scholarly journals The Role of Smooth Muscle Cells in Vessel Wall Pathophysiology and Reconstruction Using Bioactive Synthetic Polymers

2011 ◽  
pp. 419-437 ◽  
Author(s):  
M. PAŘÍZEK ◽  
K. NOVOTNÁ ◽  
L. BAČÁKOVÁ
Keyword(s):  
Cell Culture ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Tissue ◽  
Culture Media ◽  
Vascular Grafts ◽  
Chemical Properties ◽  
Vascular Diseases ◽  
Cyclic Strain ◽  
Muscle Cells

This review summarizes recent trends in the construction of bioartificial vascular replacements, i.e. hybrid grafts containing synthetic polymeric scaffolds and cells. In these advanced replacements, vascular smooth muscle cells (VSMC) should be considered as a physiological component, although it is known that activation of the migration and proliferation of VSMC plays an important role in the onset and development of vascular diseases, and also in restenosis of currently used vascular grafts. Therefore, in novel bioartificial vascular grafts, VSMCs should be kept in quiescent mature contractile phenotype. This can be achieved by (1) appropriate physical and chemical properties of the material, such as its chemical composition, polarity, wettability, surface roughness and topography, electrical charge and conductivity, functionalization with biomolecules and mechanical properties, (2) appropriate cell culture conditions, such as composition of cell culture media and dynamic load, namely cyclic strain, and (3) the presence of a confluent, mature, semipermeable, non-thrombogenic and non-immunogenic endothelial cell (EC) barrier, covering the luminal surface of the graft and separating the VSMCs from the blood. Both VSMCs and ECs can also be differentiated from stem and progenitor cells of various sources. In the case of degradable scaffolds, the material will gradually be removed by the cells and will be replaced by their own new extracellular matrix. Thus, the material component in advanced blood vessel substitutes acts as a temporary scaffold that promotes regeneration of the damaged vascular tissue.

PI-3K/AKT signal pathway modulates vascular smooth muscle cells migration under cyclic mechanical strain

VASA ◽  
2011 ◽  
Vol 40 (2) ◽  
pp. 109-116 ◽  
Author(s):  
Zhang ◽  
Zhou ◽  
Li ◽  
Xu
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Mechanical Strain ◽  
Vascular Diseases ◽  
Cyclic Strain ◽  
Muscle Cells ◽  
Sti 571 ◽  
Actin Rearrangement

Background: The migration of vascular smooth muscle cells (VSMCs), exposed to altered mechanical strain, contributes to vascular remodeling which is the key event underlying the pathogenesis of vascular diseases such as atherosclerosis and restenosis. Signal transduction pathways in VSMCs activated by mechanical strain that influence cell migration remain unclear. Herein, we provide evidence that higher mechanical strain enhances VSMCs migration, which is mediated, at least in part, through Akt/protein kinase B (PKB) included pathway. Material and methods: VSMCs were exposed to mechanical strain at 15 % elongation and 5 % elongation, 60 cycles/min using FX-4000T system from at least three independent experiments. VSMCs were incubated with 100nmol/L wortmannin, 10 uM Akti, 10 uM PD98059 and 10 uM SB202190 prior to strain for inhibitor studies, respectively. VSMCs migration,the activation of Akt/PKB, the inhibition of STI-571 and immunofluorescence for actin fibers were detected, respectively. Activation of the Akt pathway and inhibition of STI-571 were assessed with the Western blot technique. Results: (1) Our study demonstrated that VSMCs migration under 15 % strain was facilitated compared with 5 % strain (15 % strain vs. 5 % strain, P < 0.01); and the activation of P-Akt was enhanced compared to the control (15 % strain and 5 % strain vs. static control, P < 0.01, respectively); whereas wortmannin could markedly inhibit serine/threonine kinase Akt/PKB phosphorylation, reduced VSMCs migration following higher mechanical strain stimulation (15 % strain + wortmannin vs. 15 % strain, P < 0.01). Immunofluorescence revealed actin rearrangement, which could also be inhibited by wortmannin in VSMCs induced by cyclic strain. (2) Akti significantly inhibited VSMCs migration (15 % strain + Akti and 5 % strain + Akti vs. static control, P < 0.05,respectively), neither PD98059 nor SB202190 inhibited VSMCs migration (5 % strain + PD98059 or +SB202190 vs. static control, P < 0.01; 15 % strain + PD98059 or +SB202190 vs. static control P < 0.01,respectively). (3) Higher mechanical strain inhibits STI-571 activity in VSMCs (5 % strain vs. static control, P < 0.05; 15 % strain vs. static control, P < 0.01). Conclusions: Our data shows that higher mechanical strain activated-Akt/PKB is required for VSMC migration and probably functions through its effects on actin rearrangement.

