vascular Endothelial ◽  
Adrenergic Agents ◽  
Tissue Type Plasminogen Activator ◽  
Storage Compartment ◽  
Type Plasminogen Activator

Vascular endothelial cells are thought to be the main source of plasma tissue-type plasminogen activator (t-PA) and von Willebrand factor (VWF). Previous studies have suggested that both t-PA and VWF are acutely released in response to the same stimuli, both in cultured endothelial cells and in vivo. However, the subcellular storage compartment in endothelial cells has not been definitively established. We tested the hypothesis that t-PA is localized in Weibel-Palade (WP) bodies, the specialized endothelial storage granules for VWF. In cultured human umbilical vein endothelial cells (HUVECs), t-PA was expressed in a minority of cells and found in WP bodies by immunofluorescence. After up-regulation of t-PA synthesis either by vascular endothelial growth factor (VEGF) and retinoic acid or by sodium butyrate, there was a large increase in t-PA–positive cells. t-PA was exclusively located to WP bodies, an observation confirmed by immunoelectron microscopy. Incubation with histamine, forskolin, and epinephrine induced the rapid, coordinate release of both t-PA and VWF, consistent with a single storage compartment. In native human skeletal muscle, t-PA was expressed in endothelial cells from arterioles and venules, along with VWF. The 2 proteins were found to be colocalized in WP bodies by immunoelectron microscopy. These data indicate that t-PA and VWF are colocalized in WP bodies, both in HUVECs and in vivo. Release of both t-PA and VWF from the same storage pool likely accounts for the coordinate increase in the plasma level of the 2 proteins in response to numerous stimuli, such as physical activity, β-adrenergic agents, and 1-deamino-8d-arginine vasopressin (DDAVP) among others.

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