Ceruloplasmin is Involved in the Nigral Iron Accumulation of 6-OHDA-Lesioned Rats

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• 作者：Jun Wang ; Mingxia Bi ; Junxia Xie
• 关键词：6 ; OHDA ; Ceruloplasmin ; Iron ; Parkinson’s disease
• 刊名：Cellular and Molecular Neurobiology
• 出版年：2015
• 出版时间：July 2015
• 年：2015
• 卷：35
• 期：5
• 页码：661-668
• 全文大小：1,470 KB
• 参考文献：Abboud S, Haile DJ (2000) A novel mammalian iron-regulated protein involved in intracellular iron metabolism. J Biol Chem 275:19906-9912PubMed View Article
  Arnal N, Cristalli DO, de Alaniz MJ, Marra CA (2010) Clinical utility of copper, ceruloplasmin, and metallothionein plasma determinations in human neurodegenerative patients and their first-degree relatives. Brain Res 1319:118-30PubMed View Article
  Ayton S, Lei P, Duce JA, Wong BX, Sedjahtera A, Adlard PA, Bush AI, Finkelstein DI (2013) Ceruloplasmin dysfunction and therapeutic potential for Parkinson disease. Ann Neurol 73:554-59PubMed View Article
  Ayton S, Lei P, Adlard PA, Volitakis I, Cherny RA, Bush AI, Finkelstein DI (2014) Iron accumulation confers neurotoxicity to a vulnerable population of nigral neurons: implications for Parkinson’s disease. Molecular Neurodegener 9:27View Article
  Bharucha KJ, Friedman JK, Vincent AS, Ross ED (2008) Lower serum ceruloplasmin levels correlate with younger age of onset in Parkinson’s disease. J Neurol 255:1957-962PubMed View Article
  Bisaglia M, Mammi S, Bubacco L (2009) Structural insights on physiological functions and pathological effects of alpha-synuclein. FASEB J 23:329-40PubMed View Article
  Boll MC, Sotelo J, Otero E, Alcaraz-Zubeldia M, Rios C (1999) Reduced ferroxidase activity in the cerebrospinal fluid from patients with Parkinson’s disease. Neurosci Lett 265:155-58PubMed View Article
  Bradbury MW (1997) Transport of iron in the blood
  ain-cerebrospinal fluid system. J Neurochem 69:443-54PubMed View Article
  Burdo JR, Menzies SL, Simpson IA, Garrick LM, Garrick MD, Dolan KG, Haile DJ, Beard JL, Connor JR (2001) Distribution of divalent metal transporter 1 and metal transport protein 1 in the normal and Belgrade rat. J Neurosci Res 66:1198-207PubMed View Article
  De Domenico I, Ward DM, di Patti MC, Jeong SY, David S, Musci G, Kaplan J (2007) Ferroxidase activity is required for the stability of cell surface ferroportin in cells expressing GPI-ceruloplasmin. EMBO J 26:2823-831PubMed Central PubMed View Article
  Dickinson TK, Connor JR (1995) Cellular distribution of iron, transferrin, and ferritin in the hypotransferrinemic (Hp) mouse brain. J Comp Neurol 355:67-0PubMed View Article
  Donovan A, Brownlie A, Zhou Y, Shepard J, Pratt SJ, Moynihan J, Paw BH, Drejer A, Barut B, Zapata A, Law TC, Brugnara C, Lux SE, Pinkus GS, Pinkus JL, Kingsley PD, Palis J, Fleming MD, Andrews NC, Zon LI (2000) Positional cloning of zebrafish ferroportin 1 identifies a conserved vertebrate iron exporter. Nature 403:776-81PubMed View Article
  Earl CD, Reum T, Xie JX, Sautter J, Kupsch A, Oertel WH, Morgenstern R (1996) Foetal nigral cell suspension grafts influence dopamine release in the non-grafted side in the 6-hydroxydopamine rat model of Parkinson’s disease: in vivo voltammetric data. Exp Brain Res 109:179-84PubMed View Article
  Fortna RR, Watson HA, Nyquist SE (1999) Glycosyl phosphatidylinositol-anchored ceruloplasmin is expressed by rat Sertoli cells and is concentrated in detergent-insoluble membrane fractions. Biol Reprod 61:1042-049PubMed View Article
  Harris ZL, Durley AP, Man TK, Gitlin JD (1999) Targeted gene disruption reveals an essential role for ceruloplasmin in cellular iron efflux. Proc Natl Acad Sci USA 96:10812-0817PubMed Central PubMed View Article
  Jiang H, Qian ZM, Xie JX (2003) Increased DMT1 expression and iron content in MPTP-treated C57BL/6 mice. Sheng Li Xue Bao 55:571-76PubMed
  Jin L, Wang J, Zhao L, Jin H, Fei G, Zhang Y, Zeng M, Zhong C (2011) Decreased serum ceruloplasmin levels characteristically aggravate nigral iron deposition in Parkinson’s disease. Brain 134:50-8PubMed View Article
  Kaneko K, Hineno A, Yoshida K, Ikeda S (2008) Increased vulnerability to rotenone-induced neurotoxicity in ceruloplasmin-deficient mice. Neurosci Lett 446:56-8PubMed View Article
  Kaplan J, Kushner JP (2000) Mining the genome for iron. Nature 403(711):713
  Kooyman DL, Byrne GW, McClellan S, Nielsen D, Tone M, Waldmann H, Coffman TM, McCurry KR, Platt JL, Logan JS (1995) In vivo transfer of GPI-linked complement restriction factors from erythrocytes to the endothelium. Science 269:89-2PubMed View Article
  Le NT, Richardson DR (2002) Ferroportin1: a new iron export molecule? Int J Biochem Cell Biol 34:103-08PubMed View Article
  Liu B, Xie J (2004) Increased dopamine release in vivo by estradiol benzoate from the central amygdaloid nucleus of Parkinson’s disease model rats. J Neurochem 90:654-58PubMed View Article
  Martin WR, Wieler M, Gee M (2008) Midbrain iron content in early Parkinson disease: a potential biomarker of disease status. Neurology 70:1411-417PubMed View Article
  Mastroberardino PG, Hoffman EK, Horowitz MP, Betarbet R, Taylor G, Cheng D, Na HM, Gutekunst CA, Gearing M, Trojanowski JQ, Anderson M, Chu CT, Peng J, Greenamyre JT (2009) A novel transferrin/TfR2-mediated mitochondrial iron transport system
• 作者单位：Jun Wang (1)
  Mingxia Bi (1)
  Junxia Xie (1)
  
