• arterial
  • Genetically determined minor modifications in elastin and collagen in the aorta could influence the onset and evolution of arterial pathology, such as hypertension and its complications. (ahajournals.org)
  • The elastin-null mice (ELN −/− ) die of obstructive arterial disease, 2 whereas the ELN +/− mice have reduced absolute quantities of elastin and are hypertensive, phenotypes similar to those observed in patients with supravalvular aortic stenosis and Williams syndrome. (ahajournals.org)
  • Investigating the genetic basis and pathophysiological consequences of the modulation of elastin levels, rather than the impact of absolute elastin deficit, is central to our understanding of mechanisms involved in arterial pathologies. (ahajournals.org)
  • Conclusions Patients with COPD have increased skin elastin degradation compared with controls, which is related to emphysema severity and arterial stiffness. (bmj.com)
  • Is systemic elastin degradation the mechanism of increased arterial stiffness and skin wrinkling in chronic obstructive pulmonary disease? (bmj.com)
  • Men with chronic obstructive pulmonary disease (COPD) have increased skin elastin degradation compared with controls matched for age and smoking history, and this was associated with arterial stiffness and emphysema severity. (bmj.com)
  • quantitative
  • After a genome-wide search for quantitative trait loci (QTL) influencing the aortic elastin, collagen, and cell protein contents in an F2 population derived from BN and LOU rats, we identified on chromosomes 2 and 14, 3 QTL specifically controlling elastin levels, and a further highly significant QTL on chromosome 17 linked to the level of cell proteins. (ahajournals.org)
  • In this study, we have performed a genetic analysis in an F2 cohort of 161 rats derived from BN and LOU rat strains to detect genetic loci contributing to quantitative variations of aortic elastin, collagen, and cell protein contents and to test a possible relationship between these loci and those linked to susceptibility to aortic IEL ruptures. (ahajournals.org)
  • protein
  • Western blot and immuno-staining confirmed expression of elastin protein. (ahajournals.org)
  • Seven days after coronary artery ligation, BMSCs transfected with genes for either adeno-elastin (BMSC+Elastin) or adeno-green fluorescence protein (BMSC), or media (control group) were injected into the infarct area of adult rats (n=8/group). (ahajournals.org)
  • Since elastase has been shown to degrade elastin (elastin is the most resistant fibrous protein of the organisms), 3 interest has increased in the potential effects of elastase activity on atherosclerosis. (ahajournals.org)
  • gene
  • We previously demonstrated that the inbred Brown Norway (BN) rat shows an aortic elastin deficit in both abdominal and thoracic segments, partly because of a decrease in tropoelastin synthesis when compared with the LOU rat, that elastin gene polymorphisms in these strains do not significantly account for. (ahajournals.org)
  • In these patients, the elastin gene is mutated or deleted. (ahajournals.org)
  • 5 Because the elastin gene polymorphism explains only a small part of differences between parental strains, it is thus probable that other genes account for the major proportion of the interstrain differences in aortic elastin content. (ahajournals.org)
  • area
  • We attempted to restore the elastic properties of the scar by implanting the infarct area with cells expressing elastin. (ahajournals.org)
  • 0.05) scar size and surface area in the BMSC+Elastin group. (ahajournals.org)
  • Methods The authors measured cutaneous elastin degradation using immunohistochemistry (percentage area of elastin fibres) in sun-exposed (exposed) and non-sun-exposed (non-exposed) skin biopsies in 16 men with COPD and 15 controls matched for age and cigarette smoke exposure. (bmj.com)