Xiao-Yu Cheng published latest article in Neuroscience entitled Serum Response Factor Promotes Dopaminergic Neuron Survival via Activation of Beclin 1-Dependent Autophagy. This article is available in PubMed with an unique identification number PMID: 29196028 and it is published in 2017. The coauthors of this article are Cheng XY, Li SY, Mao CJ, Wang MX, Chen J, Wang F, Wang GH, Deng WB, Li XK, Liu CF.
Co-Author(s): Cheng XY, Li SY, Mao CJ, Wang MX, Chen J, Wang F, Wang GH, Deng WB, Li XK, Liu CF
Affiliation(s): Department of Neurology and Suzhou Clinical Research Center of Neurological Disease, The Second Affiliated Hospital of Soochow University, Suzhou 215004, China; Institute of Neuroscience, Soochow University, Suzhou 215123, China; Departments of Biochemistry and Molecular Medicine, University of California-Davis, Sacramento, CA 95817, USA. Electronic address: firstname.lastname@example.org.
PMID 29196028, Year 2017
Abstract: Serum response factor (SRF), a transcription factor highly expressed in neurons, is involved in neuronal survival and the pathogenesis of some neurodegenerative disorders. The ablation of SRF renders the midbrain dopaminergic (DA) neurons vulnerable to 1-methyl 4-phenyl 1,2,3,6-tetrahydropyridine-induced neurotoxicity, however, the underlying mechanisms remain poorly understood. Here, we report decreased SRF levels in the substantia nigra (SN) of rotenone-treated rats that was associated with the loss of tyrosine hydroxylase (TH)-positive neurons. SRF expression was also reduced in rotenone-treated PC12 cells in vitro. In addition, Srf knockdown augmented rotenone-induced toxicity in PC12 cells. In contrast, overexpression of Srf attenuated the cells sensitivity to rotenone and alleviated rotenone-induced ?-synuclein accumulation. The protective effect of SRF was abolished when the expression of autophagy-related proteins Beclin 1 and Atg5 was suppressed. These results suggested that SRF may promote DA neuron survival by regulating autophagy, and thus serves as a critical molecule in PD progression.
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