ArticleBritish journal of pharmacology2009
Dysfunction of endothelial and smooth muscle cells in small arteries of a mouse model of Marfan syndrome.
Article in British journal of pharmacology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 44 citations in OpenAlex.
- Article
- Exploring thoracic aorta ECM alterations in Marfan syndrome: insights into aorta wall structure.Scientific reports · 2025Article
- In vivo phenotypic vascular dysfunction extends beyond the aorta in a mouse model for fibrillin-1 (Fbn1) mutation.Scientific reports · 2024Article
- Cerebral microvascular density, blood-brain barrier permeability, and support for neuroinflammation indicate early aging in a Marfan syndrome mouse model.Frontiers in physiology · 2024Article
- Fibrillin-1 Regulates Arteriole Integrity in the Retina.Biomolecules · 2022Article
- Comprehensive Characterization of Arterial and Cardiac Function in Marfan Syndrome-Can Biomarkers Help Improve Outcome?Frontiers in physiology · 2022Article
- A Pilot Study Characterizing Flow Patterns in the Thoracic Aorta of Patients With Connective Tissue Disease: Comparison to Age- and Gender-Matched ControlsFrontiers in pediatrics · 2022Article
- Blood pressure-independent inhibition of Marfan aortic root widening by the angiotensin II receptor blocker valsartan.Physiological reports · 2021Article
- Aortic Dimensions, Biophysical Properties, and Plasma Biomarkers in Children and Adults with Marfan or Loeys-Dietz Syndrome.CJC open · 2021Article
- Stenosis coexists with compromised α1-adrenergic contractions in the ascending aorta of a mouse model of Williams-Beuren syndrome.Scientific reports · 2020Article
- Multiset sparse partial least squares path modeling for high dimensional omics data analysis.BMC bioinformatics · 2020Article
- 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
- Endothelial-Vascular Smooth Muscle Cells Interactions in Atherosclerosis.Frontiers in cardiovascular medicine · 2018Review
- AP-1 Oligodeoxynucleotides Reduce Aortic Elastolysis in a Murine Model of Marfan Syndrome.Molecular therapy. Nucleic acids · 2017Article
- Cardiovascular Benefits of Moderate Exercise Training in Marfan Syndrome: Insights From an Animal Model.Journal of the American Heart Association · 2017Article
- An iPSC-derived vascular model of Marfan syndrome identifies key mediators of smooth muscle cell death.Nature genetics · 2017Article
- Vascular smooth muscle cells in Marfan syndrome aneurysm: the broken bricks in the aortic wall.Cellular and molecular life sciences : CMLS · 2017Review
- Isometric Stretch Alters Vascular Reactivity of Mouse Aortic Segments.Frontiers in physiology · 2017Article
- A novel set-up for the ex vivo analysis of mechanical properties of mouse aortic segments stretched at physiological pressure and frequency.The Journal of physiology · 2016Article
- Losartan Attenuates Degradation of Aorta and Lung Tissue Micromechanics in a Mouse Model of Severe Marfan Syndrome.Annals of biomedical engineering · 2016Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
background and purposeMarfan syndrome, a connective tissue disorder caused by mutations in FBN1 encoding fibrillin-1, results in life-threatening complications in the aorta, but little is known about its effects in resistance vasculature. EXPERIMENTAL APPROACH: Second-order mesenteric arteries from mice at 3, 6 and 10 months of age (n= 30) heterozygous for the Fbn1 allele encoding a cysteine substitution (Fbn1(C1039G/+)) were compared with those from age-matched control littermates. KEY
resultsStress-strain curves indicated that arterial stiffness was increased at 6 and 10 months of age in Marfan vessels. Isometric force measurement revealed that contraction in response to potassium (60 mM)-induced membrane depolarization was decreased by at least 28% in Marfan vessels at all ages, while phenylephrine (3 microM)-induced contraction was reduced by at least 40% from 6 months. Acetylcholine-induced relaxation in Marfan vessels was reduced to 70% and 45% of control values, respectively, at 6 and 10 months. Sensitivity to sodium nitroprusside was reduced at 6 months (pEC(50)= 5.64 +/- 0.11, control pEC(50)= 7.34 +/- 0.04) and 10 months (pEC(50)= 5.99 +/- 0.07, control pEC(50)= 6.99 +/- 0.14). Pretreatment with N(omega)-Nitro-L-arginine methyl ester (200 microM) had no effect on acetylcholine-induced relaxation in Marfan vessels, but reduced vasorelaxation in control vessels to 57% of control values. Addition of indomethacin (10 microM) and catalase (1000 U.mL(-1)) further inhibited vasorelaxation in Marfan vessels to a greater degree compared with control vessels. CONCLUSIONS AND IMPLICATIONS: Pathogenesis of Marfan syndrome in resistance-sized arteries increases stiffness and impairs vasomotor function.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.