Endothelial Cell Recoverage and Intimal Hyperplasia after Endothelium Removal with or without Smooth Muscle Cell Necrosis in the Rabbit Carotid Artery

1996 ◽  
Vol 33 (2) ◽  
pp. 146-155 ◽  
Author(s):  
Frits N.G. Doornekamp ◽  
Cornelius Borst ◽  
Mark J. Post
Keyword(s):  
Smooth Muscle ◽  
Endothelial Cell ◽  
Carotid Artery ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Intimal Hyperplasia ◽  
Cell Necrosis ◽  
Rabbit Carotid Artery

scholarly journals Connexin37 reduces smooth muscle cell proliferation and intimal hyperplasia in a mouse model of carotid artery ligation

2017 ◽  
Vol 113 (7) ◽  
pp. 805-816 ◽  
Author(s):  
Florent Allagnat ◽  
Céline Dubuis ◽  
Martine Lambelet ◽  
Loïc Le Gal ◽  
Florian Alonso ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Smooth Muscle ◽  
Carotid Artery ◽  
Mouse Model ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Intimal Hyperplasia ◽  
Smooth Muscle Cell Proliferation ◽  
Artery Ligation ◽  
Carotid Artery Ligation

scholarly journals Heparin/heparan sulfate chelation inhibits control of vascular repair by tissue-engineered endothelial cells

1997 ◽  
Vol 273 (6) ◽  
pp. H2586-H2595 ◽  
Author(s):  
Richard O. Han ◽  
David S. Ettenson ◽  
Edward W. Y. Koo ◽  
Elazer R. Edelman
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cells ◽  
Smooth Muscle ◽  
Endothelial Cell ◽  
Smooth Muscle Cell ◽  
Conditioned Medium ◽  
Muscle Cell ◽  
Intimal Hyperplasia ◽  
Vascular Repair ◽  
Dose Dependent Fashion

The relative importance of heparin-like compounds in mediating vascular repair is unclear. We investigated how protamine, a chelator of heparin, affected endothelial cell inhibition of vascular smooth muscle cell growth and intimal hyperplasia. The 52% ( P < 0.001) reduction in smooth muscle cell proliferation produced by postconfluent endothelial cell-conditioned medium was entirely reversed by pretreatment of medium with heparinase and heparitinase and was inhibited in a dose-dependent fashion by the coadministration of protamine. Pretreatment of conditioned medium with heparinase and heparitinase largely prevented protamine’s mitogenic activity, suggesting that protamine affects growth by interacting with heparin-like compounds. Perivascular implantation of polymer-engrafted endothelial cells reduced neointima formation in denuded rat carotid arteries by 92% ( P < 0.001) and cell proliferation by 81% ( P < 0.001). Coadministration of protamine abolished the inhibitory potential of the cell implants, resulting in a nearly twofold exacerbation of intimal hyperplasia compared with controls ( P < 0.001). Thus heparin-like molecules are essential to the biochemical regulation of vascular repair provided by endothelial cells, and the continued routine clinical use of heparin chelators, like protamine, may be questionable.

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