scholarly journals Plasma microparticles of intubated COVID‐19 patients cause endothelial cell death, neutrophil adhesion and netosis, in a phosphatidylserine‐dependent manner

2021 ◽  
Author(s):  
Yohann Garnier ◽  
Livia Claude ◽  
Patricia Hermand ◽  
Evely Sachou ◽  
Aurélie Claes ◽  
...  
Keyword(s):  
Cell Death ◽  
Endothelial Cell ◽  
Neutrophil Adhesion ◽  
Dependent Manner ◽  
Endothelial Cell Death

Vascular endothelial cadherin is an endostatin receptor

Biologia ◽  
2011 ◽  
Vol 66 (4) ◽  
Author(s):  
Takahiro Nemoto ◽  
Shunichiro Kubota
Keyword(s):  
Cell Death ◽  
Endothelial Cell ◽  
Tyrosine Phosphorylation ◽  
Dependent Manner ◽  
Vascular Endothelial ◽  
Western Blots ◽  
Vascular Endothelial Cadherin ◽  
Endothelial Cell Death ◽  
Tumor Growth And Metastasis ◽  
Induced Apoptosis

AbstractAngiogenesis is involved in tumor growth and metastasis. Endostatin inhibits angiogenesis, but its precise mechanism is not fully understood. To clarify signal transduction involved in endostatin-induced angiogenesis inhibition (endothelial cell growth inhibition), it is important to identify an endostatin receptor, which is the aim of the present study. We hypothesized that vascular endothelial cadherin (VE-cadherin) is an endostatin receptor and found that endostatin induced apoptosis in cultured calf pulmonary artery endothelium (CPAE) cells. Immunoprecipitation and western blots revealed that endostatin specifically bound to VE-cadherin in a Ca2+-dependent manner. Binding of endostatin to VE-cadherin induced tyrosine phosphorylation of VE-cadherin, β-catenin recruitment, and endothelial cell death. Antisense oligonucleotides against VE-cadherin rescued endostatin-induced endothelial cell death. Inhibition of tyrosine phosphorylation of VE-cadherin inhibited endostatin-induced β-catenin recruitment and CPAE cell death. Taken together, we conclude that VE-cadherin is an endostatin receptor.

scholarly journals Role of thromboxane in retinal microvascular degeneration in oxygen-induced retinopathy

2001 ◽  
Vol 90 (6) ◽  
pp. 2279-2288 ◽  
Author(s):  
Martin H. Beauchamp ◽  
Ana Katherine Martinez-Bermudez ◽  
Fernand Gobeil ◽  
Anne Marilise Marrache ◽  
Xin Hou ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cell Death ◽  
Endothelial Cell ◽  
Oxidant Stress ◽  
Microvascular Endothelial Cell ◽  
Oxygen Induced Retinopathy ◽  
Rat Pups ◽  
Endothelial Cell Death ◽  
Peroxidation Product ◽  
Synthase Inhibitor

Microvascular degeneration is an important event in oxygen-induced retinopathy (OIR), a model of retinopathy of prematurity. Because oxidant stress abundantly generates thromboxane A2(TxA2), we tested whether TxA2plays a role in retinal vasoobliteration of OIR and contributes to such vascular degeneration by direct endothelial cytotoxicity. Hyperoxia-induced retinal vasoobliteration in rat pups (80% O2exposure from postnatal days 5–14) was associated with increased TxB2generation and was significantly prevented by TxA2synthase inhibitor CGS-12970 (10 mg · kg−1· day−1) or TxA2-receptor antagonist CGS-22652 (10 mg · kg−1· day−1). TxA2mimetics U-46619 (EC5050 nM) and I-BOP (EC505 nM) caused a time- and concentration-dependent cell death of neuroretinovascular endothelial cells from rats as well as newborn pigs but not of smooth muscle and astroglial cells; other prostanoids did not cause cell death. The peroxidation product 8-iso-PGF2, which is generated in OIR, stimulated TxA2formation by endothelial cells and triggered cell death; these effects were markedly diminished by CGS-12970. TxA2-dependent neuroretinovascular endothelial cell death was mostly by necrosis and to a lesser extent by apoptosis. The data identify an important role for TxA2in vasoobliteration of OIR and unveil a so far unknown function for TxA2in directly triggering neuroretinal microvascular endothelial cell death. These effects of TxA2might participate in other ischemic neurovascular injuries.

Homocysteine induces cerebral endothelial cell death by activating the acid sphingomyelinase ceramide pathway

2013 ◽  
Vol 45 ◽  
pp. 21-27 ◽  
Author(s):  
Jiunn-Tay Lee ◽  
Giia-Sheun Peng ◽  
Shao-Yuan Chen ◽  
Chang-Hung Hsu ◽  
Chun-Chieh Lin ◽  
...  
Keyword(s):  
Cell Death ◽  
Endothelial Cell ◽  
Acid Sphingomyelinase ◽  
Cerebral Endothelial Cell ◽  
Endothelial Cell Death

NGP1-01, a multi-targeted polycyclic cage amine, attenuates brain endothelial cell death in iron overload conditions

2012 ◽  
Vol 1489 ◽  
pp. 133-139 ◽  
Author(s):  
J.A. Lockman ◽  
W.J. Geldenhuys ◽  
M.R. Jones-Higgins ◽  
J.D. Patrick ◽  
D.D. Allen ◽  
...  
Keyword(s):  
Cell Death ◽  
Endothelial Cell ◽  
Iron Overload ◽  
Brain Endothelial Cell ◽  
Endothelial Cell Death

scholarly journals Carbamoylating Activity Associated with the Activation of the Antitumor Agent Laromustine Inhibits Angiogenesis by Inducing ASK1-Dependent Endothelial Cell Death

PLoS ONE ◽  
2014 ◽  
Vol 9 (7) ◽  
pp. e103224 ◽  
Author(s):  
Weidong Ji ◽  
Mei Yang ◽  
Alexandra Praggastis ◽  
Yonghao Li ◽  
Huanjiao Jenny Zhou ◽  
...  
Keyword(s):  
Cell Death ◽  
Endothelial Cell ◽  
Antitumor Agent ◽  
Endothelial Cell Death

scholarly journals The blood-brain barrier in primary CNS lymphomas: Ultrastructural evidence of endothelial cell death

1999 ◽  
Vol 1 (2) ◽  
pp. 89-100
Author(s):  
Peter P. Molnár ◽  
Brian P. O'Neill ◽  
Bernd W. Scheithauer ◽  
Dennis R. Groothuis
Keyword(s):  
Cell Death ◽  
Endothelial Cell ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Ultrastructural Evidence ◽  
Blood Brain ◽  
Endothelial Cell Death ◽  
Cns Lymphomas
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