Prostanoid function and cardiovascular disease

Íñiguez, Miguel A.; Cacheiro-Llaguno, Cristina; Cuesta, Natalia; Díaz-Muñoz, Manuel D.; Fresno, Manuel

doi:10.1080/13813450802180882

Cited by 46 publications

(28 citation statements)

References 85 publications

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“…Accumulating evidences suggest that alterations in the production/release of prostanoids by the endothelium directly contribute to the endothelial dysfunction in vascular diseases (Yuhki et al, 2010;Iñiguez et al, 2008). In fact, the increased vasoconstriction and the reduced vasodilatation in MSG rats were corrected after COX inhibition.…”

Section: Discussionmentioning

confidence: 93%

Improvement of metabolic parameters and vascular function by metformin in obese non-diabetic rats

et al. 2012

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Section: Discussionmentioning

confidence: 93%

Improvement of metabolic parameters and vascular function by metformin in obese non-diabetic rats

et al. 2012

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“…Prostacyclin (PGI 2 ) and thromboxane A 2 (TXA 2 ) are the two most important prostanoids modulating vascular thromboresistance [5]. PGI 2 is predominantly produced by endothelial cells and has potent anti-inflammatory, antiplatelet, anti-proliferative and vasodilatory effects [2].…”

Section: Introductionmentioning

confidence: 99%

Cyclic stretch induces cyclooxygenase-2 gene expression in vascular endothelial cells via activation of nuclear factor kappa-β

Zhao

Hiroi

Hansen

et al. 2009

Biochemical and Biophysical Research Communications

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Vascular endothelial cells respond to biomechanical forces, such as cyclic stretch and shear stress, by altering gene expression. Since endothelial-derived prostanoids, such as prostacyclin and thromboxane A 2 , are key mediators of endothelial function, we investigated the effects of cyclic stretch on the expression of genes in human umbilical vein endothelial cells controlling prostanoid synthesis: cyclooxygenase-1 (COX-1), cyclooxygenase-2 (COX-2), prostacyclin synthase (PGIS) and thromboxane A 2 synthase (TXAS). COX-2 and TXAS mRNAs were upregulated by cyclic stretch for 24 hours. In contrast, PGIS mRNA was decreased and stretch had no effect on COX-1 mRNA expression. We further show that stretch-induced upregulation of COX-2 is mediated by activation of the NF-κB signaling pathway.

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“…In order to avoid platelet activation during the centrifugation processes, inhibitors of platelet function may be used (Prostacyclin PGI2 for example), with the potential drawback that these inhibitors may induce protein changes that will interfere with proteomics analysis. However, PGI2 has a short half-life and the changes in platelet physiology induced by PGI2 are usually reversible (Garcia et al, 2005a;Iñiguez et al, 2008). The quality and purity of the final platelet suspension should be evaluated.…”

Section: A Platelet Isolationmentioning

confidence: 99%

Platelet proteomics

Zufferey

Fontana

Reny

et al. 2011

Mass Spectrometry Reviews

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Platelets are small cell fragments, produced by megakaryocytes, in the bone marrow. They play an important role in hemostasis and diverse thrombotic disorders. They are therefore primary targets of antithrombotic therapies. They are implicated in several pathophysiological pathways, such as inflammation or wound repair. In blood circulation, platelets are activated by several pathways including subendothelial matrix and thrombin, triggering the formation of the platelet plug. Studying their proteome is a powerful approach to understand their biology and function. However, particular attention must be paid to different experimental parameters, such as platelet quality and purity. Several technologies are involved during the platelet proteome processing, yielding information on protein identification, characterization, localization, and quantification. Recent technical improvements in proteomics combined with inter-disciplinary strategies, such as metabolomic, transcriptomics, and bioinformatics, will help to understand platelets biological mechanisms. Therefore, a comprehensive analysis of the platelet proteome under different environmental conditions may contribute to elucidate complex processes relevant to platelet function regarding bleeding disorders or platelet hyperreactivity and identify new targets for antiplatelet therapy.

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Prostanoid function and cardiovascular disease

Cited by 46 publications

References 85 publications

Improvement of metabolic parameters and vascular function by metformin in obese non-diabetic rats

Improvement of metabolic parameters and vascular function by metformin in obese non-diabetic rats

Cyclic stretch induces cyclooxygenase-2 gene expression in vascular endothelial cells via activation of nuclear factor kappa-β

Platelet proteomics

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