A zwitterionic hydrogel coated titanium surface with high-efficiency endothelial cell selectivity for rapid re-endothelialization

2020 ◽  
Vol 8 (19) ◽  
pp. 5441-5451
Author(s):  
Chiyu Wen ◽  
Jiamin Zhang ◽  
Yongjian Li ◽  
Weiwei Zheng ◽  
Min Liu ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Endothelial Cell ◽  
Smooth Muscle Cells ◽  
Blood Cells ◽  
Titanium Surface ◽  
High Efficiency ◽  
Muscle Cells ◽  
Selective Coating ◽  
Cell Selectivity

A bifunctional antifouling and endothelial cell selective coating, based on a zwitterionic hydrogel and the REDV peptide, can promote re-endothelialization and achieve multi-resistance of proteins, bacteria, blood cells and smooth muscle cells.

The Role of Endothelial Cell Injury and Platelet Response in Atherogenesis

1977 ◽  
Author(s):  
L. A. Harker ◽  
R. Ross ◽  
J. Glomset
Keyword(s):  
Smooth Muscle ◽  
Endothelial Cell ◽  
Connective Tissue ◽  
Smooth Muscle Cells ◽  
Lipid Accumulation ◽  
Blood Platelets ◽  
Muscle Cells ◽  
Endothelial Injury ◽  
Intimal Proliferation ◽  
Flowing Blood

Endothelium forms a resistant barrier between flowing blood and vessel wall structures. Endothelial thromboresistance is maintained in part by the synthesis of prostacyclin, a potent prostaglandin inhibitor of platelet function. Loss of endothelial cells, mediated by physical, chemical, infectious or immune mechanisms, exposes the sub endothelium to flowing blood. Platelets react to the subendothelial connective tissue structures, undergoing adhesion and release of intracellular constituents, including a factor that is mitogenic to smooth muscle cells. This growth factor is a heat stable, basic protein (IP 7.4–9.4) of 20,000 Daltons and appears to be responsible for the intimal proliferation of smooth muscle cells that follows endothelial cell desquamation. After a single injury event the intimal lesion regresses over several months. Repeated or continuous endothelial cell loss results in progressive intimal proliferation of smooth muscle cells, their secretion of connective tissue matrix components (collagen, elastin and proteoglycans) and accumulation of lipid when animals are on a hypercholesterolemic diet to form early atherosclerotic intimal lesions. Discontinuance of endothelial injury and restoration of the endothelium appear to be followed by lesion regression except when lipid accumulation is extensive. Possible approaches to atherosclerosis prevention include: 1) protection of the endothelium by interruption or avoidance of endothelial injury factors, and perhaps by pharmacologic protection; 2) inhibition of platelet reactivity; 3) modification of SMC proliferation, secretion or lipid accumulation.

Electrical activation of endothelium evokes vasodilation and hyperpolarization along hamster feed arteries

2001 ◽  
Vol 280 (1) ◽  
pp. H160-H167 ◽  
Author(s):  
Geoffrey G. Emerson ◽  
Steven S. Segal
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Endothelial Cell ◽  
Smooth Muscle Cells ◽  
Cell Damage ◽  
Muscle Cells ◽  
Sympathetic Nerves ◽  
Retractor Muscle ◽  
Receptor Interactions ◽  
Feed Arteries

Endothelial cells are considered electrically unexcitable. However, endothelium-dependent vasodilators (e.g., acetylcholine) often evoke hyperpolarization. We hypothesized that electrical stimulation of endothelial cells could evoke hyperpolarization and vasodilation. Feed artery segments (resting diameter: 63 ± 1 μm; length 3–4 mm) of the hamster retractor muscle were isolated and pressurized to 75 mmHg, and focal stimulation was performed via microelectrodes positioned across one end of the vessel. Stimulation at 16 Hz (30–50 V, 1-ms pulses, 5 s) evoked constriction (−20 ± 2 μm) that spread along the entire vessel via perivascular sympathetic nerves, as shown by inhibition with tetrodotoxin, ω-conotoxin, or phentolamine. In contrast, stimulation with direct current (30 V, 5 s) evoked vasodilation (16 ± 2 μm) and hyperpolarization (11 ± 1 mV) of endothelial and smooth muscle cells that conducted along the entire vessel. Conducted responses were insensitive to preceding treatments, atropine, or N ω-nitro-l-arginine, yet were abolished by endothelial cell damage (with air). Injection of negative current (≤1.6 nA) into a single endothelial cell reproduced vasodilator responses along the entire vessel. We conclude that, independent of ligand-receptor interactions, endothelial cell hyperpolarization evokes vasodilation that is readily conducted along the vessel wall. Moreover, electrical events originating within a single endothelial cell can drive the relaxation of smooth muscle cells throughout the entire vessel.

