Journal article
Inhibiting mitochondrial fission protects the heart against ischemia/reperfusion injury
SB Ong, S Subrayan, SY Lim, DM Yellon, SM Davidson, DJ Hausenloy
Circulation | LIPPINCOTT WILLIAMS & WILKINS | Published : 2010
Abstract
Background: Whether alterations in mitochondrial morphology affect the susceptibility of the heart to ischemia/reperfusion injury is unknown. We hypothesized that modulating mitochondrial morphology protects the heart against ischemia/reperfusion injury. Methods and Results: In response to ischemia, mitochondria in HL-1 cells (a cardiac-derived cell line) undergo fragmentation, a process that is dependent on the mitochondrial fission protein dynamin-related protein 1 (Drp1). Transfection of HL-1 cells with the mitochondrial fusion proteins mitofusin 1 or 2 or with Drp1K38A, a dominant-negative mutant form of Drp1, increased the percentage of cells containing elongated mitochondria (65±4%, 69..
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Funding Acknowledgements
S.-B. Ong is funded by a Dorothy Hodgkin Postgraduate Award (Biotechnology and Biological Sciences Research Council). We thank the British Heart Foundation for their continued support. This work was undertaken at University College London Hospital/University College London, which received a portion of funding from the Department of Health's National Institute of Health Research Biomedical Research Centres funding scheme.