Optimizing a Three Layered Electrospun Matrix to Mimic Native Arterial Architecture: Cellular and Mechanical Analysis

2011 ◽  
Author(s):  
Michael J. McClure ◽  
Scott A. Sell ◽  
David G. Simpson ◽  
Beat H. Walpoth ◽  
Gary L. Bowlin
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Mechanical Response ◽  
Muscle Cells ◽  
Vascular Wall ◽  
Biomechanical Properties ◽  
Mechanical Analysis ◽  
Elastic Behavior ◽  
Cellular Attachment ◽  
Inhibition Experiment

The architecture of the vascular wall is highly intricate and requires unique biomechanical properties in order to function properly. Native artery is composed of a mix of collagen, elastin, endothelial cells (ECs), smooth muscle cells (SMC), fibroblasts, and proteoglycans arranged into three distinct layers: the intima, media, and adventitia. Throughout artery, collagen and elastin play an important role, providing a mechanical backbone, preventing vessel rupture, and promoting recovery while undergoing pulsatile deformations [1]. The low-strain mechanical response of artery to blood flow is dominated by the elastic behavior of elastin which prevents pulsatile energy from being dissipated as heat [2]. Previous work has shown the ability to fabricate multi-layered electrospun scaffolds composed of polycaprolactone (PCL), elastin (ELAS), and collagen (COL), and their associated mechanical advantages. PCL was chosen, in this case, to provide mechanical integrity and elasticity, while elastin and collagen would provide further elasticity and bioactivity [3,4]. However, when the grafts were implanted in the descending aorta of a rat, cellular results were not as desirable as predicted. Therefore, further graft optimization was required. The hypothesis of this study was that blended polymers and biopolymers would be conducive for cellular attachment through specific integrin binding sites. To test this hypothesis, human umbilical artery smooth muscle cells (hUASMC) were seeded on electrospun PCL, COL, and ELAS blends for evaluation in a cell adhesion inhibition experiment.

scholarly journals Role of Perivascular Adipose Tissue-Derived Adiponectin in Vascular Homeostasis

Cells ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 1485
Author(s):  
Adrian Sowka ◽  
Pawel Dobrzyn
Keyword(s):  
Endothelial Cells ◽  
Adipose Tissue ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Vascular Wall ◽  
Whole Body ◽  
Perivascular Adipose Tissue

Studies of adipose tissue biology have demonstrated that adipose tissue should be considered as both passive, energy-storing tissue and an endocrine organ because of the secretion of adipose-specific factors, called adipokines. Adiponectin is a well-described homeostatic adipokine with metabolic properties. It regulates whole-body energy status through the induction of fatty acid oxidation and glucose uptake. Adiponectin also has anti-inflammatory and antidiabetic properties, making it an interesting subject of biomedical studies. Perivascular adipose tissue (PVAT) is a fat depot that is conterminous to the vascular wall and acts on it in a paracrine manner through adipokine secretion. PVAT-derived adiponectin can act on the vascular wall through endothelial cells and vascular smooth muscle cells. The present review describes adiponectin’s structure, receptors, and main signaling pathways. We further discuss recent studies of the extent and nature of crosstalk between PVAT-derived adiponectin and endothelial cells, vascular smooth muscle cells, and atherosclerotic plaques. Furthermore, we argue whether adiponectin and its receptors may be considered putative therapeutic targets.

ANG II increases TIMP-1 expression in rat aortic smooth muscle cells in vivo

2003 ◽  
Vol 284 (2) ◽  
pp. H635-H643 ◽  
Author(s):  
Giovanna Castoldi ◽  
Cira R. T. di Gioia ◽  
Federico Pieruzzi ◽  
Cristina D'Orlando ◽  
Willy M. M. van de Greef ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Vascular Wall ◽  
Dependent Manner ◽  
Ang Ii ◽  
Maximal Increase ◽  
Aortic Smooth Muscle Cells ◽  
Aortic Smooth Muscle

Matrix metalloproteinases (MMPs) and their tissue inhibitors (TIMPs) are involved in tissue remodeling processes. TIMP-1 is the main native inhibitor of MMPs and it contributes to the development of tissue fibrosis. It is known that ANG II plays a fundamental role in vascular remodeling. In this study, we investigated whether ANG II modulates TIMP-1 expression in rat aortic smooth muscle cells. In vitro, ANG II induces TIMP-1 mRNA expression in a dose-dependent manner. The maximal increase in TIMP-1 expression was present after 3 h of ANG II stimulation. The ANG II increase in TIMP-1 expression was mediated by the ANG type 1 receptors because it was blocked by losartan. The increase in TIMP-1 expression was present after the first ANG II treatment, whereas repeated treatments (3 and 5 times) did not modify TIMP-1 expression. In vivo, exogenous ANG II was administered to Sprague-Dawley rats (200 ng · kg−1· min−1sc) for 6 and 25 days. Control rats received physiological saline. After treatment, systolic blood pressure was significantly higher ( P < 0.01), whereas plasma renin activity was suppressed ( P < 0.01), in ANG II-treated rats. ANG II increased TIMP-1 expression in the aorta of ANG II-treated rats both at the mRNA ( P < 0.05) and protein levels as evaluated by Western blotting ( P < 0.05) and/or immunohistochemistry. Neither histological modifications at the vascular wall nor differences in collagen content in the tunica media were present in both the ANG II- and saline-treated groups. Our data demonstrate that ANG II increases TIMP-1 expression in rat aortic smooth muscle cells. In vivo, both short- and long-term chronic ANG II treatments increase TIMP-1 expression in the rat aorta. TIMP-1 induction by ANG II in aortic smooth muscle cells occurs in the absence of histological changes at the vascular wall.

