1
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Multimodality Imaging-Based Characterization of Regional Material Properties in a Murine Model of Aortic Dissection

      research-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Chronic infusion of angiotensin-II in atheroprone ( ApoE −/−) mice provides a reproducible model of dissection in the suprarenal abdominal aorta, often with a false lumen and intramural thrombus that thickens the wall. Such lesions exhibit complex morphologies, with different regions characterized by localized changes in wall composition, microstructure, and properties. We sought to quantify the multiaxial mechanical properties of murine dissecting aneurysm samples by combining in vitro extension-distension data with full-field multimodality measurements of wall strain and thickness to inform an inverse material characterization using the virtual fields method. A key advance is the use of a digital volume correlation approach that allows for characterization of properties not only along and around the lesion, but also across its wall. Specifically, deformations are measured at the adventitial surface by tracking motions of a speckle pattern using a custom panoramic digital image correlation technique while deformations throughout the wall and thrombus are inferred from optical coherence tomography. These measurements are registered and combined in 3D to reconstruct the reference geometry and compute the 3D finite strain fields in response to pressurization. Results reveal dramatic regional variations in material stiffness and strain energy, which reflect local changes in constituent area fractions obtained from histology but emphasize the complexity of lesion morphology and damage within the dissected wall. This is the first point-wise biomechanical characterization of such complex, heterogeneous arterial segments. Because matrix remodeling is critical to the formation and growth of these lesions, we submit that quantification of regional material properties will increase the understanding of pathological mechanical mechanisms underlying aortic dissection.

          Related collections

          Most cited references61

          • Record: found
          • Abstract: not found
          • Article: not found

          Physics-Informed Neural Networks: A Deep Learning Framework for Solving Forward and Inverse Problems Involving Nonlinear Partial Differential Equations

            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Angiotensin II promotes atherosclerotic lesions and aneurysms in apolipoprotein E-deficient mice.

            Increased plasma concentrations of angiotension II (Ang II) have been implicated in atherogenesis. To examine this relationship directly, we infused Ang II or vehicle for 1 month via osmotic minipumps into mature apoE(-/-) mice. These doses of Ang II did not alter arterial blood pressure, body weight, serum cholesterol concentrations, or distribution of lipoprotein cholesterol. However, Ang II infusions promoted an increased severity of aortic atherosclerotic lesions. These Ang II-induced lesions were predominantly lipid-laden macrophages and lymphocytes; moreover, Ang II promoted a marked increase in the number of macrophages present in the adventitial tissue underlying lesions. Unexpectedly, pronounced abdominal aortic aneurysms were present in apoE(-/-) mice infused with Ang II. Sequential sectioning of aneurysmal abdominal aorta revealed two major characteristics: an intact artery that is surrounded by a large remodeled adventitia, and a medial break with pronounced dilation and more modestly remodeled adventitial tissue. Although no atherosclerotic lesions were visible at the medial break point, the presence of hyperlipidemia was required because infusions of Ang II into apoE(+/+) mice failed to generate aneurysms. These results demonstrate that increased plasma concentrations of Ang II have profound and rapid effects on vascular pathology when combined with hyperlipidemia, in the absence of hemodynamic influences.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Mouse models of abdominal aortic aneurysms.

              Many mouse models of abdominal aortic aneurysms have been developed that use a diverse array of methods for producing the disease, including genetic manipulation and chemical induction. These models could provide insight into potential mechanisms in the development of this disease. Although experimental studies on abdominal aortic aneurysms (AAAs) have used a variety of mammalian and avian approaches, there is an increasing reliance on the use of mice. The models recapitulate some facets of the human disease including medial degeneration, inflammation, thrombus formation, and rupture. Most of the mouse models of AAA are evoked either by genetically defined approaches or by chemical means. The genetic approaches are spontaneous and engineered mutations. These include defects in extracellular matrix maturation, increased degradation of elastin and collagen, aberrant cholesterol homeostasis, and enhanced production of angiotensin peptides. The chemical approaches include the intraluminal infusion of elastase, periaortic incubations of calcium chloride, and subcutaneous infusion of AngII. A common feature of these models is the reduction of AAA incidence and severity by the prophylactic administration of matrix metalloproteinase (MMP) inhibitors or genetically engineered deficiencies of specific members of this proteolytic protein family. The validation of mouse models of AAAs will provide insight into the mechanisms of progression of the human disease.
                Bookmark

                Author and article information

                Contributors
                avril@emse.fr
                Journal
                Sci Rep
                Sci Rep
                Scientific Reports
                Nature Publishing Group UK (London )
                2045-2322
                8 June 2020
                8 June 2020
                2020
                : 10
                : 9244
                Affiliations
                [1 ]ISNI 0000000419368710, GRID grid.47100.32, Department of Biomedical Engineering, , Yale University, ; New Haven, CT USA
                [2 ]ISNI 0000 0001 2264 7217, GRID grid.152326.1, Department of Biomedical Engineering, , Vanderbilt University, ; Nashville, TN USA
                [3 ]ISNI 0000 0001 2158 1682, GRID grid.6279.a, Mines Saint-Etienne, , University of Lyon, University Jean Monnet, INSERM, ; Saint-Etienne, France
                [4 ]ISNI 0000 0004 1937 2197, GRID grid.169077.e, Weldon School of Biomedical Engineering, , Purdue University, ; West Lafayette, IN USA
                [5 ]ISNI 0000000419368710, GRID grid.47100.32, Vascular Biology and Therapeutics Program, , Yale School of Medicine, ; New Haven, CT USA
                Article
                65624
                10.1038/s41598-020-65624-7
                7280301
                32514185
                d033d238-c866-4bd0-804b-34077f462324
                © The Author(s) 2020

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

                History
                : 12 December 2019
                : 4 May 2020
                Categories
                Article
                Custom metadata
                © The Author(s) 2020

                Uncategorized
                biophysics,engineering
                Uncategorized
                biophysics, engineering

                Comments

                Comment on this article