Rapid Engineered Small Diameter Vascular Grafts from Smooth Muscle Cells

2011 ◽  
Vol 2 (3) ◽  
pp. 149-159 ◽  
Author(s):  
Wei He ◽  
Alejandro Nieponice ◽  
Yi Hong ◽  
William R. Wagner ◽  
David A. Vorp
2019 ◽  
Vol 7 (3) ◽  
pp. 914-925 ◽  
Author(s):  
Jing Liu ◽  
Yibo Qin ◽  
Yifan Wu ◽  
Zhiting Sun ◽  
Binhan Li ◽  
...  

The surrounding tissue contributes to smooth muscle cells’ regeneration and vascularization in the vascular regeneration process.


2011 ◽  
pp. 419-437 ◽  
Author(s):  
M. PAŘÍZEK ◽  
K. NOVOTNÁ ◽  
L. BAČÁKOVÁ

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.


2019 ◽  
Vol 7 (8) ◽  
pp. 1258-1269 ◽  
Author(s):  
Elena Diana Giol ◽  
Sandra Van Vlierberghe ◽  
Ronald E. Unger ◽  
Ken Kersemans ◽  
Filip de Vos ◽  
...  

The potential in vascular grafts of gelatin-modified poly(ethylene terephthalate) (PET) was shown herein via their coating stability, ability to promote endothelial cells (ECs) and smooth muscle cells (SMCs) and positive cyto- and endotoxicity assessments.


2005 ◽  
Vol 289 (6) ◽  
pp. H2461-H2467 ◽  
Author(s):  
Won Sun Park ◽  
Jin Han ◽  
Nari Kim ◽  
Jae-Hong Ko ◽  
Sung Joon Kim ◽  
...  

We examined the effects of acute hypoxia on Ba2+-sensitive inward rectifier K+ (KIR) current in rabbit coronary arterial smooth muscle cells. The amplitudes of KIR current was definitely higher in the cells from small-diameter (<100 μm) coronary arterial smooth muscle cells (SCASMC, −12.8 ± 1.3 pA/pF at −140 mV) than those in large-diameter coronary arterial smooth muscle cells (>200 μm, LCASMC, −1.5 ± 0.1 pA pF−1). Western blot analysis confirmed that Kir2.1 protein was expressed in SCASMC but not LCASMC. Hypoxia activated much more KIR currents in symmetrical 140 K+. This effect was blocked by the adenylyl cyclase inhibitor SQ-22536 (10 μM) and mimicked by forskolin (10 μM) and dibutyryl-cAMP (500 μM). The production of cAMP in SCASMC increased 5.7-fold after 6 min of hypoxia. Hypoxia-induced increase in KIR currents was abolished by the PKA inhibitors, Rp-8-(4-chlorophenylthio)-cAMPs (10 μM) and KT-5720 (1 μM). The inhibition of G protein with GDPβS (1 mM) partially reduced (∼50%) the hypoxia-induced increase in KIR currents. In Langendorff-perfused rabbit hearts, hypoxia increased coronary blood flow, an effect that was inhibited by Ba2+. In summary, hypoxia augments the KIR currents in SCASMC via cAMP- and PKA-dependent signaling cascades, which might, at least partly, explain the hypoxia-induced coronary vasodilation.


2000 ◽  
Vol 31 (5) ◽  
pp. 953-959 ◽  
Author(s):  
David J. Minion ◽  
Rudolph M. Snajdar ◽  
Maarten-Paul van de Kerkhove ◽  
John A. van Aalst ◽  
Paul L. Fox ◽  
...  

1994 ◽  
Vol 5 (10) ◽  
pp. 1211-1216 ◽  
Author(s):  
Randolph L. Geary ◽  
Alexander W. Clowes ◽  
Stella Lau ◽  
Selina Vergel ◽  
David C. Dale ◽  
...  

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