Endothelial and Smooth Muscle Cells as Antagonists in Vascular Fibrinoysis

1975 ◽  
Author(s):  
V. Noordhoek Hegt
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Blood Vessels ◽  
Plasminogen Activator ◽  
Fibrinolytic Activity ◽  
Vascular System ◽  
Muscle Cells ◽  
Vascular Wall ◽  
Vasa Vasorum ◽  
Slide Technique

Endothelial plasminogen activator activity in different types of human blood vessels obtained from fifty necropsies and thirty-five biopsies was detected and localized by means of plasminogen-rich fibrin slides. Great differences in endothelial activator activity were found along and across (vasa vasorum) the wall of the human vascular system.The same blood vessels were simultaneously investigated by a modified fibrin slide technique using plasminogen-free fibrin slides covered by plasmin to detect and localize inhibition of fibrinolysis in the vascular wall. The great variation in plasmin inhibition in different vessels revealed by this “fibrin slide sandwich technique” appeared to be closely associated with the localization and number of smooth muscle cells present in the walls of the vascular system. Strong plasmin inhibition was generally found at sites which showed no activator activity with the regular fibrin slide technique, while areas with a high endothelial fibrinolytic activity mostly revealed no inhibitory capacity.These results indicate that much of the variation in endothelial fibrinolytic activity on fibrin slides is due to inhibitory effects from the surrounding smooth muscle cells rather than to variability in the plasminogen activator content of the endothelium itself.

The Studies on Biocompatibility of Self-Expanding NiTi Stent and Apoptosis of Smooth Muscle Cells after Stenting

2005 ◽  
Vol 288-289 ◽  
pp. 587-590 ◽  
Author(s):  
Chun Jiang Li ◽  
Yu Feng Zheng ◽  
Chao Li ◽  
Lian Cheng Zhao
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Niti Alloy ◽  
Muscle Cells ◽  
Vascular Wall ◽  
Vessel Remodeling ◽  
Proliferation And Apoptosis ◽  
The Media ◽  
Atherosclerotic Process ◽  
Stent Surface

The biocompatibility of the NiTi alloy self-expanding stent, its dilating effect on the vascular wall, and the apoptosis of smooth muscle cells (SMCs) were studied by implantation of stent into the rabbit’s abdominal aorta for different period. All the animals lived throughout the study. There was no detectable migration or dissection of the stent, and there were no acute closures or sub-acute thromboses in the vessels. The rates of patency were 100% both at the beginning when the stent was implanted and at the end when the animal was sacrificed. It may be concluded that the vascular intima covers the whole stent at the 8-week point. The atherosclerotic process existed in the vascular intima in contact with the stent surface, while the proliferation and apoptosis of SMCs occured simultaneously. After stent implantation, the apoptosis happened in both intima and media, which indicated that the stent might not only stimulate the intima but also compress the media, leading to proliferation and apoptosis. This might contribute to vessel remodeling after stenting.

scholarly journals Influence of conjugated linoleic acids on functional properties of vascular cells

2009 ◽  
Vol 102 (8) ◽  
pp. 1099-1116 ◽  
Author(s):  
Robert Ringseis ◽  
Klaus Eder
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Functional Properties ◽  
Inflammatory Responses ◽  
Atherosclerotic Lesion ◽  
Muscle Cells ◽  
Vascular Wall ◽  
Mechanisms Of Action ◽  
Conjugated Linoleic Acids

Conjugated linoleic acids (CLA) are biologically highly active lipid compounds that inhibit the development of atherosclerotic plaques in experimental animals. The underlying mechanisms of action, however, are only poorly understood. Since cell-culture experiments are appropriate to provide a detailed view into the mechanisms of action of a compound, the present review summarises results from in vitro studies dealing with the effects of CLA isomers and CLA mixtures on functional properties of cells of the vascular wall, such as endothelial cells, smooth muscle cells and monocyte-derived macrophages, which are amongst the major cells contributing to atherosclerotic lesion development. Based on these studies, it can be concluded that CLA exert several beneficial actions in cells of the vascular wall through the activation of nuclear PPAR. These actions of CLA, which may, at least partially, explain the inhibition of atherogenesis by dietary CLA, include modulation of vasoactive mediator release from endothelial cells, inhibition of inflammatory and fibrotic processes in activated smooth muscle cells, abrogation of inflammatory responses in activated macrophages, and reduction of cholesterol accumulation in macrophage-derived foam cells.

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