scholarly journals Prostacyclin Synthase Gene Transfer Accelerates Reendothelialization and Inhibits Neointimal Formation in Rat Carotid Arteries After Balloon Injury

1999 ◽  
Vol 19 (3) ◽  
pp. 727-733 ◽  
Author(s):  
Yasushi Numaguchi ◽  
Keiji Naruse ◽  
Mitsunori Harada ◽  
Hiroyuki Osanai ◽  
Shinji Mokuno ◽  
...  
Stroke ◽  
1999 ◽  
Vol 30 (2) ◽  
pp. 419-426 ◽  
Author(s):  
T. Todaka ◽  
C. Yokoyama ◽  
H. Yanamoto ◽  
N. Hashimoto ◽  
I. Nagata ◽  
...  

2020 ◽  
Vol 25 (6) ◽  
pp. 570-577
Author(s):  
Nikolaos P. E. Kadoglou ◽  
Marianna Stasinopoulou ◽  
Triantafyllos Giannakopoulos ◽  
Anastasios Papapetrou ◽  
Constantinos Dimitriou ◽  
...  

Background: The purpose of the study was the comparative assessment of ticagrelor and clopidogrel effects on carotid post-balloon injury (PBI) and on post carotid artery stenting (CAS) rate of in-stent restenosis (ISR) and in-stent thrombosis in atherosclerotic rabbits. Methods: Forty-eight New Zealand white rabbits on high-fat diet were randomized into 4 groups: A1: PBI and clopidogrel (30 mg/kg/d), A2: PBI and ticagrelor (21 mg/kg twice daily), B1: PBI, CAS, and clopidogrel (30 mg/kg/d), B2: PBI, CAS, and ticagrelor (21 mg/kg twice daily). All rabbits received orally aspirin (10 mg/kg/d) and interventions were performed in their right carotid arteries (RCAs). Optical coherence tomography (OCT) and carotid angiography were performed at end point, while platelet aggregation and lipid profile were measured. After euthanasia both carotids were obtained for histological examination. Results: In B1 group, 3 rabbits presented thrombotic total occlusion of the stents, while none such episode was observed in B2 group. The neointimal areas in RCAs, calculated by OCT, did not differ between A1 and A2 groups, and between B1 and B2 groups ( P > .05). From the histological findings, the intima/(media + intima) percentage (%) in RCAs of balloon-injured rabbits did not present any difference between groups ( P = .812). Similarly, the immunohistochemically determined accumulation of endothelial cells and macrophages on vascular walls was equivalent between groups ( P > .05). Conclusion: Following carotid balloon injury and stenting, clopidogrel and ticagrelor did not show any differential effects on the extent of neointimal formation and ISR in atherosclerotic rabbits receiving aspirin. Three thrombotic stent occlusions were noted in the clopidogrel treatment group, but this finding was not statistically significant.


2000 ◽  
Vol 86 (6) ◽  
pp. 676-683 ◽  
Author(s):  
Jens W. Fischer ◽  
Michael G. Kinsella ◽  
Monika M. Clowes ◽  
Stephanie Lara ◽  
Alexander W. Clowes ◽  
...  

2014 ◽  
Vol 115 (suppl_1) ◽  
Author(s):  
Chun-Mei Cao ◽  
Ning Xie ◽  
Yuan Yao ◽  
Yan Zhang ◽  
Rui-Ping Xiao

Abnormal proliferation of vascular smooth muscle cells (VSMCs) contributes to various vascular diseases, but the factors that maintain VSMCs in a quiescent state remain poor understood. Phosphatidylinositol 3 kinases (PI3Ks) are important protein kinases that regulate vascular cell proliferation, but the biological and pathological functions of p55γ, a regulatory subunit of PI3K, and its regulation in the cardiovascular system are completely unknown. We aimed to determine the relationship between p55γ and vascular proliferation and neointimal formation. In the present study, we have demonstrated that p55γ expression is markedly downregulated in primary cultured VSMCs in response to mitogenic stimulation and in carotid arteries after balloon injury, and that overexpression p55γ profoundly inhibits mitogenic stimuli and injury induced VSMC proliferation as well as neointimal formation. p55γ overexpression inhibited, whereas knockdown of p55γ promoted PDGF-BB- and serum-induced VSMC proliferation. Importantly, in vivo adenoviral gene transfer of p55γ into carotid arteries attenuated, while knockdown of p55γenhanced balloon injury-induced neointimal formation. Furthermore, p55γ sequentially upregulated p53 and p21, resulting in cell-cycle arrest in S phase; knockdown of either p53 or p21 blocked p55γ-induced VSMC growth arrest. Mechanistically, p55γ interacted with and stabilized p53 protein by blocking MDM2-mediated p53 ubiquitination and degradation, subsequently activating its target gene p21. Concurrently, p55γ upregulated Bcl-xl expression, which counterbalanced p53-mediated apoptosis. These findings mark p55γ as a novel upstream regulator of the p53-p21 signaling pathway which negatively regulates VSMC proliferation, suggesting that malfunction of p55γ may trigger vascular proliferative disorders. * Correspondence to Chun-Mei Cao ([email protected]) or Rui-Ping Xiao ([email protected]).


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