OBJECTIVE: Neointimal formation following percutaneous coronary intervention (PCI), termed restenosis, limits therapeutic revascularization. Since reendothelialization is one of the determinant factors for the development of neointimal formation, we examined the effects of granulocyte colony-stimulating factor (G-CSF) on reendothelialization and neointimal formation after vascular injury in mice. METHODS AND RESULTS: Wire-mediated vascular injury was produced in the femoral artery of C57BL/6 mice. G-CSF pretreatment significantly accelerated reendothelialization and decreased neointimal formation following vascular injury; however, this inhibitory effect of G-CSF was diminished when G-CSF was started following the injury. Flow cytometry analysis revealed that G-CSF treatment increased the number of endothelial progenitor cells (EPCs: CD34+/Flk-1+) in the peripheral circulation. Vascular injury was also produced in 2 types of mice whose bone marrow was replaced with that of enhanced green fluorescent protein- and Tie2/LacZ-transgenic mice. In the reendothelialized artery of these mice, few bone marrow-derived EPCs were detected. Furthermore, G-CSF treatment reduced the serum level of interleukin (IL)-6. CONCLUSION: G-CSF treatment accelerated reendothelialization and decreased neointimal formation following vascular injury, although there was little contribution of bone marrow-derived EPCs to the reendothelialization of the artery. These results suggest that G-CSF pretreatment has a therapeutic potential for prevention of restenosis following PCI.
OBJECTIVE: Neointimal formation following percutaneous coronary intervention (PCI), termed restenosis, limits therapeutic revascularization. Since reendothelialization is one of the determinant factors for the development of neointimal formation, we examined the effects of granulocyte colony-stimulating factor (G-CSF) on reendothelialization and neointimal formation after vascular injury in mice. METHODS AND RESULTS: Wire-mediated vascular injury was produced in the femoral artery of C57BL/6 mice. G-CSF pretreatment significantly accelerated reendothelialization and decreased neointimal formation following vascular injury; however, this inhibitory effect of G-CSF was diminished when G-CSF was started following the injury. Flow cytometry analysis revealed that G-CSF treatment increased the number of endothelial progenitor cells (EPCs: CD34+/Flk-1+) in the peripheral circulation. Vascular injury was also produced in 2 types of mice whose bone marrow was replaced with that of enhanced green fluorescent protein- and Tie2/LacZ-transgenic mice. In the reendothelialized artery of these mice, few bone marrow-derived EPCs were detected. Furthermore, G-CSF treatment reduced the serum level of interleukin (IL)-6. CONCLUSION:G-CSF treatment accelerated reendothelialization and decreased neointimal formation following vascular injury, although there was little contribution of bone marrow-derived EPCs to the reendothelialization of the artery. These results suggest that G-CSF pretreatment has a therapeutic potential for prevention of restenosis following PCI.
Authors: Bernd Hohenstein; Mei-Chuan Kuo; Francesco Addabbo; Kaoru Yasuda; Brian Ratliff; Claudia Schwarzenberger; Kai-Uwe Eckardt; Christian P M Hugo; Michael S Goligorsky Journal: Am J Physiol Renal Physiol Date: 2010-03-17
Authors: Oliver Soehnlein; Sarawuth Wantha; Sakine Simsekyilmaz; Yvonne Döring; Remco T A Megens; Sebastian F Mause; Maik Drechsler; Ralf Smeets; Stefan Weinandy; Fabian Schreiber; Thomas Gries; Stefan Jockenhoevel; Martin Möller; Santosh Vijayan; Marc A M J van Zandvoort; Birgitta Agerberth; Christine T Pham; Richard L Gallo; Tilman M Hackeng; Elisa A Liehn; Alma Zernecke; Doris Klee; Christian Weber Journal: Sci Transl Med Date: 2011-10-05 Impact factor: 17.956
Authors: Ziad A Ali; Ruth Rinze; Gillian Douglas; Yanhua Hu; Qingzhong Xiao; Wei Qi; Eileen McNeill; Christina Bursill; Isaac George; David R Greaves; Qingbo Xu; Keith M Channon Journal: Circulation Date: 2013-09-10 Impact factor: 29.690