scholarly journals Ca2+-regulated lysosome fusion mediates angiotensin II-induced lipid raft clustering in mesenteric endothelial cells

2016 ◽  
Vol 39 (4) ◽  
pp. 227-236 ◽  
Author(s):  
Wei-Qing Han ◽  
Wen-Dong Chen ◽  
Ke Zhang ◽  
Jian-Jun Liu ◽  
Yong-Jie Wu ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Angiotensin Ii ◽  
Lipid Raft ◽  
Raft Clustering

scholarly journals CD82 Restrains Pathological Angiogenesis by Altering Lipid Raft Clustering and CD44 Trafficking in Endothelial Cells

Circulation ◽  
2014 ◽  
Vol 130 (17) ◽  
pp. 1493-1504 ◽  
Author(s):  
Quan Wei ◽  
Feng Zhang ◽  
Mekel M. Richardson ◽  
Nathan H. Roy ◽  
William Rodgers ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Lipid Raft ◽  
Pathological Angiogenesis ◽  
Raft Clustering

scholarly journals Lipid Raft Clustering and Redox Signaling Platform Formation in Coronary Arterial Endothelial Cells

Hypertension ◽  
2006 ◽  
Vol 47 (1) ◽  
pp. 74-80 ◽  
Author(s):  
Andrew Y. Zhang ◽  
Fan Yi ◽  
Guo Zhang ◽  
Erich Gulbins ◽  
Pin-Lan Li
Keyword(s):  
Endothelial Cells ◽  
Lipid Raft ◽  
Redox Signaling ◽  
Arterial Endothelial Cells ◽  
Raft Clustering

scholarly journals Actin Depolymerization Transduces the Strength of B-Cell Receptor Stimulation

2005 ◽  
Vol 16 (5) ◽  
pp. 2275-2284 ◽  
Author(s):  
Shengli Hao ◽  
Avery August
Keyword(s):  
B Cell ◽  
Lipid Raft ◽  
Cell Activation ◽  
Cell Receptor ◽  
Dependent Manner ◽  
B Cell Activation ◽  
Erk Activation ◽  
Actin Depolymerization ◽  
Transcription Factor Activation ◽  
Raft Clustering

Polymerization of the actin cytoskeleton has been found to be essential for B-cell activation. We show here, however, that stimulation of BCR induces a rapid global actin depolymerization in a BCR signal strength-dependent manner, followed by polarized actin repolymerization. Depolymerization of actin enhances and blocking actin depolymerization inhibits BCR signaling, leading to altered BCR and lipid raft clustering, ERK activation, and transcription factor activation. Furthermore actin depolymerization by itself induces altered lipid raft clustering and ERK activation, suggesting that F-actin may play a role in separating lipid rafts and in setting the threshold for cellular activation.

Pulmonary Endothelial Cells / Metabolism of Vasoactive Substances

1975 ◽  
Author(s):  
J. W. Ryan ◽  
Una S. Ryan
Keyword(s):  
Endothelial Cells ◽  
Angiotensin Ii ◽  
Angiotensin I ◽  
Clotting System ◽  
Arterial Circulation ◽  
Pulmonary Endothelial Cells ◽  
Vasoactive Substances ◽  
Metabolic Products ◽  
Relationship Of ◽  
The Relationship

The lungs metabolize a variety of vasoactive substances, including bradykinin (BK), angiotensin I (AT I), PGE2 and F2α, norepinephrine, 5-HT, 5’-ATP and 5’-AMP. In contrast, the lungs od not metabolize angiotensin II (AT II), PGA2, histamine and epinephrine. Of the substances metabolized, all (with the possible exceptions of the prostaglandins) are processed primarily by the pulmonary endothelial cells. Furthermore, the means by which the substances are processed suggest that endothelial cells determine the vasoactive substances allowed to enter the systemic arterial circulation. BK is inactivated while AT I is converted to its potent homolog, AT II. AT II enters the arterial circulation. The metabolism of BK and AT I may be effected by the same enzyme. Pulmonary endothelial cells are a rich source of thromboplastin, an enzyme capable of degrading BK and AT I. However, the relationship of thromboplastin to the fates of these hormones is not clear : The metabolic products produced are not those produced by intact lungs nor by endothelial cells in culture. In addition, thromboplastin degrades substances (e.g. AT II), which are not degraded by intact lungs. Possibly the extrinsic clotting system plays a role when activated but not under physiologic conditions.

scholarly journals Angiotensin II Evokes Angiogenic Signals within Skeletal Muscle through Co-ordinated Effects on Skeletal Myocytes and Endothelial Cells

PLoS ONE ◽  
2014 ◽  
Vol 9 (1) ◽  
pp. e85537 ◽  
Author(s):  
Jennifer L. Gorman ◽  
Sammy T. K. Liu ◽  
Dara Slopack ◽  
Khashayar Shariati ◽  
Adam Hasanee ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Endothelial Cells ◽  
Angiotensin Ii ◽  
Skeletal Myocytes

scholarly journals Inhibitory Effect of thePunica granatumFruit Extract on Angiotensin-II Type I Receptor and Thromboxane B2 in Endothelial Cells Induced by Plasma from Preeclamptic Patients

2016 ◽  
Vol 2016 ◽  
pp. 1-6 ◽  
Author(s):  
Widya Kusumawati ◽  
Kusnarman Keman ◽  
Setyawati Soeharto
Keyword(s):  
Endothelial Cells ◽  
Angiotensin Ii ◽  
Vascular Endothelial Cells ◽  
Ethanolic Extract ◽  
Punica Granatum ◽  
Normal Pregnancy ◽  
Inhibitory Effect ◽  
Thromboxane B2 ◽  
High Dose ◽  
Type I

This study aims to evaluate whether thePunica granatumfruit extract modulates the Angiotensin-II Type I receptor (AT1-R) and thromboxane B2 level in endothelial cells induced by plasma from preeclamptic patients. Endothelial cells were obtained from human umbilical vascular endothelial cells. At confluence, endothelial cells were divided into five groups, which included endothelial cells exposed to 2% plasma from normal pregnancy (NP), endothelial cells exposed to 2% plasma from preeclamptic patients (PP), and endothelial cells exposed to PP in the presence of ethanolic extract ofPunica granatum(PP + PG) at the following three doses: 14; 28; and 56 ppm. The expression of AT1-R was observed by immunohistochemistry technique, and thromboxane B2 level was done by immunoassay technique. Plasma from PP significantly increased AT1-R expression and thromboxane B2 levels compared to cells treated by normal pregnancy plasma. The increasing of AT1-R expression significantly (P<0.05) attenuated by high dose treatments ofPunica granatumextract. Moreover, the increasing of thromboxane B2 levels significantly (P<0.05) attenuated by lowest dose treatments ofPunica granatumextract. We further concluded thatPunica granatumfruit protects and inhibits the sensitivity of endothelial cells to plasma from preeclamptic patients due to inhibition of AT1-R expression (56 ppm) and reduced thromboxane B2 levels (14 ppm).

scholarly journals Angiotensin II Type 1 Receptor Blocker Reduces Monocyte Adhesion to Endothelial Cells in Spontaneously Hypertensive Rats

2007 ◽  
Vol 54 (4) ◽  
pp. 605-612 ◽  
Author(s):  
Fuki IKEDA ◽  
Kosuke AZUMA ◽  
Takeshi OGIHARA ◽  
Yukiko TOYOFUKU ◽  
Aiko OTSUKA ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Angiotensin Ii ◽  
Spontaneously Hypertensive Rats ◽  
Receptor Blocker ◽  
Monocyte Adhesion ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive
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