Necrostatin-1 protection of dopaminergic neurons

Neural Regeneration Research
Jing-Ru WuYanbo Cheng

Abstract

Necroptosis is characterized by programmed necrotic cell death and autophagic activation and might be involved in the death process of dopaminergic neurons in Parkinson's disease. We hypothesized that necrostatin-1 could block necroptosis and give protection to dopaminergic neurons. There is likely to be crosstalk between necroptosis and other cell death pathways, such as apoptosis and autophagy. PC12 cells were pretreated with necroststin-1 1 hour before exposure to 6-hydroxydopamine. We examined cell viability, mitochondrial membrane potential and expression patterns of apoptotic and necroptotic death signaling proteins. The results showed that the autophagy/lysosomal pathway is involved in the 6-hydroxydopamine-induced death process of PC12 cells. Mitochondrial disability induced overactive autophagy, increased cathepsin B expression, and diminished Bcl-2 expression. Necrostatin-1 within a certain concentration range (5-30 μM) elevated the viability of PC12 cells, stabilized mitochondrial membrane potential, inhibited excessive autophagy, reduced the expression of LC3-II and cathepsin B, and increased Bcl-2 expression. These findings suggest that necrostatin-1 exerted a protective effect against injury on dopaminergic neuron...Continue Reading

References

May 3, 2003·Nature Reviews. Neuroscience·Miquel Vila, Serge Przedborski
Jan 13, 2006·Nature Chemical Biology·Alexei DegterevJunying Yuan
May 19, 2007·Toxicology in Vitro : an International Journal Published in Association with BIBRA·Xiaogang KangBairen Wang
Aug 1, 2007·Cardiovascular Drugs and Therapy·Christopher C T SmithDerek M Yellon
Apr 15, 2008·Nature Chemical Biology·Alexei DegterevJunying Yuan
Jun 24, 2010·Journal of Cerebral Blood Flow and Metabolism : Official Journal of the International Society of Cerebral Blood Flow and Metabolism·Frances J NorthingtonLee J Martin
May 14, 2011·Journal of Cellular and Molecular Medicine·Christopher C T Smith, Derek M Yellon
May 31, 2011·Antioxidants & Redox Signaling·Celine PerierMiquel Vila
Feb 24, 2012·Journal of Biosciences·Ying-Tsen TungYung-Feng Liao
Apr 5, 2012·Cold Spring Harbor Perspectives in Medicine·Melinda A Lynch-DayDaniel J Klionsky
May 4, 2012·Basic Research in Cardiology·Martinus I F J OerlemansJoost P G Sluijter
Aug 22, 2012·Cold Spring Harbor Perspectives in Medicine·Katerina Venderova, David S Park
Jan 11, 2013·Journal of Cellular and Molecular Medicine·Mayur V JainMarek Łos
Jun 19, 2013·Biochimica Et Biophysica Acta·Vassiliki NikoletopoulouNektarios Tavernarakis
Oct 25, 2013·CNS & Neurological Disorders Drug Targets·S M FayazG K Rajanikant
Nov 21, 2013·Journal of Parkinson's Disease·Vera DiasM Maral Mouradian
Nov 23, 2013·Parkinsonism & Related Disorders·Ping-Yue Pan, Zhenyu Yue
Dec 21, 2013·Médecine sciences : M/S·Lauriane CabonSantos A Susin
Jan 31, 2014·The New England Journal of Medicine·Andreas Linkermann, Douglas R Green
Mar 29, 2014·International Journal of Molecular Medicine·Young Sik Cho
Oct 21, 2014·The FEBS Journal·Maria Feoktistova, Martin Leverkus

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Citations

Apr 7, 2017·Neurochemical Research·Lifei ShaoYilu Gao
Jul 1, 2017·Cell Death & Disease·Shuo ZhangYu-Ming Xu
Nov 24, 2018·Nature Reviews. Neuroscience·Junying YuanDimitry Ofengeim
Oct 9, 2019·Cell Death and Differentiation·Maritza OñateFelipe A Court
Jun 19, 2020·Antioxidants·Eva Alegre-CortésSokhna M S Yakhine-Diop
Oct 19, 2016·Journal of Huazhong University of Science and Technology. Medical Sciences = Hua Zhong Ke Ji Da Xue Xue Bao. Yi Xue Ying De Wen Ban = Huazhong Keji Daxue Xuebao. Yixue Yingdewen Ban·Shuang ChenKun Xiong
Oct 6, 2017·Acta Biochimica Et Biophysica Sinica·Lvshuang LiaoKun Xiong
Oct 21, 2018·Cell Death and Differentiation·Bradlee L HeckmannDouglas R Green
Apr 25, 2018·Scientific Reports·Mi-Bo TangYu-Ming Xu
Jul 8, 2018·Journal of Neuroinflammation·Yogesh K Dhuriya, Divakar Sharma
Nov 22, 2018·Frontiers in Neurology·Paulina Troncoso-EscuderoRene L Vidal
Jan 9, 2021·Cell Death and Differentiation·Marlene F SchmidtGrant Dewson
Nov 26, 2020·Antioxidants & Redox Signaling·Illyane Sofia LimaRaffaella Gozzelino
Nov 13, 2020·Pharmacological Research : the Official Journal of the Italian Pharmacological Society·Liyuan Cao, Wei Mu
Oct 30, 2020·Frontiers in Aging Neuroscience·Caroline L Benn, Lee A Dawson
Mar 2, 2021·Neural Regeneration Research·Eva Alegre-CortesSokhna M S Yakhine-Diop
Jul 30, 2020·Progress in Neurobiology·Laura Mahoney-SánchezJean-Christophe Devedjian
Jul 30, 2021·Frontiers in Pharmacology·Ziyu YuYehong Zhuo

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Methods Mentioned

BETA
protein assay

Software Mentioned

SPSS

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