Publications

Vascular Applications of Micro- and Nanotechnology

927: Alterations in Ex VIVO Biomechanical Properties and Functional Properties of the Proximal Urethra in a Rat Model of Birth Trauma Induced by Vaginal Distension

You have accessJournal of UrologyPodium, Monday, May 23, 2005, 3:30 - 5:30 pm1 Apr 2005927: Alterations in Ex VIVO Biomechanical Properties and Functional Properties of the Proximal Urethra in a Rat Model of Birth Trauma Induced by Vaginal Distension Rachelle L. Prantil, Ronald J. Jankowski, Yasuhiro Haiho, William C. de Groat, Michael B. Chancellor, Naoki Yoshimura, and David A. Vorp Rachelle L. PrantilRachelle L. Prantil More articles by this author , Ronald J. JankowskiRonald J. Jankowski More articles by this author , Yasuhiro HaihoYasuhiro Haiho More articles by this author , William C. de GroatWilliam C. de Groat More articles by this author , Michael B. ChancellorMichael B. Chancellor More articles by this author , Naoki YoshimuraNaoki Yoshimura More articles by this author , and David A. VorpDavid A. Vorp More articles by this author View All Author Informationhttps://doi.org/10.1016/S0022-5347(18)35083-3AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookLinked InTwitterEmail "927: Alterations in Ex VIVO Biomechanical Properties and Functional Properties of the Proximal Urethra in a Rat Model of Birth Trauma Induced by Vaginal Distension." The Journal of Urology, 173(4S), pp. 250–251 © 2016 by American Urological AssociationFiguresReferencesRelatedDetails Volume 173Issue 4SApril 2005Page: 250-251 Advertisement Copyright & Permissions© 2016 by American Urological AssociationMetricsAuthor Information Rachelle L. Prantil More articles by this author Ronald J. Jankowski More articles by this author Yasuhiro Haiho More articles by this author William C. de Groat More articles by this author Michael B. Chancellor More articles by this author Naoki Yoshimura More articles by this author David A. Vorp More articles by this author Expand All Advertisement PDF downloadLoading ...

Experimental system for<i>ex vivo</i>measurement of murine aortic stiffness

While vascular stiffness is universally studied using pulse wave velocity, this method overestimates the stiffness of small calibre blood vessels. We have developed and rigorously validated an ex vivo system for measuring stiffness of the mouse aorta. The system consists of a temperature-controlled tissue bath, a pressurization loop and a helium-neon laser micrometer. We harvested thoracic aortas from 8 (n = 56), 11 (n = 6) and 14 (n = 6) week male C57BL/6J mice, mounted them within a tissue chamber and applied an intraluminal pressure waveform while measuring mid vessel outer diameter. Vessel stiffness (E(p), mmHg) was calculated from the pressure-diameter response. Vessels were then stained for endothelial cells, smooth muscle cells, elastin fibres and collagen. The data indicate highly reproducible stiffness measurements in 8 week mice (E(p) = 602.4 +/- 160.2; p = 0.934), age-related stiffening between 11 and 14 week mice (11 week E(p) = 646.9 +/- 62.4, 14 week E(p) = 795.4 +/- 87.5, p = 0.008), and a morphologically intact vessel wall. These results represent the first ex vivo measurements of murine aortic stiffness and illustrate that our methods are feasible and reliable. Since we demonstrate that the system is sensitive to age-related stiffening and does not damage the vessel, this approach is useful for investigating the pathophysiology of vascular disease from biomechanical and histological perspectives.

