scholarly journals Tissue-Engineered Vascular Graft with Co-Culture of Smooth Muscle Cells and Human Endothelial Vein Cells on an Electrospun Poly(lactic-co-glycolic acid) Microtube Array Membrane

Membranes ◽  
2021 ◽  
Vol 11 (10) ◽  
pp. 732
Author(s):  
Chee Ho Chew ◽  
Bo-Long Sheu ◽  
Amanda Chen ◽  
Wan-Ting Huang ◽  
Tsai-Mu Cheng ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Graft ◽  
Glycolic Acid ◽  
Bypass Graft ◽  
Graft Infection ◽  
Small Diameter ◽  
Muscle Cells ◽  
Synthetic Grafts ◽  
Microtube Array

Coronary artery disease is one of the major diseases that plagues today’s modern society. Conventional treatments utilize synthetic vascular grafts such as Dacron® and Teflon® in bypass graft surgery. Despite the wide adaptation, these synthetic grafts are often plagued with weaknesses such as low hemocompatibility, thrombosis, intimal hyperplasia, and risks of graft infection. More importantly, these synthetic grafts are not available at diameters of less than 6 mm. In view of these challenges, we strived to develop and adapt the electrospun Poly Lactic-co-Glycolic Acid (PLGA) Microtube Array Membrane (MTAM) vascular graft for applications smaller than 6 mm in diameter. Homogenously porous PLGA MTAMs were successfully electrospun at 5.5–8.5 kV under ambient conditions. Mechanically, the PLGA MTAMs registered a maximum tensile strength of 5.57 ± 0.85 MPa and Young’s modulus value of 1.134 ± 0.01 MPa; while MTT assay revealed that seven-day Smooth Muscle Cells (SMCs) and Human Umbilical Vein Endothelial Cells (HUVECs) registered a 6 times and 2.4 times higher cell viability when cultured in a co-culture setting in medium containing α-1 haptaglobulin. When rolled into a vascular graft, the PLGA MTAMs registered an overall degradation of 82% after 60 days of cell co-culture. After eight weeks of culturing, immunohistochemistry staining revealed the formation of a monolayer of HUVECs with tight junctions on the surface of the PLGA MTAM, and as for the SMCs housed within the lumens of the PLGA MTAMs, a monolayer with high degree of orientation was observed. The PLGA MTAM registered a burst pressure of 1092.2 ± 175.3 mmHg, which was sufficient for applications such as small diameter blood vessels. Potentially, the PLGA MTAM could be used as a suitable substrate for vascular engineering

Coculture of endothelial and smooth muscle cells on a collagen membrane in the development of a small-diameter vascular graft

Biomaterials ◽  
2007 ◽  
Vol 28 (7) ◽  
pp. 1385-1392 ◽  
Author(s):  
Hsi-Chin Wu ◽  
Tzu-Wei Wang ◽  
Pei-Leun Kang ◽  
Yang-Hwei Tsuang ◽  
Jui-Sheng Sun ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Graft ◽  
Small Diameter ◽  
Muscle Cells ◽  
Collagen Membrane

Coronary artery spasm

2021 ◽  
pp. 16-18
Author(s):  
Hiroaki Shimokawa ◽  
Jun Takahashi
Keyword(s):  
Smooth Muscle ◽  
Coronary Artery ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Coronary Artery Spasm ◽  
Bypass Graft ◽  
Rho Kinase ◽  
Muscle Cells ◽  
Inflammatory Changes

Coronary artery spasm is a condition in which an epicardial coronary artery or coronary bypass graft exhibits abnormal transient constriction with the possible or subsequent development of myocardial ischaemia. Porcine models have demonstrated the important role of atherosclerotic/inflammatory changes of the coronary artery and established that hypercontraction of vascular smooth muscle cells plays a central role in the genesis of spasm and is, in part, dependent on activation of Rho-kinase, a molecular switch for vascular smooth muscle cell contraction. Fasudil, which is used for the treatment of cerebral vasospasm in Japan, is metabolized to hydroxyfasudil and functions as a selective Rho-kinase inhibitor. Recent studies demonstrated that inflammatory changes in the adventitia of the coronary artery play an important role for Rho-kinase activation of vascular smooth muscle cells. Prevention and treatment of coronary spasm is important in preventing acute coronary syndromes and sudden cardiac death.

