Age-Related Changes in the Elastic Tissue of the Human Aorta

Abstract

Background: Age-related arterial alterations affecting cells, matrix and biomolecules are the main culprit for initiation and progression of cardiovascular disease. The objective of this study is to gain further insights into the complex mechanism of elastic tissue ageing in human aortic blood vessels. Methods: One hundred and nineteen human aortic tissue samples were collected from adult patients (101 males, 18 females; age 40–86 years) undergoing coronary artery bypass grafting. Overall extracellular matrix architecture was examined by multiphoton laser scanning microscopy and histology. Matrix metalloproteinases 2 and 9, corresponding tissue inhibitors 1 and 2 as well as desmosine were determined. mRNA levels of tropoelastin were assessed by quantitative RT-PCR. Results: Age-related destruction of the vascular elastic laminas as well as a loss of interlamina cross-links were observed by laser scanning microscopy. These results were confirmed by histology indicating increasing interlamina gaps. There were no significant differences in matrix turnover or desmosine content. A steady decrease in tropoelastin mRNA by about 50% per 10 years of age increase was observed. Conclusions: Our findings indicate that ageing is accompanied by a destruction of the elastic vascular structure. However, tropoelastin expression analysis suggests that elastogenesis occurs throughout life with constantly decreasing levels.

Elastins from patients with Williams–Beuren syndrome and healthy individuals differ on the molecular level

“…by results obtained in a study on aortic punch biopsies similar to the ones used in this work, which revealed a decrease of the amount of interlaminar elastin and a decrease of tropoelastin mRNA levels with increased age, respectively [Fritze et al, 2011]. The similarities in the amounts of elastin found between aortic samples from WBS patients and healthy subjects may also be associated with an increase of the number of the elastic lamellae [O'Connor et al, 1985;Li et al, 1998], which may partly compensate for the lower amounts of elastin that are produced.…”

Aging and Alzheimer’s disease: Comparison and associations from molecular to system level

“…Endothelial dysfunction may be due to diminished bioavailability of nitric oxide (Taddei et al, 2001; Tschudi et al, 1996). Arterial stiffness results primarily from loss of elastic fibers and an increase in collagen (Fritze et al, 2012). Like AD, cardiovascular disease is another aging‐related disease that brings a great burden for the patients and healthcare systems (Paneni, Diaz Cañestro, Libby, Lüscher, & Camici, 2017).…”

The Effect of Ageing on Vascular Smooth Muscle Cell Behaviour - A Mini-Review

“…In addition to MCP-1, numerous studies have reported increased MMP expression and activity in the ageing vascular wall which may also facilitate increased VSMC migration. Specifically, MMP-13 [36], MMP-9 [10,37] and MMP-2 expression and activity were elevated in the ageing vascular wall [10,12,13,36,37]. It has been proposed that increased MMP-2 activation is due to a combination of elevated levels of the MMP-2 activator MMP-14 and reduced levels of tissue inhibitor of metalloproteinase-2 in the ageing intima [13].…”