ArticleBritish journal of pharmacology2007
Imbalanced synthesis of cyclooxygenase-derived thromboxane A2 and prostacyclin compromises vasomotor function of the thoracic aorta in Marfan syndrome.
Article in British journal of pharmacology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 34 citations in OpenAlex.
- The aorta in Marfan syndrome: from molecular mechanisms to mechanobiological dysfunction.Cardiovascular research · 2026Review
- Fibrillin-1 Deficiency Perturbs Aortic Cholinergic Relaxation and Adrenergic Contraction in a Mouse Model of Early Onset Progressively Severe Marfan Syndrome.Journal of vascular research · 2025Article
- The extracellular matrix glycoprotein fibrillin-1 in health and disease.Frontiers in cell and developmental biology · 2023Review
- Autosomal recessive cutis laxa type Ib-Successful redo aortic root and arch replacement.Clinical case reports · 2022Article
- ADAMTS proteases in cardiovascular physiology and disease.Open biology · 2020Review
- Reactive Oxygen Species and Oxidative Stress in the Pathogenesis and Progression of Genetic Diseases of the Connective Tissue.Antioxidants (Basel, Switzerland) · 2020Review
- An integrative systems approach identifies novel candidates in Marfan syndrome-related pathophysiology.Journal of cellular and molecular medicine · 2019Article
- In vivo characterization of doxycycline-mediated protection of aortic function and structure in a mouse model of Marfan syndrome-associated aortic aneurysm.Scientific reports · 2019Article
- Marfan syndrome; A connective tissue disease at the crossroads of mechanotransduction, TGFβ signaling and cell stemness.Matrix biology : journal of the International Society for Matrix Biology · 2018Review
- The Effect of a Nonpeptide Angiotensin II Type 2 Receptor Agonist, Compound 21, on Aortic Aneurysm Growth in a Mouse Model of Marfan Syndrome.Journal of cardiovascular pharmacology · 2018Article
- Participation of Arachidonic Acid Metabolism in the Aortic Aneurysm Formation in Patients with Marfan Syndrome.Frontiers in physiology · 2018Article
- The Evaluation of Flow-Mediated Vasodilation in the Brachial Artery Correlates With Endothelial Dysfunction Evaluated by Nitric Oxide Synthase Metabolites in Marfan Syndrome Patients.Frontiers in physiology · 2018Article
- A Novel Murine Model of Marfan Syndrome Accelerates Aortopathy and Cardiomyopathy.The Annals of thoracic surgery · 2017Article
- Differences in the Thoracic Aorta by Region and Sex in a Murine Model of Marfan Syndrome.Frontiers in physiology · 2017Article
- Article
- Cardiovascular Effects of the Essential Oil ofEvidence-based complementary and alternative medicine : eCAM · 2016Article
- Vascular dysfunctions in the isolated aorta of double-transgenic hypertensive mice developing aortic aneurysm.Pflugers Archiv : European journal of physiology · 2015Article
- Dimorphic effects of transforming growth factor-β signaling during aortic aneurysm progression in mice suggest a combinatorial therapy for Marfan syndrome.Arteriosclerosis, thrombosis, and vascular biology · 2015Article
- Biomechanical phenotyping of central arteries in health and disease: advantages of and methods for murine models.Annals of biomedical engineering · 2013Review
- Induction of macrophage chemotaxis by aortic extracts from patients with Marfan syndrome is related to elastin binding protein.PloS one · 2011Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeThoracic aortic dissection is a life-threatening complication of Marfan syndrome, a connective tissue disorder caused by mutations in the gene encoding fibrillin-1. We have demonstrated that nitric oxide-mediated endothelial-dependent relaxation is impaired in the thoracic aorta in Marfan syndrome. In the present study, we determined whether the cyclooxygenase (COX)-pathway is involved in the compromised aortic vasomotor function. EXPERIMENTAL APPROACH: Thoracic aortae from mice at 3, 6 and 9 months of age, heterozygous for the Fbn1 allele encoding a cysteine substitution (Fbn1 (C1039G/+), 'Marfan', n=35), were compared with those from age-matched controls (n=35). KEY
resultsIsometric force measurement revealed that preincubation with indomethacin, a non-specific COX inhibitor, but not valeryl salicylate, a specific COX-1 inhibitor, improved the phenylephrine-induced contractions (at 6 months, EC(50) and E(max) were increased 4.5-fold and by 45%, respectively) in Marfan aortae. Sensitivity to acetylcholine-induced relaxation was improved 10-fold. Blockade of the thromboxane-endoperoxide receptor by SQ-29548 did not affect phenylephrine-mediated contractions in Marfan aortae, although they did respond to the thromboxane analogue, U46619. From 6 months on, phenylephrine-induced secretion of prostacyclin and thromboxane A(2) in Marfan aortae was 200% and 40%, respectively, of those in controls. Reduced COX-1 expression was detected in Marfan aortae at 3 and 9 months, whilst COX-2 expression was increased from 3 months on. CONCLUSIONS AND IMPLICATIONS: The compromised vasomotor function in Marfan thoracic aortae is associated with an imbalanced synthesis of thromboxane A(2) and prostacyclin resulting from the differential protein expression of COX-1 and COX-2.
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