OBJECTIVES: The aim of this study was to investigate whether the mobilization and recruitment of bone marrow stem cells (BMSCs) contribute to cardioprotection in the late phase after ischemic pre-conditioning (IPC). BACKGROUND: IPC is an innate phenomenon in which brief exposure to sublethal ischemia provides tissue protection from subsequent ischemia/reperfusion (I/R) injury. A delayed cardioprotection also occurs after IPC, but the precise mechanism is unclear. METHODS: IPC was created with 4 cycles of 5-min occlusion and reperfusion of the abdominal aorta in mice. Heart I/R injury was induced by occluding the left anterior descending artery for 30 min immediately (early phase) or 24 h (late phase) after IPC. RESULTS: Serum vascular endothelial growth factor and stromal cell-derived factor-1alpha levels were increased significantly 1 and 3 h after IPC, but CD34+ and CD34+/flk-1+ stem cells in the peripheral blood were increased significantly 12 and 24 h after IPC (p < 0.05). Compared with the control treatment, both the early and late phases of IPC protected the heart against I/R injury. However, the recruitment of BMSCs was significantly greater in the heart when I/R injury was induced in late phase than in the early phase of IPC (p < 0.01). Interestingly, the blockade of the recruitment of BMSCs significantly attenuated the cardioprotective effect of IPC in the late phase (p < 0.01) but did not change in the early phase. CONCLUSIONS: Cardioprotection was observed in the early and late phases of IPC; however, the enhanced mobilization and recruitment of BMSCs played an important role in the late phase of IPC.
OBJECTIVES: The aim of this study was to investigate whether the mobilization and recruitment of bone marrow stem cells (BMSCs) contribute to cardioprotection in the late phase after ischemic pre-conditioning (IPC). BACKGROUND: IPC is an innate phenomenon in which brief exposure to sublethal ischemia provides tissue protection from subsequent ischemia/reperfusion (I/R) injury. A delayed cardioprotection also occurs after IPC, but the precise mechanism is unclear. METHODS: IPC was created with 4 cycles of 5-min occlusion and reperfusion of the abdominal aorta in mice. Heart I/R injury was induced by occluding the left anterior descending artery for 30 min immediately (early phase) or 24 h (late phase) after IPC. RESULTS: Serum vascular endothelial growth factor and stromal cell-derived factor-1alpha levels were increased significantly 1 and 3 h after IPC, but CD34+ and CD34+/flk-1+ stem cells in the peripheral blood were increased significantly 12 and 24 h after IPC (p < 0.05). Compared with the control treatment, both the early and late phases of IPC protected the heart against I/R injury. However, the recruitment of BMSCs was significantly greater in the heart when I/R injury was induced in late phase than in the early phase of IPC (p < 0.01). Interestingly, the blockade of the recruitment of BMSCs significantly attenuated the cardioprotective effect of IPC in the late phase (p < 0.01) but did not change in the early phase. CONCLUSIONS: Cardioprotection was observed in the early and late phases of IPC; however, the enhanced mobilization and recruitment of BMSCs played an important role in the late phase of IPC.
Authors: Paulino A Alvarez; Ernst R Schwarz; Rajesh Ramineni; Phil Myatt; Clay Barbin; Carlos Boissonnet; Anita Phan; Aldo Maggioni; Alejandro Barbagelata Journal: Clin Res Cardiol Date: 2012-09-28 Impact factor: 5.460
Authors: Patrick G Lyons; Frank J Zadravecz; Dana P Edelson; Babak Mokhlesi; Matthew M Churpek Journal: J Hosp Med Date: 2015-06-13 Impact factor: 2.960
Authors: Meghan M Nickerson; Caitlin W Burke; Joshua K Meisner; Casey W Shuptrine; Ji Song; Richard J Price Journal: Angiogenesis Date: 2009-09-24 Impact factor: 9.596