scholarly journals P715Regulation of elastic fibers and smooth muscle cells in the mechanism of fibrosis found in patients with initial and intense varicose lesions: a clinical correlation

2014 ◽  
Vol 103 (suppl 1) ◽  
pp. S130.3-S131 ◽  
Author(s):  
J Regadera ◽  
JP Velasco-Martin ◽  
G Espana-Caparros ◽  
LM Reparaz ◽  
LA Condezo-Hoyos ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Elastic Fibers ◽  
Clinical Correlation

scholarly journals Proteoglycans in primate arteries. I. Ultrastructural localization and distribution in the intima.

1975 ◽  
Vol 67 (3) ◽  
pp. 660-674 ◽  
Author(s):  
T N Wight ◽  
R Ross
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Ultrastructural Localization ◽  
Ruthenium Red ◽  
Basement Membranes ◽  
Macaca Nemestrina ◽  
Elastic Fibers ◽  
Surface Coat ◽  
The Matrix

Proteoglycans were identified and localized histochemically and ultrastructurally in normal and hyperplastic arterial intimas in nonhuman primates (Macaca nemestrina). These regions were consistently more alcianophilic than the adjacent medial layers and this alcianophilia was absent after treatment with glycosaminoglycan-degradative enzymes. Ultrastructurally, the intimal intercellular matrix consisted of numerous, irregularly shaped, 200-500-A diameter granules possessing 30--60-A diameter filamentous projections, and these granules were dispersed between collagen and elastic fibers. The granules exhibited a marked affinity for ruthenium red and were interconnected via their filamentous projections. The ruthenium red-positive granules were intimately associated with the plasma membrane of intimal smooth muscle cells and attached to collagen fibrils and elastic fibers. The matrix granules were completely removed after testicular hyaluronidase or chondroitinase ABC digestion but only partially removed after leech hyaluronidase treatment. These results suggest that the matrix granules contain some hyaluronic acid and one or more isomers of chondroitin sulfate. In addition to the large ruthenium red-positive matrix granules, a smaller class of ruthenium red-positive granule (100--200-A diameter) was present within the basement membranes beneath the endothelium and surrounding the smooth muscle cells. Ruthenium red also exhibited an affinity for the surface coat of the smooth muscle cells. The potential importance of proteoglycans in arterial intimal hyperplasia is discussed.

ORGANIZATION AND RELATIVE CONTENT OF SMOOTH MUSCLE CELLS, COLLAGEN AND ELASTIC FIBERS IN THE CORPUS CAVERNOSUM OF RAT PENIS

2000 ◽  
Vol 164 (5) ◽  
pp. 1802-1806 ◽  
Author(s):  
ANA C.A.D. PINHEIRO ◽  
WALDEMAR S. COSTA ◽  
LUIS E.M. CARDOSO ◽  
FRANCISCO J.B. SAMPAIO
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Corpus Cavernosum ◽  
Muscle Cells ◽  
Relative Content ◽  
Elastic Fibers

scholarly journals Extracellular Vesicles Derived from Primary Adipose Stromal Cells Induce Elastin and Collagen Deposition by Smooth Muscle Cells within 3D Fibrin Gel Culture

2021 ◽  
Vol 8 (5) ◽  
pp. 51
Author(s):  
Eoghan M. Cunnane ◽  
Aneesh K. Ramaswamy ◽  
Katherine L. Lorentz ◽  
David A. Vorp ◽  
Justin S. Weinbaum
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Stromal Cells ◽  
Biological Effects ◽  
Muscle Cells ◽  
Arterial Disease ◽  
Protein Quantification ◽  
Elastic Fibers ◽  
Positive Effects ◽  
Adipose Derived Stromal Cells