  1. Department of Physiology, Shandong Provincial Key Laboratory of Pathogenesis and Prevention of Neurological Disorders, Shandong Provincial Collaborative Innovation Center for Neurodegenerative Disorders and State Key Disciplines: Physiology, Medical College of Qingdao University, Qingdao, 266071, China
  
• 刊物类别：Biomedical and Life Sciences
• 刊物主题：Biomedicine
  Neurosciences
  Animal Anatomy, Morphology and Histology
  
• 出版者：Springer Netherlands
• ISSN：1573-6830

文摘

Elevated iron levels in the substantia nigra (SN) participate in neuronal death in Parkinson’s disease (PD), while the mechanisms underlying the increased iron are still unknown. Ceruloplasmin (CP), a ferroxidase, converts highly toxic ferrous iron to its non-toxic ferric form, which cooperated with ferroportin1 (FP1) facilitating the export of iron from cells. To elucidate if the abnormal expression of CP is involved in the nigral iron accumulation, here, we investigated CP expression in the SN of rats lesioned by 6-hydroxydopamine (6-OHDA). We showed that FP1 and CP colocalized in the rat SN. One day after 6-OHDA lesion, when there was a half reduction in the number of dopaminergic neurons, the iron level was increased compared with the normal rats; both the mRNA and protein expressions of CP decreased compared with the control. When rats began showing rotation behavior induced by apomorphine, usually after 6?weeks since 6-OHDA lesion, they are considered PD models. In these PD models, almost no dopaminergic neurons can be detected in the lesioned SN and nigral iron level was further increased. At this time point, a further decrease of CP was observed. These results show that FP1 and CP colocalize in the rat brain, indicating the coordinated actions of the two proteins in the?cellular iron export, and suggest that decreased expression of CP in the SN is involved in the nigral iron accumulation of 6-OHDA-lesioned rats.