Prostacyclin protects vascular integrity via PPAR/14-3-3 pathway
| Autor: | Jun-Yang Liou, Kenneth K. Wu, Ling-Yun Chu |
|---|---|
| Rok vydání: | 2015 |
| Předmět: |
medicine.medical_specialty
Vascular smooth muscle Platelet Aggregation Physiology Cell Myocytes Smooth Muscle Peroxisome Proliferator-Activated Receptors Peroxisome proliferator-activated receptor Prostacyclin Biology Biochemistry Muscle Smooth Vascular Downregulation and upregulation Internal medicine medicine Animals Humans Receptor Pharmacology chemistry.chemical_classification Endothelial Cells Cell Biology Protective Factors Epoprostenol Cell biology Endocrinology medicine.anatomical_structure chemistry 14-3-3 Proteins Apoptosis cardiovascular system Phosphorylation lipids (amino acids peptides and proteins) Endothelium Vascular medicine.drug Signal Transduction |
| Zdroj: | Prostaglandinsother lipid mediators. |
| ISSN: | 1098-8823 |
| Popis: | Vascular integrity is protected by the lining endothelial cells (ECs) through structural and molecular protective mechanisms. In response to external stresses, ECs are dynamic in producing protective molecules such as prostacyclin (PGI2). PGI2 is known to inhibit platelet aggregation and controls smooth muscle cell contraction via IP receptors. Recent studies indicate that PGI2 defends endothelial survival and protects vascular smooth muscle cell from apoptosis via peroxisome-proliferator activated receptors (PPAR). PPAR activation results in 14-3-3 upregulation. Increase in cytosolic 14-3-3ɛ or 14-3-3β enhances binding and sequestration of Akt-mediated phosphorylated Bad and reduces Bad-mediated apoptosis via the mitochondrial pathway. Experimental data indicate that administration of PGI2 analogs or augmentation of PGI2 production by gene transfer attenuates endothelial damage and organ infarction caused by ischemia-reperfusion injury. The protective effect of PGI2 is attributed in part to preserving endothelial integrity. |
| Databáze: | OpenAIRE |
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