Macromolecular components of the vascular extracellular matrix (ECM), particularly elastic fibers and collagen fibers, are critical for the proper physiological function of arteries. When the unique biomechanical combination of these fibers is disrupted, or in the ultimate extreme where fibers are completely lost, arterial disease can emerge. Bioengineers in the realms of vascular tissue engineering and regenerative medicine must therefore ideally consider how to create tissue engineered vascular grafts containing the right balance of these fibers and how to develop regenerative treatments for situations such as an aneurysm where fibers have been lost. Previous work has demonstrated that the primary cells responsible for vascular ECM production during development, arterial smooth muscle cells (SMCs), can be induced to make new elastic fibers when exposed to secreted factors from adipose-derived stromal cells. To further dissect how this signal is transmitted, in this study, the factors were partitioned into extracellular vesicle (EV)-rich and EV-depleted fractions as well as unseparated controls. EVs were validated using electron microscopy, dynamic light scattering, and protein quantification before testing for biological effects on SMCs. In 2D culture, EVs promoted SMC proliferation and migration. After 30 days of 3D fibrin construct culture, EVs promoted SMC transcription of the elastic microfibril gene FBN1 as well as SMC deposition of insoluble elastin and collagen. Uniaxial biomechanical properties of strand fibrin constructs were no different after 30 days of EV treatment versus controls. In summary, it is apparent that some of the positive effects of adipose-derived stromal cells on SMC elastogenesis are mediated by EVs, indicating a potential use for these EVs in a regenerative therapy to restore the biomechanical function of vascular ECM in arterial disease.

A new adhesive protein mediating the interaction between mesenchymal cells and elastin fibers: Elastonectin

1988 ◽  
Vol 53 (1) ◽  
pp. 209-211
Author(s):  
Ladislas Robert ◽  
William Hornebeck
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Atherosclerotic Plaque ◽  
Muscle Cells ◽  
Mesenchymal Cells ◽  
Elastic Fibers ◽  
Elastic Tissue ◽  
Adhesive Protein

An inducible adhesive protein was demonstrated in smooth muscle cells and fibroblasts which mediate the adhesion of mesenchymal cells to elastic fibers. It is proposed to designate it elastonectin. This protein plays probably an important role in the morphogenesis of elastic tissue and its degradation is probably involved in the formation of the atherosclerotic plaque.

scholarly journals An electron stain for elastic fibers using orcein.

1977 ◽  
Vol 25 (4) ◽  
pp. 306-308 ◽  
Author(s):  
H Nakamura ◽  
C Kanai ◽  
V Mizuhira
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Uranyl Acetate ◽  
Elastic Fibers ◽  
Lead Citrate ◽  
Thin Sections ◽  
Electron Microscopes ◽  
Orcein Staining

Orcein was found to be useful as an electron-opaque stain for elastic fibers in epoxy-sections. Ultra-thin sections of aorta were treated with elastica stain containing 0.1-0.3% orcein and counterstained in uranyl acetate and lead citrate. Elastic fibers were densely and specifically demonstrated in the stroma and near smooth muscle cells. The result of orcein staining has a comparable appearance under both light and electron microscopes.

scholarly journals The Effects of Elastic Fiber Protein Insufficiency and Treatment on the Modulus of Arterial Smooth Muscle Cells

2014 ◽  
Vol 136 (2) ◽  
Author(s):  
M. Gabriela Espinosa ◽  
William S. Gardner ◽  
Lisa Bennett ◽  
Bradley A. Sather ◽  
Hiromi Yanagisawa ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Elastic Fiber ◽  
Muscle Cells ◽  
Elastic Fibers ◽  
Force Microscopy ◽  
Altered Gene Expression ◽  
Atomic Force ◽  
Fiber Protein ◽  
Altered Gene

Elastic fibers are critical for the mechanical function of the large arteries. Mechanical effects of elastic fiber protein deficiency have been investigated in whole arteries, but not in isolated smooth muscle cells (SMCs). The elastic moduli of SMCs from elastin (Eln-/-) and fibulin-4 (Fbln4-/-) knockout mice were measured using atomic force microscopy. Compared to control SMCs, the modulus of Eln-/- SMCs is reduced by 40%, but is unchanged in Fbln4-/- SMCs. The Eln-/- SMC modulus is rescued by soluble or α elastin treatment. Altered gene expression, specifically of calponin, suggests that SMC phenotypic modulation may be responsible for the modulus changes.

P1937Deficiency of PI 3-kinase isoform p110alpha in smooth muscle cells impairs vascular integrity and promotes aortic aneurysm formation

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
M Vantler ◽  
E M Berghausen ◽  
M Zierden ◽  
M Mollenhauer ◽  
D Mehrkens ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Inflammation ◽  
Elastic Fiber ◽  
Muscle Cells ◽  
Aortic Aneurysms ◽  
Elastic Fibers ◽  
Infrarenal Aorta ◽  
Vascular Integrity ◽  
Anti Inflammatory

