Neuroprotection by Orexin-A via HIF-1α induction in a cellular model of Parkinson's disease.
Identifieur interne : 000026 ( PubMed/Curation ); précédent : 000025; suivant : 000027Neuroprotection by Orexin-A via HIF-1α induction in a cellular model of Parkinson's disease.
Auteurs : Ya Feng [République populaire de Chine] ; Te Liu [République populaire de Chine] ; Xin Li [États-Unis] ; Ye Liu [République populaire de Chine] ; Xiao Zhu [République populaire de Chine] ; Joseph Jankovic [États-Unis] ; Tian Pan [États-Unis] ; Yun Wu [République populaire de Chine]Source :
- Neuroscience letters ; 2014.
English descriptors
- KwdEn :
- Cell Line, Humans, Hypoxia-Inducible Factor 1, alpha Subunit (biosynthesis), Intracellular Signaling Peptides and Proteins (pharmacology), MPTP Poisoning (chemically induced), MPTP Poisoning (pathology), Neuropeptides (pharmacology), Neuroprotective Agents (pharmacology), Orexins, Suppression, Genetic (drug effects), Vascular Endothelial Growth Factor A (metabolism).
- MESH :
- chemical , biosynthesis : Hypoxia-Inducible Factor 1, alpha Subunit.
- chemical , metabolism : Vascular Endothelial Growth Factor A.
- chemical , pharmacology : Intracellular Signaling Peptides and Proteins, Neuropeptides, Neuroprotective Agents.
- chemically induced : MPTP Poisoning.
- drug effects : Suppression, Genetic.
- pathology : MPTP Poisoning.
- Cell Line, Humans, Orexins.
Abstract
Orexin-A, a neuropeptide secreted by hypothalamic neurons, may be neuroprotective in many neurological conditions such as cerebral ischaemia. One mechanism postulated to be involved in the neuroprotection by Orexin-A is the induction of hypoxia inducible factor 1 alpha (HIF-1α). Parkinson's disease (PD) is a progressive neurodegenerative disorder and mitochondrial dysfunction has been demonstrated to play a role in its pathogenesis. Mitochondrial dysfunction may cause reduction of O2 consumption and subsequently activate prolyl hydroxylase, which leads to decreased level of HIF-1α. In this study, we used MPP(+)-treated SH-SY5Y cells as an in vitro cellular model of PD to test the role of Orexin-A as an inducer of HIF-1α. Our results showed that Orexin-A not only induced HIF-1α but also activated downstream targets of HIF-1α, such as vascular endothelial growth factor and erythropoietin. Thus, Orexin-A treatment attenuated MPP(+)-induced cell injury and this effect was blocked when HIF-1α was suppressed. Hence, we conclude that induction of HIF-1α is one of the mechanisms involved in the neuroprotection by Orexin-A.
DOI: 10.1016/j.neulet.2014.07.014
PubMed: 25038418
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<front><div type="abstract" xml:lang="en">Orexin-A, a neuropeptide secreted by hypothalamic neurons, may be neuroprotective in many neurological conditions such as cerebral ischaemia. One mechanism postulated to be involved in the neuroprotection by Orexin-A is the induction of hypoxia inducible factor 1 alpha (HIF-1α). Parkinson's disease (PD) is a progressive neurodegenerative disorder and mitochondrial dysfunction has been demonstrated to play a role in its pathogenesis. Mitochondrial dysfunction may cause reduction of O2 consumption and subsequently activate prolyl hydroxylase, which leads to decreased level of HIF-1α. In this study, we used MPP(+)-treated SH-SY5Y cells as an in vitro cellular model of PD to test the role of Orexin-A as an inducer of HIF-1α. Our results showed that Orexin-A not only induced HIF-1α but also activated downstream targets of HIF-1α, such as vascular endothelial growth factor and erythropoietin. Thus, Orexin-A treatment attenuated MPP(+)-induced cell injury and this effect was blocked when HIF-1α was suppressed. Hence, we conclude that induction of HIF-1α is one of the mechanisms involved in the neuroprotection by Orexin-A.</div>
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<Abstract><AbstractText>Orexin-A, a neuropeptide secreted by hypothalamic neurons, may be neuroprotective in many neurological conditions such as cerebral ischaemia. One mechanism postulated to be involved in the neuroprotection by Orexin-A is the induction of hypoxia inducible factor 1 alpha (HIF-1α). Parkinson's disease (PD) is a progressive neurodegenerative disorder and mitochondrial dysfunction has been demonstrated to play a role in its pathogenesis. Mitochondrial dysfunction may cause reduction of O2 consumption and subsequently activate prolyl hydroxylase, which leads to decreased level of HIF-1α. In this study, we used MPP(+)-treated SH-SY5Y cells as an in vitro cellular model of PD to test the role of Orexin-A as an inducer of HIF-1α. Our results showed that Orexin-A not only induced HIF-1α but also activated downstream targets of HIF-1α, such as vascular endothelial growth factor and erythropoietin. Thus, Orexin-A treatment attenuated MPP(+)-induced cell injury and this effect was blocked when HIF-1α was suppressed. Hence, we conclude that induction of HIF-1α is one of the mechanisms involved in the neuroprotection by Orexin-A.</AbstractText>
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