Various cells release a stable small molecule that inhibits endothelium-dependent relaxation

1995 ◽  
Vol 269 (4) ◽  
pp. H1303-H1311
Author(s):  
J. J. Liu ◽  
B. Xie ◽  
P. J. Thurlow ◽  
J. S. Wiley ◽  
J. R. Chen
Keyword(s):  
Smooth Muscle ◽  
Endothelial Cell ◽  
Tumor Cell ◽  
Smooth Muscle Cells ◽  
Cell Line ◽  
Tumor Cell Line ◽  
Muscle Cells ◽  
Cardiac Cells ◽  
Endothelial Cell Line ◽  
Endothelium Dependent Relaxation

Previous studies have shown that neutrophils release a stable factor that inhibits endothelium-dependent relaxation. In the present studies, the effects of supernatants derived from various cells on endothelium-dependent relaxation were studied. Cells were obtained from seven sources: human hematopoietic cells including mononuclear leukocytes (MONO), polymorphonuclear leukocytes (PMNs), and chronic lymphocytic leukemia (CLL) cells; cells of the cardiovascular system including human endothelial cell line ECV304, human smooth muscle cells, and rat myocardial cells; and the tumor cell line HPB. These isolated or cultured cells were incubated for 1 h in Krebs solution to release the factor. The results showed that the supernatants from 10(5) cells/ml of all cells except the tumor cell line HPB produced a potent inhibitory effect on endothelium-dependent relaxation of rat aortic rings in response to acetylcholine and Ca2+ ionophores A23187 and ionomycin but not on endothelium-independent relaxation to nitroprusside and glyceryl trinitrate. When the concentration increased to 10(6) cell/ml, the supernatants from the tumor cell line HPB also slightly but significantly inhibited endothelium-dependent relaxation. The potency order was PMNs = MONO = CLL cells > cardiac cells > smooth muscle cells > the endothelial cell line ECV304 > the tumor cell line HPB. It seems that the hematopoietic cells and the cardiac cells are more active in release of the factor. The effect of this factor was rapid in onset and hard to wash out. A cyclooxygenase inhibitor or a thromboxane A2-prostaglandin H2 receptor antagonist partially but significantly reduced the effect of the factor.(ABSTRACT TRUNCATED AT 250 WORDS)

Communication Among Endothelial and Smooth Muscle Cells Coordinates Blood Flow Control During Exercise

Physiology ◽  
1992 ◽  
Vol 7 (4) ◽  
pp. 152-156 ◽  
Author(s):  
SS Segal
Keyword(s):  
Blood Flow ◽  
Smooth Muscle ◽  
Endothelial Cell ◽  
Locus Of Control ◽  
Smooth Muscle Cells ◽  
Flow Control ◽  
Muscle Cells ◽  
Peripheral Blood Flow ◽  
Metabolic Demand ◽  
Blood Flow Control

Peripheral blood flow control during exercise is coordinated among several vascular locations. The locus of control shifts upstream from distal arterioles into feeding arteries as metabolic demand increases. This shift occurs by cell-to-cell conduction and by flow-dependent endothelial cell-mediated relaxation of smooth muscle cells.

scholarly journals Smooth muscle cells improve endothelial cell retention on polytetrafluoroethylene grafts in vivo

2003 ◽  
Vol 38 (3) ◽  
pp. 557-563 ◽  
Author(s):  
Hong Yu ◽  
Wangde Dai ◽  
Zhe Yang ◽  
Paul Kirkman ◽  
Fred A. Weaver ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Endothelial Cell ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Cell Retention
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