Document Detail


Dysfunction in elastic fiber formation in fibulin-5 null mice abrogates the evolution in mechanical response of carotid arteries during maturation.
MedLine Citation:
PMID:  23241326     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Elastin fragmentation is a common characteristic of vascular diseases, such as abdominal aortic aneurysms, peripheral arterial disease, and aortic dissection. Examining growth and remodeling in the presence of dysfunctional elastic fibers provides insight into the adaptive or maladaptive changes that tissues undergo in compensating for structural deficiencies. This study used the maturation of fibulin-5 knockout (KO) and wild-type mice to study the effects of fragmented elastic fibers on the growth and remodeling of carotid arteries. The microstructural content and organization and the biaxial mechanical behavior of common carotid arteries were measured, and parameter estimation performed from KO and WT mice aged 3, 4, 8, and 13 wk. Gross measurements and biaxial tests revealed significant differences in pressure-diameter behavior, in vivo axial stretch, opening angle, compliance, and wall stresses during maturation of wild-type arteries, but little change in these values in KO mice. Multiphoton microscopy used to image collagen fibers across the vessel wall in pressurized and stretched arteries suggests that there is little variation in fiber angles between different ages. Parameter estimation revealed significant differences in material parameters between genotypes and age groups. This study suggests that neonatal formation and cross-linking of functional elastic fibers, followed by increases in artery size due to growth with little remodeling of the elastic fibers, endow arteries with large distensibility and contribute to the evolution of mechanical behavior of arteries during maturation. Dysfunction in neonatal formation of elastic fibers abrogates many of the changes in mechanical response that take place during the maturation.
Authors:
William Wan; Rudolph L Gleason
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2012-12-15
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  304     ISSN:  1522-1539     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2013 Mar 
Date Detail:
Created Date:  2013-03-04     Completed Date:  2013-04-18     Revised Date:  2014-03-07    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H674-86     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Animals
Animals, Newborn
Biomechanical Phenomena / physiology
Carotid Arteries / growth & development*,  pathology,  physiology*
Carotid Artery Diseases / genetics,  pathology,  physiopathology*
Collagen / physiology
Elastic Tissue / physiology*
Elastin / physiology
Extracellular Matrix / pathology,  physiology
Extracellular Matrix Proteins / genetics,  physiology*
Male
Mice
Mice, 129 Strain
Mice, Inbred C57BL
Mice, Knockout
Models, Cardiovascular*
Recombinant Proteins / genetics
Stress, Mechanical
Vascular Stiffness / genetics,  physiology
Grant Support
ID/Acronym/Agency:
HL-070531/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Extracellular Matrix Proteins; 0/Fbln5 protein, mouse; 0/Recombinant Proteins; 9007-34-5/Collagen; 9007-58-3/Elastin
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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