scholarly journals Smooth Muscle and Other Cell Sources for Human Blood Vessel Engineering

2012 ◽  
Vol 195 (1-2) ◽  
pp. 15-25 ◽  
Author(s):  
Sumati Sundaram ◽  
Laura E. Niklason
Keyword(s):  
Smooth Muscle ◽  
Blood Vessel ◽  
Human Blood ◽  
Cell Sources ◽  
Blood Vessel Engineering

Effect of Ridogrel on Vascular Contractions Gaused by Vasoactive Substances Released during Platelet Activation

1990 ◽  
Vol 64 (01) ◽  
pp. 091-096 ◽  
Author(s):  
W J Janssens ◽  
F J S Cools ◽  
L A M Hoskens ◽  
J M Van Nueten
Keyword(s):  
Smooth Muscle ◽  
Blood Vessel ◽  
Platelet Activation ◽  
Prostaglandin F2α ◽  
Thromboxane A2 ◽  
Femoral Arteries ◽  
Vasoactive Substances ◽  
Caudal Artery ◽  
Isolated Rat ◽  
Rat Platelets

SummaryRidogrel (6.3 × 10−6 to 10−4 M) inhibited contractions of isolated rat caudal arteries and rabbit femoral arteries caused by U-46619. The slope of an Arunlakshana-Schild plot (pA2-value: 3.4 × 10−6 M) on the caudal artery was slightly higher than one (1.14). This effect was maximal within}D min of incubation of the blood vessel with the compound and easily reversible. Ridogrel antagonised contractions of isolated rabbit femoral arteries caused by prostaglandin Fzo2α in the same concentration range. Ridogrel also inhibited contractions induced by aggregating rat platelets on isolated rat caudal arteries (itt the presence of ketanserin 4 × 10−7 M) and on isolated rabbit pulmonary and femoral arteries (in the absence of ketanserin). Ridogrel had no effect on Ca2+-induced contractions in depolarised isolated rabbit femoral arteries, and at 10−4 M antagonised serotonin-induced contractions in this blood vessel. Its effect on serotonin-induced contractions was statistically significant but very small on isolated rat caudal arteries. These observations indicate that ridogrel is an antagonist of prostaglandin endoperoxide/thromboxane A2 and prostaglandin F2α raCeptors on vascular smooth muscle.

scholarly journals COARCTATION OF THE AORTA AT THE LEVEL OF THE DIAPHRAGM TREATED SUCCESSFULLY WITH A PRESERVED HUMAN BLOOD VESSEL GRAFT

1951 ◽  
Vol 21 (5) ◽  
pp. 506-512 ◽  
Author(s):  
Edward J. Beattie ◽  
Francis N. Cooke ◽  
John S. Paul ◽  
James A. Orbison
Keyword(s):  
Blood Vessel ◽  
Human Blood ◽  
Coarctation Of The Aorta

scholarly journals An in vivo model allowing continuous observation of human vascular formation in the same animal over time

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Yohei Tsukada ◽  
Fumitaka Muramatsu ◽  
Yumiko Hayashi ◽  
Chiaki Inagaki ◽  
Hang Su ◽  
...  
Keyword(s):  
Blood Vessel ◽  
Blood Vessels ◽  
Human Blood ◽  
Molecular Mechanisms ◽  
Human Tumor ◽  
Continuous Observation ◽  
In Vivo Models ◽  
Cranial Window ◽  
Pathological Conditions

AbstractAngiogenesis contributes to numerous pathological conditions. Understanding the molecular mechanisms of angiogenesis will offer new therapeutic opportunities. Several experimental in vivo models that better represent the pathological conditions have been generated for this purpose in mice, but it is difficult to translate results from mouse to human blood vessels. To understand human vascular biology and translate findings into human research, we need human blood vessel models to replicate human vascular physiology. Here, we show that human tumor tissue transplantation into a cranial window enables engraftment of human blood vessels in mice. An in vivo imaging technique using two-photon microscopy allows continuous observation of human blood vessels until at least 49 days after tumor transplantation. These human blood vessels make connections with mouse blood vessels as shown by the finding that lectin injected into the mouse tail vein reaches the human blood vessels. Finally, this model revealed that formation and/or maintenance of human blood vessels depends on VEGFR2 signaling. This approach represents a useful tool to study molecular mechanisms of human blood vessel formation and to test effects of drugs that target human blood vessels in vivo to show proof of concept in a preclinical model.

Differential Expression of Melanocytic Markers in Myoid, Lipomatous, and Vascular Components of Renal Angiomyolipomas

2007 ◽  
Vol 131 (1) ◽  
pp. 122-125 ◽  
Author(s):  
Andres A. Roma ◽  
Cristina Magi-Galluzzi ◽  
Ming Zhou
Keyword(s):  
Smooth Muscle ◽  
Blood Vessel ◽  
Blood Vessels ◽  
Differential Expression ◽  
Tumor Cells ◽  
Tissue Microarray ◽  
Expression Patterns ◽  
Renal Angiomyolipoma ◽  
Melanocytic Lesions ◽  
Hmb 45

Abstract Context.—Renal angiomyolipoma is a tumor composed of varying amounts of fat, smooth muscle, and blood vessels. Characteristically, tumor cells express melanocytic markers such as HMB-45 and Melan-A. Recently, several other markers have been described as having excellent diagnostic sensitivity in cutaneous melanocytic lesions. Objectives.—To compare the sensitivities of 5 melanocytic markers in renal angiomyolipoma and to study the expression patterns of these markers in the 3 different components of angiomyolipoma. Design.—A tissue microarray of 20 renal angiomyolipomas was constructed. For each case, 3 cores containing fat, blood vessels, and smooth muscle were taken. The tissue microarray was then stained for HMB-45, Melan-A, tyrosinase, NK1-C3, and CD117. Results.—HMB-45 was positive in 95%, Melan-A in 85%, NK1-C3 in 70%, tyrosinase in 50%, and CD117 in 40% of the cases. All (20/20) were positive for HMB-45 and Melan-A combined. These 5 markers had different sensitivities in the 3 components. HMB-45 was positive in 90%, 85%, and 80% of fat, smooth muscle, and blood vessel components, respectively; Melan-A in 70%, 60%, and 40%; NK1-C3 in 55%, 55%, and 45%; tyrosinase in 30%, 40%, and 10%; and CD117 in 20%, 40%, and 10%, respectively, of these 3 components. Conclusions.—HMB-45 and Melan-A combined were positive in 100% of the renal angiomyolipomas. We recommend the use of these 2 markers in the workup of this entity, including those with predominantly 1 component. Other melanocytic markers are of limited use. A tissue block comprising predominantly fat or smooth muscle components should be used when performing melanocytic marker immunostain.

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