Kinetics of prostacyclin synthesis in PGHS-1-overexpressed endothelial cells.

  title={Kinetics of prostacyclin synthesis in PGHS-1-overexpressed endothelial cells.},
  author={Sudershan K. Sanduja and Ah-lim Tsai and Nevenka Matijevic-Aleksic and Kenneth K. Wu},
  journal={The American journal of physiology},
  volume={267 5 Pt 1},
The availability of a human endothelial cell overexpressed with prostaglandin H synthase-1 (PGHS-1) by retrovirus-mediated gene transfer made it possible to quantify the kinetics of prostacyclin [prostaglandin (PG)I2] synthesis and PGHS-1 turnover. Prostacyclin synthesis in response to arachidonate (AA) and ionophore A-23187 fit a single exponential kinetics. The rate constants for AA- and ionophore-treated cells were 0.064 min-1 [half-life (t1/2) of 11 min] and 0.032 min-1 (t1/2 = 22 min… 
Selective Augmentation of Prostacyclin Production by Combined Prostacyclin Synthase and Cyclooxygenase-1 Gene Transfer
Prostacyclin synthesis can be selectively augmented by cotransfecting endothelial cells with an optimal ratio of COX-1 to PGIS, which has the potential for therapeutic augmentation of prostacyClin.
Upregulation of prostacyclin synthesis-related gene expression by shear stress in vascular endothelial cells.
The results suggest that the elevated P GI2 production by shear stress is mediated by increased arachidonic acid release and a combination of increased expression of COXs and PGI2 synthase.
Shear Stress Differentially Regulates PGHS-1 and PGHS-2 Protein Levels in Human Endothelial Cells
The regulation of PGHS-1 andPGHS-2 protein levels by shear stress indicates that these proteins play an important role in the maintenance of cardiovascular homeostasis as regulators of PGI2production.
Cyclooxygenase-1 and Bicistronic Cyclooxygenase-1/Prostacyclin Synthase Gene Transfer Protect Against Ischemic Cerebral Infarction
COX-1–based gene transfer has potential for treating ischemic stroke by augmenting prostacyclin and suppressing leukotriene productions and reducing cerebral infarct volume.
Induction of cyclooxygenase-2 in human umbilical vein endothelial cells by lysophosphatidylcholine.
The results suggest that the induction of endothelial cyclooxygenase-2 by lysoPC may be an important vasoprotective mechanism that limits progression of atherosclerotic lesions and promotes their regression.
Induction of Prostacyclin/PGI2 Synthase Expression After Cerebral Ischemia–Reperfusion
  • Yao-Ching Fang, Jui‐Sheng Wu, Teng-Nan Lin
  • Biology, Medicine
    Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism
  • 2006
Findings indicate that PGIS protects the brain by enhancing PGI2 synthesis and creating a favorable P GI2/TXA2 ratio.
Protection of Endothelial Survival by Peroxisome Proliferator-Activated Receptor-&dgr; Mediated 14-3-3 Upregulation
PGI2 protects ECs from H2O2-induced apoptosis by inducing PPAR&dgr; binding to 14-3-3ϵ promoter, thereby upregulating 14- 3-3 ϵ protein expression and augments Bad sequestration and prevents Bad-triggered apoptosis.
Cyclooxygenase‐2‐Derived Prostaglandin E2 Protects Mouse Embryonic Stem Cells from Apoptosis
Results indicate that mES cells constitutively express COX‐2 and PGE synthases and produce PGE2, which confers resistance to apoptosis via EP2‐mediated activation of PI‐3K to the Akt pathway.
Role of endothelium in thrombosis and hemostasis.
Endothelium produces and secretes von Willebrand factor, which mediates platelet adhesion and shear-stress-induced aggregation, and releases prostacyclin and nitric oxide, potent inhibitors of platelet and monocyte activation and vasodilators.
Phospholipid association reduces the gastric mucosal toxicity of aspirin in human subjects
The present study shows that acute aspirin-induced damage to the gastric mucosa can be reduced by chemically associating ASA with PC, and the mechanism of mucosal protection provided by this compound is not related to any alteration in the ability of ASA to inhibit mucosal COX activity.


Cultured endothelial cells synthesize both platelet-activating factor and prostacyclin in response to histamine, bradykinin, and adenosine triphosphate.
Endothelial cell-generated PAF, a potent activator of platelets and neutrophils with endothelial cells, may mediate some of the inflammatory properties of histamine and bradykinin and be a factor in the formation of a thrombogenic vascular surface.
Selectivity of nonsteroidal antiinflammatory drugs as inhibitors of constitutive and inducible cyclooxygenase.
BF 389, an experimental drug currently being tested in humans, was the most potent and most selective inhibitor of COX-2 in intact cells, indicating there are clear pharmacological differences between the two enzymes.
Bovine prostacyclin synthase: purification and isolation of partial cDNA.
Results based on elution profile of the Mono Q column, two-dimensional gel electrophoresis and N-terminal amino acid sequence suggested that PGIS is heterogenous, and a partial cDNA fragment was isolated.
Subcellular localization of prostaglandin-forming cyclooxygenase in Swiss mouse 3T3 fibroblasts by electron microscopic immunocytochemistry.
The results establish that conversion of arachidonic acid to the prostaglandin endoperoxide precursor of PGE2 actually takes place on the endoplasmic reticulum and the nuclear envelope.