scholarly journals A model of atherosclerosis using nicotine with balloon overdilation in a porcine

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Munki Kim ◽  
Han Byul Kim ◽  
Dae Sung Park ◽  
Kyung Hoon Cho ◽  
Dae Young Hyun ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Intimal Hyperplasia ◽  
Smooth Muscle Actin ◽  
Border Zone ◽  
Cardiovascular Research ◽  
Porcine Coronary Artery ◽  
Tunica Media ◽  
Atherosclerotic Lesions ◽  
Coronary Artery Atherosclerosis ◽  
Cluster Of Differentiation

AbstractPigs are important experimental animals for cardiovascular research. Few porcine coronary atherosclerosis models have been developed; however, their induction requires more than six months. We developed a porcine coronary artery atherosclerosis model using nicotine injection with a balloon overdilation. A coronary balloon was placed in the porcine coronary artery and overdilated to induce a mechanical injury. Nicotine was administrated via intramuscular injection every day, and changes in the coronary artery were observed after four weeks. Coronary angiography revealed nicotine injection with a balloon overdilation group showed narrowing of the coronary artery at the injury site. The combination of balloon and nicotine significantly increased the intimal hyperplasia in optical coherence tomography analysis. Proliferated tunica media were noted in the nicotine injection with balloon overdilation groups and lack of collagen was observed in the tunica media at eight weeks. Quantitative analysis showed increased smooth muscle actin alpha (SMA), cluster of differentiation 68 (CD68), and Krüppel-like factor 4 (KLF4) in the nicotine injection with balloon overdilation groups. Immunohistochemistry results showed CD68-positive cells displayed SMA- and KLF4-positive reactivity in the border zone of the intimal hyperplasia. Our results show that nicotine injection with balloon overdilation can induce atherosclerotic lesions within one month, which can serve as an alternative pig animal model for the development of coronary stents.

scholarly journals A Model of Atherosclerosis using Nicotine with Balloon Overdilation in a Porcine

2021 ◽  
Author(s):  
Munki Kim ◽  
Han Byul Kim ◽  
Dae Sung Park ◽  
Kyung Hoon Cho ◽  
Dae Young Hyun ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Intimal Hyperplasia ◽  
Smooth Muscle Actin ◽  
Border Zone ◽  
Cardiovascular Research ◽  
Porcine Coronary Artery ◽  
Positive Reactivity ◽  
Coronary Artery Atherosclerosis ◽  
Human Atherosclerosis ◽  
Cluster Of Differentiation

Abstract Pigs are one of the important experimental animals for cardiovascular research. Few porcine coronary atherosclerosis models have been developed; however, the induction of which requires longer than 6 months. We developed a porcine coronary artery atherosclerosis model using nicotine injection with a balloon overdilation. A coronary balloon was placed in the porcine coronary artery and was over dilated to induce a mechanical injury. Nicotine was administrated via intramuscular injection every day and changes in the coronary artery were observed after 4 weeks. Coronary angiography revealed nicotine injection with a balloon overdilation groups showed narrowing of the coronary artery at the injury site. Combination of balloon and nicotine significantly increased the intimal hyperplasia on optical coherence tomography analysis. Proliferated tunica media was noted in the nicotine injection with balloon overdilation groups. Quantitative analysis showed increased smooth muscle actin alpha (SMA), cluster of differentiation 68 (CD68), and Krüppel-like factor 4 (KLF4) in the nicotine injection with balloon overdilation groups. The immunohistochemistry results showed CD68-positive cells displayed SMA- and KLF4-positive reactivity in the border zone of intimal hyperplasia. Our results show that nicotine injection with balloon overdilation can induce an atherosclerosis lesion within one month, which mimics the human atherosclerosis.

Abstract 028: Endothelial Nogo-B Controls Sphingolipid de novo Biosynthesis to Impact Coronary Artery Atherosclerosis

Hypertension ◽  
2017 ◽  
Vol 70 (suppl_1) ◽  
Author(s):  
Yi Zhang ◽  
Linda Sasset ◽  
Ren Xu ◽  
Matthew Blake Greenblatt ◽  
Annarita Di Lorenzo
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery ◽  
Molecular Mechanisms ◽  
De Novo ◽  
Vascular Inflammation ◽  
High Cholesterol Diet ◽  
Serine Palmitoyltransferase ◽  
Atherosclerotic Lesions ◽  
Coronary Artery Atherosclerosis ◽  
Artery Disease

Coronary artery disease is a leading cause of myocardial infarction (MI) worldwide. Alterations in sphingolipid levels have been linked to atherosclerosis although specific molecular mechanisms are poorly understood. Recently, we discovered that endothelial Nogo-B, a membrane protein of the ER, regulates vascular functions by inhibiting serine palmitoyltransferase (SPT), the rate-limiting enzyme of the de novo sphingolipid biosynthesis. Mice lacking Nogo-B are resistant to hypertension and heart failure. Here, we employed a novel model of coronary atherosclerotic lesions induced by hypercholesterolemia and hypertension, well-known risk factors for atherosclerosis. To this aim, transverse aortic constriction (TAC) surgery was performed in mice lacking endothelial Nogo-B in ApoE -/- background and ApoE -/- mice as control. ApoE -/- mice developed coronary atherosclerotic lesions within 6 weeks following TAC, (without the need of long-term high-cholesterol diet) and 70% of the mice died of MI at 6-week post-TAC. On the contrary, mice lacking Nogo-B specifically in endothelial cells were markedly resistant to the development of coronary atherosclerotic lesions and MI (20%). Mechanistically, in the absence of endothelial Nogo-B, the biosynthesis of sphingolipids, particularly S1P, is upregulated, protecting the endothelium from hypertension and hypercholesterolemia-triggered vascular inflammation and atherogenesis. This study identifies an important and novel role of endothelial Nogo-B-dependent regulation of sphingolipid de novo biosynthesis in the coronary atherosclerosis, a primary cause of myocardial infarction.

