Postnatal alterations in elastic fiber organization precede resistance artery narrowing in SHR

2006 ◽  
Vol 291 (2) ◽  
pp. H804-H812 ◽  
Author(s):  
José M. González ◽  
Ana M. Briones ◽  
Beatriz Somoza ◽  
Craig J. Daly ◽  
Elisabet Vila ◽  
...  
Keyword(s):  
Time Course ◽  
Elastic Fiber ◽  
Elastic Fibers ◽  
Early Event ◽  
Resistance Artery ◽  
Internal Elastic Lamina ◽  
Wall Stiffness ◽  
Fiber Deposition ◽  
Fiber Organization ◽  
Elastic Lamina

Resistance artery narrowing and stiffening are key elements in the pathogenesis of essential hypertension, but their origin is not completely understood. In mesenteric resistance arteries (MRA) from spontaneously hypertensive rats (SHR), we have shown that inward remodeling is associated with abnormal elastic fiber organization, leading to smaller fenestrae in the internal elastic lamina. Our current aim is to determine whether this alteration is an early event that precedes vessel narrowing, or if elastic fiber reorganization in SHR arteries occurs because of the remodeling process itself. Using MRA from 10-day-old, 30-day-old, and 6-mo-old SHR and normotensive Wistar Kyoto rats, we investigated the time course of the development of structural and mechanical alterations (pressure myography), elastic fiber organization (confocal microscopy), and amount of elastin (radioimmunoassay for desmosine) and collagen (picrosirius red). SHR MRA had an impairment of fenestrae enlargement during the first month of life. In 30-day-old SHR, smaller fenestrae and more packed elastic fibers in the internal elastic lamina were paralleled by increased wall stiffness. Collagen and elastin levels were unaltered at this age. MRA from 6-mo-old SHR also had smaller fenestrae and a denser network of adventitial elastic fibers, accompanied by increased collagen content and vessel narrowing. At this age, elastase digestion was less effective in SHR MRA, suggesting a lower susceptibility of elastic fibers to enzymatic degradation. These data suggest that abnormal elastic fiber deposition in SHR increases resistance artery stiffness at an early age, which might participate in vessel narrowing later in life.

scholarly journals Elastic Fibers of the Internal Elastic Lamina Are Unraveled But Not Created With Expanding Arterial Diameter in Arteriogenesis

2020 ◽  
Vol 1 ◽  
pp. 247
Author(s):  
Derek Afflu ◽  
Dylan D. McCreary ◽  
Nolan Skirtich ◽  
Kathy Gonzalez ◽  
Edith Tzeng ◽  
...  
Keyword(s):  
Elastic Fibers ◽  
Internal Elastic Lamina ◽  
Arterial Diameter ◽  
Elastic Lamina

A comparison of acute vascular damage caused by ADAPT versus a stent retriever device after thrombectomy in acute ischemic stroke: a histological and ultrastructural study in an animal model

2016 ◽  
Vol 9 (8) ◽  
pp. 743-749 ◽  
Author(s):  
S Peschillo ◽  
F Diana ◽  
J Berge ◽  
P Missori
Keyword(s):  
Arterial Wall ◽  
Elastic Fibers ◽  
Cell Alignment ◽  
Internal Elastic Lamina ◽  
Endothelial Lining ◽  
Tissue Samples ◽  
First Pass ◽  
Stent Retrievers ◽  
Ultrastructural Damage ◽  
Elastic Lamina

BackgroundIt has been amply demonstrated that endovascular procedures can be successful treatment for stroke, both in terms of revascularization and clinical outcome. There is not, however, a published comparison of any histological or ultrastructural damage to the vessels that may be caused by a direct aspiration first pass technique (ADAPT) or stent retrievers (SR) used in these procedures. This study analyses and compares acute damage to the arterial wall caused by ADAPT or SR.Material and methodsDamage to the walls of swine extracranial arteries was evaluated after ADAPT with the Penumbra system or thrombectomy with an SR (Solitaire 6×30). The procedures were performed after injecting thrombi into the selected arteries (arteries with diameters similar to those of the human internal carotid artery and first segment of the middle cerebral artery). After the procedures, the animal was euthanized and 12 arterial samples were obtained for analysis by optical and electronic microscopy.ResultsTissue samples from the vessels treated with SR showed almost complete loss of endothelium, thickening of the internal elastic lamina, and degeneration of the elastic fibers of the bordering lamina media and adventitia. In contrast, tissue samples of the vessels treated with ADAPT had a clear integral internal elastic lamina and uninterrupted endothelial lining, although cell alignment was altered and there were surface lacerations due to manipulation of the samples.ConclusionsBoth techniques caused acute damage to the vessel walls, however, thrombectomy with SR appeared to be more harmful to all layers of the arterial wall, particularly the endothelium.

