MiPsummer Programme pdf - Mitochondrial Physiology Society

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52 Tuesday 27 th Heart Abstracts # 24 – 29
53 Abstract # 24 Reperfusion-induced mitochondrial dysfunction in the porcine heart is reduced by TRO40303 in the area at risk predominantly through preservation of outer mitochondrial membrane intactness M.J. Hansson 1, 2 , S. Morota 1 , S. Koul 3 , R. Jablonowski 2 , J. van der Pals 3 , M. Kanski 2 , P. Gilje 3 , H. Engblom 2 and D. Erlinge 3 . 1. Mitochondrial Pathophysiology Unit, 2. Department of Clinical Physiology and 3. Department of Cardiology, Lund University, Lund, Sweden. Background Mitochondria are considered to play critical roles in cell death pathways following ischemia-reperfusion injury. Objectives The objective of the present study was to perform a functional assessment of mitochondria following ischemia-reperfusion injury of the porcine heart as well as to evaluate mitochondrial effects of hypothermia and the outer membrane translocator protein (TSPO) ligand TRO40303. Methods Pigs were subjected to 40 min occlusion of the left anterior descending artery followed by 4 hours of reperfusion [1]. Three groups of pigs were treated either by administration of 15 mg/kg TRO40303 or the same volume of saline (1 ml/kg) at normothermia 5 min before reperfusion, or by hypothermia (32°C) initiated prior to occlusion, n=8 for all groups. Transmural needle biopsies were taken from the non-ischemic area in the left lateral wall, from the area at risk in the midventricular anterior wall and from the ischemic core area in the apical anterior wall. Mitochondrial respiratory function was evaluated polarographically in skinned heart fibers using specific substrates and inhibitors [2,3]. In the control group, heart fibers from both ischemic areas demonstrated a general reduction of respiratory states. However, respiration linked to respiratory complex I was more affected than that to complex II indicating loss of soluble matrix components such as NAD(H). Addition of exogenous cytochrome c (CytC) increased the level of respiration several fold in both ischemic areas indicating increased permeability of the outer membrane and that CytC loss contributed to the reduced levels of respiration. These changes were diminished by hypothermia in both ischemic areas. TRO40303 attenuated inhibition of respiration involving complex II and reduced the stimulatory effects of CytC in the area at risk, but did not significantly reduce the altered ratio of complex I- and II-mediated respiration, and was without effect in the ischemic core area. Conclusion It is concluded that mitochondria in both the ischemic core area and the area at risk undergo significant alterations in respiratory function following ischemia-reperfusion injury consistent with both inner and outer mitochondrial membrane permeabilization which can be inhibited by hypothermia initiated prior to occlusion. Administration of TRO40303 prior to reperfusion appears to reduce reperfusion-induced mitochondrial dysfunction in the area at risk mainly by preserving outer membrane intactness and limiting CytC release. References 1. Gotberg M, Olivecrona GK, Engblom H, Ugander M, van der Pals J, et al. (2008) Rapid shortduration hypothermia with cold saline and endovascular cooling before reperfusion reduces microvascular obstruction and myocardial infarct size. BMC Cardiovasc Disord 8: 7. 2. Veksler VI, Kuznetsov AV, Sharov VG, Kapelko VI, Saks VA (1987) Mitochondrial respiratory parameters in cardiac tissue: a novel method of assessment by using saponin‐skinned fibers. Biochim Biophys Acta 892: 191‐ 196. 3. Pesta D, Gnaiger E (2012) High‐resolution respirometry: OXPHOS protocols for human cells and permeabilized fibers from small biopsies of human muscle. Methods Mol Biol 810: 25‐58.
Page 1 and 2: COPENHAGEN MiP SUMMER 2013 MITOCHON
Page 3 and 4: 3 MiPs - The Mitochondrial Physiolo
Page 5 and 6: 5 Finding your way at the Panum Ins
Page 7 and 8: 7 PANUM INSTITUTE HOTEL ØSTERPORT
Page 9 and 10: 9 Afternoon programme Monday 26th A
Page 11 and 12: 11 Poster walk/talk The poster sess
Page 13 and 14: 13 Overview of workshops Tuesday, A
Page 15 and 16: 15 Overview of workshops Thursday,
Page 17 and 18: 17 Participants Adelheid Weidinger
Page 19 and 20: 19 Participants Giulia Girolimetti
Page 21 and 22: 21 Participants Michel van Schaarde
Page 23 and 24: 23 Speakers Albert Gjedde Universit
Page 25 and 26: 25 Organizers & teachers Bjørn Qui
Page 27 and 28: 27 Abstract # 1 Nicotinamide phosph
Page 29 and 30: 29 Abstract # 3 Aerobic interval tr
Page 31 and 32: 31 Abstract # 5 The progressive eff
Page 33 and 34: 33 Abstract # 7 Exercise with low g
Page 35 and 36: 35 Tuesday 27 th Aging, Development
Page 37 and 38: 37 Abstract # 10 Overexpression of
Page 39 and 40: 39 Abstract # 12 Physical Propertie
Page 41 and 42: 41 Abstract # 14 MITOCHONDRIAL RHOM
Page 43 and 44: 43 Tuesday 27 th Neuro Abstracts #
Page 45 and 46: 45 Abstract # 17 Mitochondrial comp
Page 47 and 48: 47 Abstract # 19 Over Expression of
Page 49 and 50: 49 Abstract # 21 Flux control analy
Page 51: 51 Abstract # 23 Developing models
Page 55 and 56: 55 Abstract # 26 Myocardial Fatty A
Page 57 and 58: 57 Time dependence of diet-induced
Page 59 and 60: 59 Thursday 29 th Models, Structure
Page 61 and 62: 61 Abstract # 31 Generation of a Dr
Page 63 and 64: 63 Abstract # 33 The human N-termin
Page 65 and 66: 65 Abstract # 35 Mitochondrial memb
Page 67 and 68: 67 Thursday 29 th Inflammation, Oxi
Page 69 and 70: 69 Abstract # 38 Evidence that fibr
Page 71 and 72: 71 Abstract # 40 Linking placental
Page 73 and 74: 73 Abstract # 42 CVB3-induced oxida
Page 75 and 76: 75 Abstract # 43 Metabolic flexibil
Page 77 and 78: 77 Abstract # 45 Dietary restrictio
Page 79 and 80: 79 Abstract # 47 Insulin sensitivit
Page 81 and 82: 81 Abstract # 49 Mitochondrial toxi
Page 83 and 84: 83 Altered mitochondrial DNA conten

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