Raw Materials and Processing Issues in the Development of Vascugel, a Cell Therapy for Vascular Disease

2000 ◽  
Author(s):  
James S. Sigler
Keyword(s):  
Smooth Muscle ◽  
Coronary Artery ◽  
Coronary Artery Bypass Graft ◽  
Smooth Muscle Cells ◽  
Coronary Artery Bypass ◽  
Artery Bypass ◽  
Bypass Graft ◽  
Muscle Cells ◽  
Arterial Disease ◽  
Artery Bypass Graft

Abstract Vascular arterial disease is the most common cause of death in the United States. Cardiovascular surgery such as coronary artery bypass graft surgery and therapies such as angioplasty and stenting are the current standard of care. However, a large number of these procedures fail due to a form of arterial disease known as restenosis. Restenosis is the re-narrowing of the treated blood vessel following vessel wall injury resulting in decreased blood flow. This re-narrowing occurs in large part because the smooth muscle cells in the wall of the vessel proliferate after the vessel is damaged. This proliferation occurs because the endothelial cells lining the inside of the vessel, which normally control proliferation, are damaged and can no longer provide the physiological function of keeping the underlying smooth muscle cells in a steady state. Of the approximately 1.5 million procedures per year, over 500,000 are coronary artery bypass graft surgeries (1996 and 1998 data from Medical Data International). Coronary artery bypass grafts experience restenosis at a 12 to 20% rate after one year.

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
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Grafts ◽  
Small Diameter ◽  
Muscle Cells ◽  
Small Diameter Vascular Grafts

Activation of inward rectifier K+ channels by hypoxia in rabbit coronary arterial smooth muscle cells

2005 ◽  
Vol 289 (6) ◽  
pp. H2461-H2467 ◽  
Author(s):  
Won Sun Park ◽  
Jin Han ◽  
Nari Kim ◽  
Jae-Hong Ko ◽  
Sung Joon Kim ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Acute Hypoxia ◽  
Large Diameter ◽  
Small Diameter ◽  
Muscle Cells ◽  
Inward Rectifier ◽  
Arterial Smooth Muscle ◽  
Arterial Smooth Muscle Cells ◽  
Adenylyl Cyclase Inhibitor

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.

scholarly journals Lipoprotein(a) in Cardiovascular Diseases

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Michele Malaguarnera ◽  
Marco Vacante ◽  
Cristina Russo ◽  
Giulia Malaguarnera ◽  
Tijana Antic ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Risk Factor ◽  
Cardiovascular Diseases ◽  
Smooth Muscle Cells ◽  
Bypass Graft ◽  
Muscle Cells ◽  
Tissue Type ◽  
Apo B ◽  
Lipoprotein A

Lipoprotein(a) (Lp(a)) is an LDL-like molecule consisting of an apolipoprotein B-100 (apo(B-100)) particle attached by a disulphide bridge to apo(a). Many observations have pointed out that Lp(a) levels may be a risk factor for cardiovascular diseases. Lp(a) inhibits the activation of transforming growth factor (TGF) and contributes to the growth of arterial atherosclerotic lesions by promoting the proliferation of vascular smooth muscle cells and the migration of smooth muscle cells to endothelial cells. Moreover Lp(a) inhibits plasminogen binding to the surfaces of endothelial cells and decreases the activity of fibrin-dependent tissue-type plasminogen activator. Lp(a) may act as a proinflammatory mediator that augments the lesion formation in atherosclerotic plaques. Elevated serum Lp(a) is an independent predictor of coronary artery disease and myocardial infarction. Furthermore, Lp(a) levels should be a marker of restenosis after percutaneous transluminal coronary angioplasty, saphenous vein bypass graft atherosclerosis, and accelerated coronary atherosclerosis of cardiac transplantation. Finally, the possibility that Lp(a) may be a risk factor for ischemic stroke has been assessed in several studies. Recent findings suggest that Lp(a)-lowering therapy might be beneficial in patients with high Lp(a) levels. A future therapeutic approach could include apheresis in high-risk patients in order to reduce major coronary events.

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