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Hypoxic Preconditioning (hypoxic + preconditioning)

Distribution by Scientific Domains

Life Sciences	75%

Selected Abstracts

Hypoxic preconditioning protects rat hearts against ischaemia,reperfusion injury: role of erythropoietin on progenitor cell mobilization

THE JOURNAL OF PHYSIOLOGY, Issue 23 2008
Jih-Shyong Lin
Preconditioning, such as by brief hypoxic exposure, has been shown to protect hearts against severe ischaemia. Here we hypothesized that hypoxic preconditioning (HPC) protects injured hearts by mobilizing the circulating progenitor cells. Ischaemia,reperfusion (IR) injury was induced by left coronary ligation and release in rats kept in room air or preconditioned with 10% oxygen for 6 weeks. To study the role of erythropoietin (EPO), another HPC + IR group was given an EPO receptor (EPOR) antibody via a subcutaneous mini-osmotic pump 3 weeks before IR induction. HPC alone gradually increased haematocrit, cardiac and plasma EPO, and cardiac vascular endothelial growth factor (VEGF) only in the first two weeks. HPC improved heart contractility, reduced ischaemic injury, and maintained EPO and EPOR levels in the infarct tissues of IR hearts, but had no significant effect on VEGF. Interestingly, the number of CD34+CXCR4+ cells in the peripheral blood and their expression in HPC-treated hearts was higher than in control. Preconditioning up-regulated cardiac expression of stromal derived factor-1 (SDF-1) and prevented its IR-induced reduction. The EPOR antibody abolished HPC-mediated functional recovery, and reduced SDF-1, CXCR4 and CD34 expression in IR hearts, as well as the number of CD34+CXCR4+ cells in blood. The specificity of neutralizing antibody was confirmed in an H9c2 culture system. In conclusion, exposure of rats to moderate hypoxia leads to an increase in progenitor cells in the heart and circulation. This effect is dependent on EPO, which induces cell homing by increased SDF-1/CXCR4 and reduces the heart susceptibly to IR injury. [source]

Potentiation of angiogenic response by ischemic and hypoxic reconditioning of the heart

JOURNAL OF CELLULAR AND MOLECULAR MEDICINE, Issue 1 2002
Nilanjana Maulik
Abstract This review is intended to discuss the newly discovered role of preconditioning which should make it an attractive therapeutic stimulus for repairing the injured myocardium. We recently found that apart from rendering the myocardium tolerant to ischemic reperfusion injury, preconditioning also potentiates angiogenesis. Our study demonstrated for the first time that both ischemic and hypoxic preconditioning triggered myocardial angiogenesis at the capillary and arteriolar levels which nicely corroborated with the improved myocardial contractile function.Hypoxic preconditioning resulted in the stimulation of VEGF, the most potent angiogenic factor known to date. In concert, endothelial cell specific tyrosine kinase receptors, Tie 1, Tie 2 and Flt-1 and Flk-1 were also significantly enhanced in the preconditioned myocardium. The redox-regulated transcription factor NFkB was found to play an essential role in the preconditioning regulation of angiogenesis [source]

Neuron-specific phosphorylation of mitogen- and stress-activated protein kinase-1 involved in cerebral hypoxic preconditioning of mice

JOURNAL OF NEUROSCIENCE RESEARCH, Issue 6 2007
Ping Huang
Abstract Studies have demonstrated the involvement of mitogen-activated protein kinase (MAPK) cascade pathways in the development of cerebral ischemic/hypoxic preconditioning (I/HPC). However, the role of mitogen- and stress-activated protein kinase 1 (MSK1), an important downstream kinase of MAPK signaling pathways, in cerebral I/HPC is unclear. By using Western blot and immunostaining methods, we applied our unique "autohypoxia"-induced I/HPC mouse model to investigate the effects of repetitive hypoxic exposure (H0,H6, n = 6 for each group) on phosphorylation and protein expression levels of MSK1 in the brain of mice. We found that the levels of phosphorylation on threonine 645 (Thr645) and serine 375 (Ser375) of MSK1, but not the protein expression, increased significantly both in hippocampus and in cortex of mice from H1,H6 groups (P < 0.05) over that of the normoxic group (H0, n = 6). Similarly, enhanced phosphorylations on Thr645 and Ser375 of MSK1 were also observed by immunostaining in both the cortex and the hippocampus of mice following three series of hypoxic exposures (H3). In addition, we found by using double-immunofluorescence labeling that phosphorylated Thr645-MSK1 colocalized with a neuron-specific protein, neurogranin, in both cortex and hippocampus of I/HPC mice (H3). These results suggest that the increased neuron-specific phosphorylation of MSK1 on Thr645 and Ser375, not protein expression, might be involved in the development of cerebral I/HPC in mice. © 2007 Wiley-Liss, Inc. [source]