Abstract Background The pathobiology of aortic aneurysms is characterized by vascular inflammation, extracellular matrix degeneration, and particularly by loss and dedifferentiation of vascular smooth muscle cells (SMCs). In SMCs, the PI 3-kinase isoform p110α mediates receptor tyrosine kinase dependent proliferation, chemotaxis, and survival. Smooth muscle specific p110α deficient mice (SM-p110α−/− mice) display reduced medial wall thickness, substantially reduced neointima formation and media hypertrophy after balloon injury of the carotid artery. Objective We hypothesized that loss of p110α signaling impairs vascular integrity and promotes development and progression of abdominal aortic aneurysms (AAA). We aimed to elucidate the impact of p110α deficiency on vascular integrity, SMC phenotypic modulation, vascular inflammation, and AAA formation. Methods and results Ultra-structural characterization of aortic wall morphology in abdominal aortas from SM-p110α−/− mice by transmission electron microscopy (TEM) revealed disarranged structure of tunica media as indicated by disorganized elastic fibers, detached SMCs, and elastic fiber breaks. Western blots showed reduced elastin and fibrillin expression in SMCs from p110α−/− mice. Media thickness was significantly reduced in abdominal aortas from SM-p110α−/− mice compared to wild type (WT) controls (29.0±3.1 vs. 42.5±4.1 μm). Lack of p110α decreased expression of differentiation markers SM-α-actin and SM-MHC. p110α deficiency significantly diminished responsiveness of aortic rings to vasodilator acetylcholine. These data indicate loss of differentiation and impaired contractility of p110α−/− SMCs. We subjected SM-p110α−/− mice and WT littermate controls to the porcine pancreatic elastase (PPE) model of AAA. PPE was infused into the infrarenal aorta, respectively, to induce AAA formation. Ultrasonic examination of abdominal aortas demonstrated an enlarged aortic diameter in PPE challenged mice. AAA formation was significantly (p<0.01) enhanced in SM-p110α−/− (0.46±0.12 mm, n=8) compared to SM-p110α+/+ mice (0.18±0.03 mm, n=4). These data indicate a protective function of p110α in AAA formation. Immunocytochemistry of the aortic medial compartment from PPE-perfused SM-p110α−/− mice revealed significantly increased MOMA-2+ monocyte/macrophage content indicating augmented aortic inflammation during AAA formation compared to WT controls. Furthermore, SMCs from SM-p110α−/− mice expressed reduced amounts of anti-inflammatory angiopoietin1 compared to p110α+/+ SMCs. Moreover, frequent apoptotic/necrotic SMCs were found in the aortic media of SM-p110α−/− mice by TEM, potentially contributing to vascular inflammation in a critical fashion. Conclusion These data indicate that p110α signaling critically contributes to vascular integrity via maintaining SMC plasticity, elastic fiber homeostasis, and anti-inflammatory processes. Consequently, lack of proper p110α signaling promotes progression of AAA formation.

Mechanics of Aortic Smooth Muscle Cells in Tissue Constructs: Effects of Matrix Composition

2008 ◽  
Author(s):  
Wei Du ◽  
Kenneth M. Pryse ◽  
Elliot L. Elson ◽  
Ruth J. Okamoto
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Cyclic Stretch ◽  
Matrix Composition ◽  
Elastic Fibers ◽  
Aortic Dilatation ◽  
Mechanical Responses ◽  
Tissue Constructs ◽  
Cardio Vascular

Remodeling of arteries in response to altered loads is an area of intense interest to cardio-vascular clinicians and researchers. In humans, changes due to cardiovascular diseases (e.g. aortic dilatation) may occur slowly over many years, and mathematical models that describe the remodeling response are needed for predicting the course, and possible treatment, of these diseases. Recently, Humphrey and coworkers have proposed constrained mixture models [1] that can describe these acute and chronic changes[2, 3]. These models consider local stresses in the arterial wall to be the sum of individual contributions from collagen, elastic fibers, and vascular smooth muscle cells (VSMCs) Therefore, the mechanical behavior of VSMCs (presumed to be mechanically in parallel) should be independent of the exact composition of the extracellular matrix (ECM) at any specified stage of tissue remodeling. Previously we have studied the mechanics of VSMCs in 3-D bio-artificial tissue constructs made with collagen [4]. In this study, we made 3-D constructs using fibrin, and investigated whether VSMC morphology and mechanics are dependent on the ECM composition. Because previous studies have shown that VSMCs respond to cyclic stretch by increasing alignment and extra-cellular matrix production[5], we measured the mechanical responses of the VSMCs under continuous cyclic stretch.

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