Vessel asymmetry as an additional diagnostic tool in the assessment of abdominal aortic aneurysms

Relative Contributions of Age and Atherosclerosis to Vascular Stiffness

To determine the relative contributions of aging and atherosclerosis to vascular stiffness, we studied aortic stiffness, plaque, and elastin in 8-, 16-, 25-, and 34-week-old male ApoE-KO and C57BL/6J control mice (N = 48). Stiffness increased gradually in both strains up to 25 weeks (p < 0.05), and dramatically between 25 and 34 weeks in ApoE-KO (p < 0.001). Aging ApoE-KO demonstrated increased plaque (p = 0.02), medial thickening (p < 0.001), and severe elastin fragmentation (p < 0.001). We conclude that the contribution of aging to vascular stiffness is relatively minor compared with the influence of atherosclerosis. However, the effect of atherosclerosis on stiffness is significant only with advanced stages of plaque formation.

Effect of intraluminal thrombus on wall stress in patient-specific models of abdominal aortic aneurysm

Computational modeling of arterial biomechanics: Insights into pathogenesis and treatment of vascular disease

Association of Wall Stress of Human Intracranial Saccular Aneurysm With Coil Packing Density After Coil Embolization

Coil embolization has become a widely accepted endovascular procedure for intracranial aneurysms, as an alternative to surgical clipping [1,2]. This procedure involves treating an aneurysm from the inside out, whereby metallic coils are placed into the aneurysm to induce thrombosis of the lumen and eliminate the risk of rupture and hemorrhage. Successful endosaccular packing mainly depends on the morphological features and size of the aneurysm, and the relationship of the aneurysm to the cerebral arteries.

Elasticity and geometry: a computational model of the Heineke–Mikulicz strictureplasty

Analytically derived material properties of multilaminated extracellular matrix devices using the ball-burst test

Mechanical, compositional and morphological characterisation of the human male urethra for the development of a biomimetic tissue engineered urethral scaffold

Dynamic Motion Analysis of Human Coronary Artery Vein Grafts In-Vivo

Abstract It has previously been shown that the coronary arteries undergo cyclic flexure, stretching and twisting due to their attachment to the beating heart [3,7,10]. We hypothesize that vein grafts to the coronary arteries also undergo such cyclic motion. Characterizing the heart-induced deformation of coronary artery vein grafts (CAVG) is important in order to study its possible role in their pathogenesis.

Aging of the skeletal muscle extracellular matrix drives a stem cell fibrogenic conversion

Age-related declines in skeletal muscle regeneration have been attributed to muscle stem cell (MuSC) dysfunction. Aged MuSCs display a fibrogenic conversion, leading to fibrosis and impaired recovery after injury. Although studies have demonstrated the influence of in vitro substrate characteristics on stem cell fate, whether and how aging of the extracellular matrix (ECM) affects stem cell behavior has not been investigated. Here, we investigated the direct effect of the aged muscle ECM on MuSC lineage specification. Quantification of ECM topology and muscle mechanical properties reveals decreased collagen tortuosity and muscle stiffening with increasing age. Age-related ECM alterations directly disrupt MuSC responses, and MuSCs seeded ex vivo onto decellularized ECM constructs derived from aged muscle display increased expression of fibrogenic markers and decreased myogenicity, compared to MuSCs seeded onto young ECM. This fibrogenic conversion is recapitulated in vitro when MuSCs are seeded directly onto matrices elaborated by aged fibroblasts. When compared to young fibroblasts, fibroblasts isolated from aged muscle display increased nuclear levels of the mechanosensors, Yes-associated protein (YAP)/transcriptional coactivator with PDZ-binding motif (TAZ), consistent with exposure to a stiff microenvironment in vivo. Accordingly, preconditioning of young fibroblasts by seeding them onto a substrate engineered to mimic the stiffness of aged muscle increases YAP/TAZ nuclear translocation and promotes secretion of a matrix that favors MuSC fibrogenesis. The findings here suggest that an age-related increase in muscle stiffness drives YAP/TAZ-mediated pathogenic expression of matricellular proteins by fibroblasts, ultimately disrupting MuSC fate.

