Effects of Hypoxia (Oxygen Glucose Deprivation) on Endothelial Progenitor Cell Function and Shh Signaling Pathway in Rats
摘要
The nature of pressure ulcer is ischemia and hypoxia leading to tissue necrosis, and the role of Shh protein in oxygen–glucose deprivation (OGD) may increase the vascular capacity of endothelial progenitor cells (EPCs), thereby reducing the degree of tissue necrosis after pressure ulcer.
Purpose of the StudyTo explore the effects of ischemia on EPCs.
MethodsWe established the EPCs in vitro ischemia model induced by OGD and detected the expression of Sonic Hedgehog (Shh).
ResultsThe results show that the expression level of Shh was reduced obviously in EPCs cultured under the OGD conditions. Invasion, migration, and tube formation abilities were significantly decreased in OGD-EPCs, as well as the ratio between the level of serine/threonine kinase B (AKT) and phosphorylated AKT (p-AKT), the ratio between the level of glycogen synthase kinase-3β (GSK-3β) and phosphorylated GSK-3β (p-GSK-3β), and the expression of mammalian target of rapamycin (mTOR) in OGD-EPCs, while they were recovered remarkably after adding smoothened agonist (SAG), insulin-like growth factor-1 (IGF-1), or IGF-1 + SAG.
ConclusionIn conclusion, invasion, migration, tube formation abilities, and angiogenic factors were increased in OGD-EPCs by activation of the Shh signaling pathway and the Akt/GSK-3β/mTOR pathway.