scholarly journals Pigmentation Affects Elastic Fiber Patterning and Biomechanical Behavior of the Murine Aortic Valve

2021 ◽  
Vol 8 ◽  
Author(s):  
Sana Nasim ◽  
Popular Pandey ◽  
Rosemeire M. Kanashiro-Takeuchi ◽  
Jin He ◽  
Joshua D. Hutcheson ◽  
...  
Keyword(s):  
Aortic Valve ◽  
Elastic Fiber ◽  
Biomechanical Properties ◽  
Systemic Circulation ◽  
Elastic Fibers ◽  
Multiphoton Imaging ◽  
Force Microscopy ◽  
Biomechanical Behavior ◽  
Atomic Force ◽  
Fiber Organization

The aortic valve (AoV) maintains unidirectional blood distribution from the left ventricle of the heart to the aorta for systemic circulation. The AoV leaflets rely on a precise extracellular matrix microarchitecture of collagen, elastin, and proteoglycans for appropriate biomechanical performance. We have previously demonstrated a relationship between the presence of pigment in the mouse AoV with elastic fiber patterning using multiphoton imaging. Here, we extended those findings using wholemount confocal microscopy revealing that elastic fibers were diminished in the AoV of hypopigmented mice (KitWv and albino) and were disorganized in the AoV of K5-Edn3 transgenic hyperpigmented mice when compared to wild type C57BL/6J mice. We further used atomic force microscopy to measure stiffness differences in the wholemount AoV leaflets of mice with different levels of pigmentation. We show that AoV leaflets of K5-Edn3 had overall higher stiffness (4.42 ± 0.35 kPa) when compared to those from KitWv (2.22 ± 0.21 kPa), albino (2.45 ± 0.16 kPa), and C57BL/6J (3.0 ± 0.16 kPa) mice. Despite the striking elastic fiber phenotype and noted stiffness differences, adult mutant mice were found to have no overt cardiac differences as measured by echocardiography. Our results indicate that pigmentation, but not melanocytes, is required for proper elastic fiber organization in the mouse AoV and dictates its biomechanical properties.

scholarly journals IUGR decreases elastin mRNA expression in the developing rat lung and alters elastin content and lung compliance in the mature rat lung

2011 ◽  
Vol 43 (9) ◽  
pp. 499-505 ◽  
Author(s):  
Lisa A. Joss-Moore ◽  
Yan Wang ◽  
Xing Yu ◽  
Michael S. Campbell ◽  
Christopher W. Callaway ◽  
...  
Keyword(s):  
Elastic Fiber ◽  
Lung Compliance ◽  
Fiber Formation ◽  
Elastic Fibers ◽  
Mrna Levels ◽  
Rat Lung ◽  
Mrna Transcript ◽  
Transcript Levels ◽  
Alveolar Development ◽  
Fiber Deposition

Complications of intrauterine growth restriction (IUGR) include increased pulmonary morbidities and impaired alveolar development. Normal alveolar development depends upon elastin expression and processing, as well as the formation and deposition of elastic fibers. This is true of the human and rat. In this study, we hypothesized that uteroplacental insufficiency (UPI)-induced IUGR decreases mRNA levels of elastin and genes required for elastin fiber synthesis and assembly, at birth (prealveolarization) and postnatal day 7 (midalveolarization) in the rat. We further hypothesized that this would be accompanied by reduced elastic fiber deposition and increased static compliance at postnatal day 21 (mature lung). We used a well characterized rat model of IUGR to test these hypotheses. IUGR decreases mRNA transcript levels of genes essential for elastic fiber formation, including elastin, at birth and day 7. In the day 21 lung, IUGR decreases elastic fiber deposition and increases static lung compliance. We conclude that IUGR decreases mRNA transcript levels of elastic fiber synthesis genes, before and during alveolarization leading to a reduced elastic fiber density and increased static lung compliance in the mature lung. We speculate that the mechanism by which IUGR predisposes to pulmonary disease may be via decreased lung elastic fiber deposition.

scholarly journals The role of caveolin-1 in pulmonary matrix remodeling and mechanical properties

