Role of autophagy and proteasome degradation pathways in apoptosis of PC12 cells overexpressing human α-synuclein
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Acknowledgements
We are grateful to Dr. Ping Feng and Bingyan Li of Soochow University for their advice, generosity and extraordinary support with facilities and reagents. We also thank Professor IC Bruce for critical reading of the manuscript. Supported by grants from the National Natural Science Foundation of China (number 30870869) and the Jiangsu Province Foundation of China (07KJB320109).
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2014, Autophagy: Cancer, Other Pathologies, Inflammation, Immunity, Infection, and AgingProtein damage, repair and proteolysis
2014, Molecular Aspects of MedicineCitation Excerpt :Expression of mutant LRRK2 (leucine rich repeated kinase 2) that is observed in familial PD patients, also increases autophagic vacuole and autophagy-dependent shortening of neurites (Plowey et al., 2008). Excessive autophagic induction that leads to neuronal loss has been associated with overexpression of A53T α-synuclein and pharmacological induction of PD with MPP+ (Choubey et al., 2011; Kirik et al., 2002; Stefanis et al., 2001; Xilouri et al., 2009; Yang et al., 2009). In accordance with the inhibition of autophagy through the 3-methylamphetamine (3-MA) inhibitor, inhibition or knock-down of ATG5 or ATG12 expression attenuates neurodegeneration (Wong et al., 2011).
Reynosin protects against neuronal toxicity in dopamine-induced SH-SY5Y cells and 6-hydroxydopamine-lesioned rats as models of Parkinson's disease: Reciprocal up-regulation of E6-AP and down-regulation of α-synuclein
2013, Brain ResearchCitation Excerpt :Human neuroblastoma SH-SY5Y cells (ATCC no. CRL-2266) were cultured in DMEM supplemented with 10% heat-inactivated FBS and 1% penicillin/streptomycin (Meiji Seika, Tokyo, Japan), at 37 °C in a humidified 5% CO2 atmosphere. SH-SY5Y cells were cultured for 24 h and then treated with reynosin (0.08, 0.4, and 2 µM) or 2 µM of APO (a positive control compound) (Hara et al., 2006) for 24 h, followed by subsequent treatment with DA (600 μM) for an additional 24 h. Cell viability was analyzed by flow cytometry (FACS) (Calibur, Becton Dickinson, USA) using PI staining (Yang et al., 2009). Male Sprague-Dawley rats were purchased from Samtako Bio Korea (Osan, Korea) and housed in groups (2–3 rats/cage) at room temperature for 1 week prior to the experiments in a humidity-controlled environment with a 12/12-light-dark cycle and unlimited access to food and water.
Retinoic acid protects against proteasome inhibition associated cell death in SH-SY5Y cells via the AKT pathway
2013, Neurochemistry InternationalCitation Excerpt :It is now generally accepted that abnormal protein accumulation is central to the pathophysiology of AD and PD (Cook and Petrucelli, 2009; Keller and Markesbery, 2000; Lopez Salon et al., 2000; McNaught and Olanow, 2003). Recent reports have suggested the involvement of autophagy, either independently or in conjunction with apoptosis in PD (Cheung and Ip, 2009; Gonzalez-Polo et al., 2005; Yang et al., 2009a). To develop therapeutic strategies for these diseases, it will be important both to identify and characterize mechanisms that regulate the proteasome–ubiquitination system, and to find ways to prevent dysfunction and cell death where abnormal protein aggregation has occurred.
Apoptosis in Parkinson's disease: Is p53 the missing link between genetic and sporadic Parkinsonism?
2011, Cellular SignallingCitation Excerpt :More recently α-synuclein was shown to be cleared by chaperone-mediated autophagy (CMA) and macroautophagy in several neuronal cell lines [23], a control abolished by either pathogenic mutations or by drugs such as dopamine able to promote α-synuclein aggregation [24]. α-Synuclein was shown to block the interaction of the transcription factor MEF2D (myocyte enhancer factor 2D) with the chaperone protein Hsc70 leading to increased cell death due to impairment of CMA [25]. Other PD-associated gene products were also shown to control type II PCD.