Abstract
Hypoxia is a condition of decreased availability of oxygen. When cells are exposed to a low oxygen environment, they impel the hypoxia responses to adapt to new situation. The hypoxia response leads to the activation of various cellular signaling pathways. The aim of this study was to evaluate the effect of ghrelin on angiogenesis, Hypoxia-Inducible-Factor-1α (HIF-1) and Vascular endothelial growth factor (VEGF) levels in normobaric hypoxia situation. Twenty four animals were divided into 4 groups (n=6): control (C), ghrelin (Gh), hypoxia (H), and hypoxic animals that received ghrelin (H+Gh). Hypoxia (11%) was induced by an Environmental Chamber System GO2 Altitude. Animals in ghrelin groups received a subcutaneous injection of ghrelin (150 μg/kg/day) for 14 days. Our results showed that hypoxia significantly (p<0.05) increased angiogenesis without any significant changes on HIF-1 and VEGF levels, whereas ghrelin significantly (p<0.05) decreased angiogenesis, expression of HIF-1 and VEGF in this condition. Ghrelin administration did not show any significant changes in normal conditions. Ghrelin had no effect on angiogenesis, expression of HIF-1 and VEGF in normal oxygen conditions but it reduced angiogenesis process in lung tissue with reducing the level of HIF and VEGF in hypoxic condition. Therefore, effect of ghrelin on angiogenesis could be related to blood oxygen level.
Highlights
Hypoxia is a common characteristic of many respiratory diseases resulting from inadequate alveolar ventilation, such as chronic obstructive lung disease or pulmonary edema due to heart failure or acute lung injury.[1]
Our results showed that hypoxia significantly (p
Effects of hypoxia and ghrelin on HIF 1-α and VEGF protein levels in lung tissue The effect of two weeks of ghrelin (150 μg/kg/day) treatment on HIF-1 α protein level in lung tissue in control and chronic hypoxia conditions showed that induction of hypoxia (O2 11%) did not significantly change HIF1-α level in hypoxia group compared with control group (Figure 1)
Summary
Hypoxia is a common characteristic of many respiratory diseases resulting from inadequate alveolar ventilation, such as chronic obstructive lung disease or pulmonary edema due to heart failure or acute lung injury.[1] When cells are exposed to a low oxygen environment that is a mortal stress[1,2] they impel the hypoxia responses to adapt to new situation. The hypoxia response leads to the activation of various cellular signaling pathways involved in metabolism, cell survival and respiration.[2] cells shift to the glycolysis pathway and induce the expression of glycolytic enzyme and inhibit enzymes leading to the tricarboxylic acid (TCA) cycle, such as pyruvate dehydrogenase for energy production and to reduce consumption of oxygen.[2] Hypoxia-Inducible-Factor-1α (HIF-1α) is one of the most important signaling pathways that are activated during hypoxia response.[2]. HIF-1 target genes contribute in some processes, including encoding proliferation/survival factors, glucose transporters, glycolytic enzymes, and angiogenic factors,[3] such as VEGF.[3,4]
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