Spatial dynamics of intracellular calcium in agonist-stimulated vascular smooth muscle cells

1990 ◽  
Vol 259 (4) ◽  
pp. C675-C686 ◽  
Author(s):  
C. B. Neylon ◽  
J. Hoyland ◽  
W. T. Mason ◽  
R. F. Irvine
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Vascular Tissue ◽  
Spatial Dynamics ◽  
Muscle Cells ◽  
Smooth Muscle Contraction ◽  
The Novel ◽  
Internal Mammary

Vasoconstrictor agonists stimulate smooth muscle contraction by inducing a rise in intracellular free Ca2+. Digital-imaging microscopy of fura-2 fluorescence from single vascular smooth muscle cells cultured from the human internal mammary artery has allowed us to record the subcellular alterations in Ca2+ that occur immediately after stimulation by receptor agonists. The thrombin-induced rise in cytoplasmic free Ca2+ begins in a discrete region typically located close to the end of the cell. Subsequently, this region of elevated Ca2+ expands until Ca2+ is elevated throughout the cell cytoplasm. The rate of spreading in the region of elevated Ca2+ in a linear direction averaged 10.1 microns/s, enabling it to traverse the length of most cells within approximately 5 s, and involved rises in Ca2+ of between 200 and 500 nM. In some cells, the Ca2+ rise began at both ends and collided midway. Similar dynamic changes in the spatial distribution of Ca2+ were recorded in cells stimulated by acetylcholine. The novel observation that vasoconstrictor agonists induce an elevation of Ca2+ in a localized region which subsequently expands throughout the cytoplasm of single smooth muscle cells may provide new insight into the nature of Ca2+ signaling in vascular tissue.

Secretion of Brain Natriuretic Peptide in Cultured Human Coronary Vascular Smooth Muscle Cells

2000 ◽  
Vol 6 (S2) ◽  
pp. 598-599
Author(s):  
J. Lin ◽  
C. Wei
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Brain Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Vascular Smooth Muscle Cells ◽  
Vascular Tone ◽  
Culture Media ◽  
Muscle Cells ◽  
Ventricular Myocardium

Brain natriuretic peptide (BNP) is a peptide of cardiac origin which regulates plasma volume as well as vascular tone and growth. Recently, we have reported that brain natriuretic peptide is a potent inhibitor of endothelin-1-mediated proliferation in human coronary vascular smooth muscle cells (HCoVSMC). While brain natriuretic peptide has been reported to be produced and released from atrial and ventricular myocardium, we hypothesize that brain natriuretic peptide may be present and secreted from human coronary vascular smooth muscle cells.Therefore, the present study was designed to investigate the secretion of brain natriuretic peptide in cultured human coronary vascular smooth muscle cells (HCoVSMC: Clonetics, San Diego, CA). The concentration of brain natriuretic peptide, and its second messenger cGMP, in culture media (48 hours) was determined by radioimmunoassay (Phoenix, Mountain View, CA). The presence of brain natriuretic peptide was determined by immunohistochemical staining using a human brain natriuretic peptide polyclonal antibody.

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