Peroxisome proliferator activated receptor (PPAR)-γ co-activator 1-α and hypoxia induced factor-1α mediate neuro- and vascular protection by hypoxic preconditioning in vitro

Autor: Chaoying Li, Ru-xun Huang, Huan Wei, Ying Peng, Jia Zhao, Zhong Pei, Bo Zhang, Yuqian Tao, Ying Wang, Ling Li
Rok vydání: 2011
Předmět:
medicine.medical_specialty
Endothelium
Cell Survival
Peroxisome proliferator-activated receptor
Biology
medicine.disease_cause
PC12 Cells
chemistry.chemical_compound
Random Allocation
Internal medicine
medicine
Animals
Viability assay
Molecular Biology
Cell damage
Cells
Cultured
Cell Line
Transformed
chemistry.chemical_classification
Neurons
General Neuroscience
RNA-Binding Proteins
Hypoxia (medical)
medicine.disease
Hypoxia-Inducible Factor 1
alpha Subunit
Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha
Cell Hypoxia
Cell biology
Rats
Vascular endothelial growth factor
Endothelial stem cell
Endocrinology
medicine.anatomical_structure
Neuroprotective Agents
chemistry
Neurology (clinical)
Endothelium
Vascular
medicine.symptom
Reactive Oxygen Species
Oxidative stress
Developmental Biology
Transcription Factors
Zdroj: Brain research. 1447
ISSN: 1872-6240
Popis: Preconditioning-induced cellular adaptation is a new therapeutic strategy for ischemic stroke. This research aims to examine the role of peroxisome proliferator activated receptor (PPAR)-γ co-activator 1-α (PGC-1α) and hypoxia induced factor-1α (HIF-1α) in hypoxic preconditioning-induced protection. In this study, rat artery endothelial cells and neuronal PC12 cells were preconditioned with hypoxia before oxygen-glucose deprivation (OGD) insult. Cell viability, protein expression and oxidative stress were then evaluated. PGC-1α and HIF-1α were knocked down by RNA interference. We found that hypoxic preconditioning significantly reduced cell damage, enhanced the expression of PGC-1α, HIF-1α and VEGF and attenuated oxidative stress in endothelial and PC12 cells in OGD model. The protective effects of hypoxic preconditioning were hardly detected in HIF-1α or PGC-1α deficit cells. The loss of protection was accompanied with a significant loss of VEGF expression in HIF-1α or PGC-1α deficit PC12 cells and PGC-1α deficit endothelial cells as well as a considerable decrease of anti-oxidative effects in PGC-1α knocked-down endothelial cells. The present study demonstrated that both PGC-1α and HIF-1α played crucial roles in hypoxic preconditioning in endothelial and neuronal cells.
Databáze: OpenAIRE
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