Development of a tissue-engineered vascular graft combining a biodegradable scaffold, muscle-derived stem cells and a rotational vacuum seeding technique

Regional Association of Biological and Hemodynamic Parameters in Distal End-to-Side Vascular Anastomoses Perfused Ex Vivo

Vascular bypass graft failure is a significant clinical problem and is frequently due to the formation of intimal hyperplasia (IH) [1–3]. IH is characterized by the accumulation of smooth muscle cells (SMC) and extracellular matrix in the intima of the vessel, which occurs when the normal balance between vascular cell proliferation and apoptosis (regulated cell death) is altered [4]. The disturbed flow present at the anastomosis has been implicated in the formation of IH and the link between hemodynamics and graft failure is via a complex cascade of events whereby biomechanical forces cause biological responses [5, 6]. For example, immediate early genes (IEG) such as c-fos, c-jun and egr-1 are involved in the signaling pathways for proliferation and apoptosis. When extracellular biomechanical stimuli (e.g. shear stress) cause the expression of IEG, their protein products translocate to the nucleus. These proteins regulate the expression of a number of genes implicated in cardiovascular disease including growth factors, adhesion molecules, proapoptotic substrates and coagulation factors [7–9]. Because IEG are involved in both proliferation and apoptosis, their expression may upset the normal balance between cell proliferation and apoptosis and could play a vital role in the IH formation in vascular bypass grafts.

<i>In Vivo</i> Assessment of a Tissue-Engineered Vascular Graft Combining a Biodegradable Elastomeric Scaffold and Muscle-Derived Stem Cells in a Rat Model

Limited autologous vascular graft availability and poor patency rates of synthetic grafts for bypass or replacement of small-diameter arteries remain a concern in the surgical community. These limitations could potentially be improved by a tissue engineering approach. We report here our progress in the development and in vivo testing of a stem-cell-based tissue-engineered vascular graft for arterial applications. Poly(ester urethane)urea scaffolds (length = 10 mm; inner diameter = 1.2 mm) were created by thermally induced phase separation (TIPS). Compound scaffolds were generated by reinforcing TIPS scaffolds with an outer electrospun layer of the same biomaterial (ES-TIPS). Both TIPS and ES-TIPS scaffolds were bulk-seeded with 10 x 10(6) allogeneic, LacZ-transfected, muscle-derived stem cells (MDSCs), and then placed in spinner flask culture for 48 h. Constructs were implanted as interposition grafts in the abdominal aorta of rats for 8 weeks. Angiograms and histological assessment were performed at the time of explant. Cell-seeded constructs showed a higher patency rate than the unseeded controls: 65% (ES-TIPS) and 53% (TIPS) versus 10% (acellular TIPS). TIPS scaffolds had a 50% mechanical failure rate with aneurysmal formation, whereas no dilation was observed in the hybrid scaffolds. A smooth-muscle-like layer of cells was observed near the luminal surface of the constructs that stained positive for smooth muscle alpha-actin and calponin. LacZ+ cells were shown to be engrafted in the remodeled construct. A confluent layer of von Willebrand Factor-positive cells was observed in the lumen of MDSC-seeded constructs, whereas acellular controls showed platelet and fibrin deposition. This is the first evidence that MDSCs improve patency and contribute to the remodeling of a tissue-engineered vascular graft for arterial applications.

Pericyte-based human tissue engineered vascular grafts

Effects of Ovariectomy and Estrogen Replacement on the Urethral Continence Reflex During Sneezing in Rats

Results indicate that ovariectomy significantly impairs urethral function from the early stage (3 weeks) but does not induce stress urinary incontinence until the late stage (6 weeks). Also, estrogen replacement restores only the urethral baseline pressure parameter, leading to partial prevention of stress urinary incontinence. Since urethral baseline pressure and urethral response amplitude during sneezing parameters are related to urethral smooth and striated muscle activity, respectively, based on our previous studies, hormone replacement therapy may be partially effective for stress urinary incontinence by enhancing smooth muscle mediated urethral activity under stress conditions such as sneezing.