2008 ◽  
Vol 295 (6) ◽  
pp. L1007-L1017 ◽  
Author(s):  
O. Le Saux ◽  
K. Teeters ◽  
S. Miyasato ◽  
J. Choi ◽  
G. Nakamatsu ◽  
...  
Keyword(s):  
Mechanical Properties ◽  
Signal Transduction ◽  
Airway Resistance ◽  
Transforming Growth Factor ◽  
Interstitial Fibrosis ◽  
Elastic Fiber ◽  
Elastic Fibers ◽  
Matrix Remodeling ◽  
Caveolin 1 ◽  
Fiber Deposition

Caveolin-1 (cav1) is a 22-kDa membrane protein essential to the formation of small invaginations in the plasma membrane, called caveolae. The cav1 gene is expressed primarily in adherent cells such as endothelial and smooth muscle cells and fibroblasts. Caveolae contain a variety of signaling receptors, and cav1 notably downregulates transforming growth factor (TGF)-β signal transduction. In pulmonary pathologies such as interstitial fibrosis or emphysema, altered mechanical properties of the lungs are often associated with abnormal ECM deposition. In this study, we examined the physiological functions and the deposition of ECM in cav1−/− mice at various ages (1–12 mo). Cav1−/− mice lack caveolae and by 3 mo of age have significant reduced lung compliance and increased elastance and airway resistance. Pulmonary extravasation of fluid, as part of the cav1−/− mouse phenotype, probably contributed to the alteration of compliance, which was compounded by a progressive increase in deposition of collagen fibrils in airways and parenchyma. We also found that the increased elastance was caused by abundant elastic fiber deposition primarily around airways in cav1−/− mice at least 3 mo old. These observed changes in the ECM composition probably also contribute to the increased airway resistance. The higher deposition of collagen and elastic fibers was associated with increased tropoelastin and col1α2 and col3α1 gene expression in lung tissues, which correlated tightly with increased TGF-β/Smad signal transduction. Our study illustrates that perturbation of cav1 function may contribute to several pulmonary pathologies as the result of the important role played by cav1, as part of the TGF-β signaling pathway, in the regulation of the pulmonary ECM.

scholarly journals Elastic Laminar Reorganization Occurs with Outward Diameter Oxidase for Stabilization

Cells ◽  
2021 ◽  
Vol 11 (1) ◽  
pp. 7
Author(s):  
Ryan M. McEnaney ◽  
Dylan D. McCreary ◽  
Nolan O. Skirtich ◽  
Elizabeth A. Andraska ◽  
Ulka Sachdev ◽  
...  
Keyword(s):  
Structural Changes ◽  
Elastic Fiber ◽  
Multiphoton Microscopy ◽  
Fold Increase ◽  
Fiber Formation ◽  
Elastic Fibers ◽  
Large Artery ◽  
Internal Elastic Lamina ◽  
Luminal Diameter ◽  
Collateral Arteries

When a large artery becomes occluded, hemodynamic changes stimulate remodeling of arterial networks to form collateral arteries in a process termed arteriogenesis. However, the structural changes necessary for collateral remodeling have not been defined. We hypothesize that deconstruction of the extracellular matrix is essential to remodel smaller arteries into effective collaterals. Using multiphoton microscopy, we analyzed collagen and elastin structure in maturing collateral arteries isolated from ischemic rat hindlimbs. Collateral arteries harvested at different timepoints showed progressive diameter expansion associated with striking rearrangement of internal elastic lamina (IEL) into a loose fibrous mesh, a pattern persisting at 8 weeks. Despite a 2.5-fold increase in luminal diameter, total elastin content remained unchanged in collaterals compared with control arteries. Among the collateral midzones, baseline elastic fiber content was low. Outward remodeling of these vessels with a 10–20 fold diameter increase was associated with fractures of the elastic fibers and evidence of increased wall tension, as demonstrated by the straightening of the adventitial collagen. Inhibition of lysyl oxidase (LOX) function with β-aminopropionitrile resulted in severe fragmentation or complete loss of continuity of the IEL in developing collaterals. Collateral artery development is associated with permanent redistribution of existing elastic fibers to accommodate diameter growth. We found no evidence of new elastic fiber formation. Stabilization of the arterial wall during outward remodeling is necessary and dependent on LOX activity.