scholarly journals 20(S)-Protopanaxadiol Saponins Mainly Contribute to the Anti-Atherogenic Effects of Panax notoginseng in ApoE Deficient Mice

Molecules ◽  
2019 ◽  
Vol 24 (20) ◽  
pp. 3723 ◽  
Author(s):  
Conghui Liu ◽  
Ruibing Feng ◽  
Jian Zou ◽  
Fangbo Xia ◽  
Jian-Bo Wan
Keyword(s):  
Collagen Fiber ◽  
Nuclear Factor Kappa B ◽  
Smooth Muscle Actin ◽  
Vascular Inflammation ◽  
Panax Notoginseng ◽  
Panax Notoginseng Saponins ◽  
Atherosclerotic Lesions ◽  
En Face ◽  
Cluster Of Differentiation ◽  
Deficient Mice

Atherosclerosis mainly contributes to cardiovascular disease, a leading cause of global morbidity and mortality. Panax notoginseng saponins (PNS) are proved to therapeutically attenuate the formation of atherosclerotic lesions. According to different sapogenin, PNS are generally classified into 20(S)-protopanaxadiol saponins (PDS) and 20(S)-protopanaxatriol saponins (PTS). It was reported that PDS and PTS might exert diverse or even antagonistic bioactivities. In this study, the probable effects of PTS and PDS on atherosclerotic development were investigated and compared in ApoE-deficient mice (ApoE−/−). Male mice were gavaged daily by PNS (200 mg/kg/d), PTS (100 mg/kg/d), or PDS (100 mg/kg/d), respectively for eight weeks. The treatments of PNS and PDS, but not PTS, showed decreased atherosclerotic lesions in the entire aorta by 45.6% and 41.3%, respectively, as evaluated by an en-face method. Both PNS and PDS can improve the plaque vulnerability, as evidenced by the increased collagen fiber, increased expression of α- smooth muscle actin (α-SMA), and decreased Cluster of differentiation 14 (CD14). Additionally, PDS also inhibit the nuclear factor kappa B (NF-κB)-mediated vascular inflammation in the aorta. In conclusion, PDS, but not PTS, might mainly contribute to the anti-atherosclerosis of P. notoginseng.

scholarly journals 99mTC-Annexin V imaging for detection of atherosclerotic lesions in porcine coronary artery

2003 ◽  
Vol 41 (6) ◽  
pp. 445 ◽  
Author(s):  
Lynne L. Johnson ◽  
Navneet Narula ◽  
Lorraine Schofield ◽  
Leonard Chaves ◽  
Jaget Narula
Keyword(s):  
Coronary Artery ◽  
Annexin V ◽  
Porcine Coronary Artery ◽  
Atherosclerotic Lesions

scholarly journals Effects of cytochalasin D-eluting stents on intimal hyperplasia in a porcine coronary artery model

2006 ◽  
Vol 69 (2) ◽  
pp. 536-544 ◽  
Author(s):  
K SALU ◽  
J BOSMANS ◽  
Y HUANG ◽  
M HENDRIKS ◽  
M VERHOEVEN ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Intimal Hyperplasia ◽  
Cytochalasin D ◽  
Porcine Coronary Artery

Characterization of Thromboxane A2/Prostaglandin H2 Receptors in Porcine Coronary Artery -The Inhibitory Effect of a Novel Dibenzoxepin Derivative, KW-3635

1992 ◽  
Vol 67 (05) ◽  
pp. 582-584 ◽  
Author(s):  
Ichiro Miki ◽  
Akio Ishii
Keyword(s):  
Coronary Artery ◽  
Binding Sites ◽  
Thromboxane A2 ◽  
Inhibitory Effect ◽  
Scatchard Analysis ◽  
Single Class ◽  
Porcine Coronary Artery ◽  
Equilibrium Binding ◽  
H2 Receptors

SummaryWe characterized the thromboxane A2/prostaglandin H2 receptors in porcine coronary artery. The binding of [3H]SQ 29,548, a thromboxane A2 antagonist, to coronary arterial membranes was saturable and displaceable. Scatchard analysis of equilibrium binding showed a single class of high affinity binding sites with a dissociation constant of 18.5 ±1.0 nM and the maximum binding of 80.7 ± 5.2 fmol/mg protein. [3H]SQ 29,548 binding was concentration-dependently inhibited by thromboxane A2 antagonists such as SQ 29,548, BM13505 and BM13177 or the thromboxane A2 agonists such as U46619 and U44069. KW-3635, a novel dibenzoxepin derivative, concentration-dependently inhibited the [3H]SQ 29,548 binding to thromboxane A2/prosta-glandin H2 receptors in coronary artery with an inhibition constant of 6.0 ± 0.69 nM (mean ± S.E.M.).

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