Journal article
Modulation of Cellular Hsp72 Levels in Undifferentiated and Neuron-Like SH-SY5Y Cells Determines Resistance to Staurosporine-Induced Apoptosis
Lesley Cheng, Danielle J Smith, Robin L Anderson, Phillip Nagley
PLOS ONE | PUBLIC LIBRARY SCIENCE | Published : 2011
Abstract
Increased expression of Hsp72 accompanies differentiation of human neuroblastoma SH-SY5Y cells to neuron-like cells. By modulating cellular levels of Hsp72, we demonstrate here its anti-apoptotic activity both in undifferentiated and neuron-like cells. Thermal preconditioning (43°C for 30 min) induced Hsp72, leading to cellular protection against apoptosis induced by a subsequent treatment with staurosporine. Preconditioned staurosporine-treated cells displayed decreased Bax recruitment to mitochondria and subsequent activation, as well as reduced cytochrome c redistribution from mitochondria. The data are consistent with Hsp72 blocking apoptosis upstream of Bax recruitment to mitochondria. ..
View full abstractGrants
Awarded by National Health and Medical Research Council of Australia (NHMRC)
Awarded by Australian Research Council (ARC), Centre of Excellence in Structural and Functional Microbial Genomics
Awarded by National Institutes of Health/National Cancer Institute
Funding Acknowledgements
Funding was obtained from grants from the National Health and Medical Research Council of Australia (NHMRC), www.nhmrc.gov.au, Program Grant on Brain Injury and Repair (Grant ID 236805); the Australian Research Council (ARC), www.arc.gov.au, Centre of Excellence in Structural and Functional Microbial Genomics (Grant CE034819) to P. Nagley; and the National Institutes of Health/National Cancer Institute, www.cancer.gov, (Grant CA81421) to R. Anderson. L. Cheng was supported by a Ph.D. training scholarship from Neurosciences Victoria, www.neurosciencesvic.com.au. R. Anderson was supported by a fellowship from the National Breast Cancer Foundation of Australia, www.nbcf.org.au. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.