Changes in aortic stiffness related to elastic fiber network anomalies in the Brown Norway rat during maturation and aging

2010 ◽  
Vol 299 (1) ◽  
pp. H144-H152 ◽  
Author(s):  
Mary Osborne-Pellegrin ◽  
Carlos Labat ◽  
Nathalie Mercier ◽  
Pascal Challande ◽  
Patrick Lacolley
Keyword(s):  
Elastic Fiber ◽  
Wall Stress ◽  
Brown Norway ◽  
Internal Elastic Lamina ◽  
Fiber Network ◽  
Norway Rat ◽  
Age Related ◽  
Brown Norway Rat ◽  
Opposing Effects ◽  
Elastic Lamina

Adult Brown Norway (BN) rats exhibit numerous internal elastic lamina (IEL) ruptures in the abdominal aorta (AA) and a lower aortic elastin-to-collagen ratio (E/C) compared with other strains. We studied here AA mechanical properties in BN compared with control strains. AA stiffness (assessed by plotting elastic modulus/wall-stress curves obtained under anesthesia), thoracic aorta elastin and collagen contents, and IEL ruptures in AA were measured in male BN and LOU rats aged 6, 10, and 15 wk. The Long Evans (LE) control strain was compared with BN at more advanced ages (15, 28, and 64 wk). At all ages, aortic E/C was lower in BN than in control strains. At 6 wk, AA stiffness was greater in BN than in LOU. In both strains, AA stiffness decreased between 6 and 10 wk, more so in BN than in LOU, and then increased, reaching similar values at 15 wk. BN AA stiffness was not different from that of LE at 15 and 28 wk, but was significantly lower at 64 wk. The increased stiffness in young BN rat AA may be due to the decreased E/C. IEL rupture onset in the BN around 7–8 wk, which decreases stiffness, as suggested by its pharmacological modulation, abolished such differences by 15 wk. Thereafter, age-related AA stiffness increased less in BN than in LE, likely due to the numerous IEL ruptures. We conclude that, in the BN rat, the lower E/C and the presence of IEL ruptures have opposing effects on arterial stiffness.

scholarly journals EXPERIMENTAL ARTERIOSCLEROSIS

1972 ◽  
Vol 136 (4) ◽  
pp. 769-789 ◽  
Author(s):  
Michael B. Stemerman ◽  
Russell Ross
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Balloon Catheter ◽  
Muscle Cells ◽  
Endothelial Injury ◽  
Macaca Nemestrina ◽  
Elastic Fibers ◽  
Internal Elastic Lamina ◽  
Principal Factors ◽  
Elastic Lamina

Arteriosclerotic lesions have been produced in monkeys (Macaca nemestrina) by selective removal of the vascular endothelium with an intra-arterial balloon catheter. Immediately after de-endothelialization a platelet layer covers the denuded area. This thrombus is gradually removed and by 7 days the vessel appears to be largely reendothelialized. Beginning at day 4, smooth muscle cells undergo modification and migrate through fenestrae in the internal elastic lamina into the intima where they proliferate. By 28 days, the intimal lesion consists of multiple layers of smooth muscle cells surrounded by collagen and elastic fibers and basement-like material. After 3 months the lesions are markedly hyperplastic and contain new extracellular connective tissue elements. In contrast, with no further injury after 6 months the lesion has decreased markedly in size suggesting that it may be reversible in the absence of continued endothelial injury. The importance of endothelial "injury" exposing medial smooth muscle to plasma constituents may be the principal factors associated with the migration and proliferation of the smooth muscle cells into the intima resulting in the lesion. The smooth muscle cells do not contain lipid. The similarities of this lesion to the fibromusculo-elastic lesion or preatherosclerotic intimal hyperplasia in man makes it a useful model for the further study of atherosclerosis.

Anchoring Fibrils in Arterial Endothelium

1969 ◽  
Vol 27 ◽  
pp. 274-275
Author(s):  
A. Trillo
Keyword(s):  
Carotid Arteries ◽  
Animal Species ◽  
Cell Layer ◽  
Present Communication ◽  
Internal Elastic Lamina ◽  
Endothelial Cell Layer ◽  
Structural Details ◽  
Rats And Mice ◽  
Arterial Endothelium ◽  
Elastic Lamina

There are conflicting reports regarding some fine structural details of arteries from several animal species. Buck denied the existence of a sub-endothelial space, while Karrer and Keech described a space of variable width which separates the endothelium from the underlying internal elastic lamina in aortas of aging rats and mice respectively.The present communication deals with the ultrastrueture of the interface between the endothelial cell layer and the internal elastic lamina as observed in carotid arteries from rabbits of varying ages.

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