Detail
Článek
Článek online
FT
Medvik - BMČ
  • Je něco špatně v tomto záznamu ?

Selective replacement of mitochondrial DNA increases the cardioprotective effect of chronic continuous hypoxia in spontaneously hypertensive rats

J. Neckář, A. Svatoňová, R. Weissová, Z. Drahota, P. Zajíčková, I. Brabcová, D. Kolář, P. Alánová, J. Vašinová, J. Šilhavý, M. Hlaváčková, K. Tauchmannová, M. Milerová, B. Ošťádal, L. Červenka, J. Žurmanová, M. Kalous, O. Nováková, J. Novotný, M....

. 2017 ; 131 (9) : 865-881. [pub] 20170314

Jazyk angličtina Země Anglie, Velká Británie

Typ dokumentu časopisecké články

Perzistentní odkaz   https://www.medvik.cz/link/bmc17023210

Mitochondria play an essential role in improved cardiac ischaemic tolerance conferred by adaptation to chronic hypoxia. In the present study, we analysed the effects of continuous normobaric hypoxia (CNH) on mitochondrial functions, including the sensitivity of the mitochondrial permeability transition pore (MPTP) to opening, and infarct size (IS) in hearts of spontaneously hypertensive rats (SHR) and the conplastic SHR-mt(BN) strain, characterized by the selective replacement of the mitochondrial genome of SHR with that of the more ischaemia-resistant brown Norway (BN) strain. Rats were adapted to CNH (10% O2, 3 weeks) or kept at room air as normoxic controls. In the left ventricular mitochondria, respiration and cytochrome c oxidase (COX) activity were measured using an Oxygraph-2k and the sensitivity of MPTP opening was assessed spectrophotometrically as Ca(2+)-induced swelling. Myocardial infarction was analysed in anaesthetized open-chest rats subjected to 20 min of coronary artery occlusion and 3 h of reperfusion. The IS reached 68±3.0% and 65±5% of the area at risk in normoxic SHR and SHR-mt(BN) strains, respectively. CNH significantly decreased myocardial infarction to 46±3% in SHR. In hypoxic SHR-mt(BN) strain, IS reached 33±2% and was significantly smaller compared with hypoxic SHR. Mitochondria isolated from hypoxic hearts of both strains had increased detergent-stimulated COX activity and were less sensitive to MPTP opening. The maximum swelling rate was significantly lower in hypoxic SHR-mt(BN) strain compared with hypoxic SHR, and positively correlated with myocardial infarction in all experimental groups. In conclusion, the mitochondrial genome of SHR modulates the IS-limiting effect of adaptation to CNH by affecting mitochondrial energetics and MPTP sensitivity to opening.

Citace poskytuje Crossref.org

000      
00000naa a2200000 a 4500
001      
bmc17023210
003      
CZ-PrNML
005      
20240314092742.0
007      
ta
008      
170720s2017 enk f 000 0|eng||
009      
AR
024    7_
$a 10.1042/CS20170083 $2 doi
035    __
$a (PubMed)28292971
040    __
$a ABA008 $b cze $d ABA008 $e AACR2
041    0_
$a eng
044    __
$a enk
100    1_
$a Neckář, Jan $u Institute of Physiology, Czech Academy of Sciences, Vídeňská 1083, Prague, 14220, Czech Republic jan.neckar@fgu.cas.cz.
245    10
$a Selective replacement of mitochondrial DNA increases the cardioprotective effect of chronic continuous hypoxia in spontaneously hypertensive rats / $c J. Neckář, A. Svatoňová, R. Weissová, Z. Drahota, P. Zajíčková, I. Brabcová, D. Kolář, P. Alánová, J. Vašinová, J. Šilhavý, M. Hlaváčková, K. Tauchmannová, M. Milerová, B. Ošťádal, L. Červenka, J. Žurmanová, M. Kalous, O. Nováková, J. Novotný, M. Pravenec, F. Kolář,
520    9_
$a Mitochondria play an essential role in improved cardiac ischaemic tolerance conferred by adaptation to chronic hypoxia. In the present study, we analysed the effects of continuous normobaric hypoxia (CNH) on mitochondrial functions, including the sensitivity of the mitochondrial permeability transition pore (MPTP) to opening, and infarct size (IS) in hearts of spontaneously hypertensive rats (SHR) and the conplastic SHR-mt(BN) strain, characterized by the selective replacement of the mitochondrial genome of SHR with that of the more ischaemia-resistant brown Norway (BN) strain. Rats were adapted to CNH (10% O2, 3 weeks) or kept at room air as normoxic controls. In the left ventricular mitochondria, respiration and cytochrome c oxidase (COX) activity were measured using an Oxygraph-2k and the sensitivity of MPTP opening was assessed spectrophotometrically as Ca(2+)-induced swelling. Myocardial infarction was analysed in anaesthetized open-chest rats subjected to 20 min of coronary artery occlusion and 3 h of reperfusion. The IS reached 68±3.0% and 65±5% of the area at risk in normoxic SHR and SHR-mt(BN) strains, respectively. CNH significantly decreased myocardial infarction to 46±3% in SHR. In hypoxic SHR-mt(BN) strain, IS reached 33±2% and was significantly smaller compared with hypoxic SHR. Mitochondria isolated from hypoxic hearts of both strains had increased detergent-stimulated COX activity and were less sensitive to MPTP opening. The maximum swelling rate was significantly lower in hypoxic SHR-mt(BN) strain compared with hypoxic SHR, and positively correlated with myocardial infarction in all experimental groups. In conclusion, the mitochondrial genome of SHR modulates the IS-limiting effect of adaptation to CNH by affecting mitochondrial energetics and MPTP sensitivity to opening.
650    _2
$a zvířata $7 D000818
650    _2
$a western blotting $7 D015153
650    _2
$a chronická nemoc $7 D002908
650    _2
$a mitochondriální DNA $x genetika $7 D004272
650    _2
$a respirační komplex IV $x genetika $x metabolismus $7 D003576
650    _2
$a genom mitochondriální $x genetika $7 D054629
650    12
$a hypoxie $7 D000860
650    _2
$a mužské pohlaví $7 D008297
650    _2
$a srdeční mitochondrie $x genetika $x metabolismus $7 D008929
650    _2
$a transportní proteiny mitochondriální membrány $x metabolismus $7 D033681
650    _2
$a mitochondriální proteiny $x genetika $x metabolismus $7 D024101
650    _2
$a infarkt myokardu $x genetika $x metabolismus $x patologie $7 D009203
650    _2
$a reperfuzní poškození myokardu $x genetika $x metabolismus $x patofyziologie $7 D015428
650    _2
$a krysa rodu Rattus $7 D051381
650    _2
$a potkani inbrední BN $7 D011914
650    _2
$a potkani inbrední SHR $7 D011918
650    _2
$a potkani transgenní $7 D055647
650    _2
$a polymerázová řetězová reakce s reverzní transkripcí $7 D020133
655    _2
$a časopisecké články $7 D016428
700    1_
$a Svatoňová, Anna $u Institute of Physiology, Czech Academy of Sciences, Vídeňská 1083, Prague, 14220, Czech Republic.
700    1_
$a Weissová, Romana $u Institute of Physiology, Czech Academy of Sciences, Vídeňská 1083, Prague, 14220, Czech Republic. Department of Cell Biology, Faculty of Science, Charles Univesity, Viničná 7, Prague, 12800, Czech Republic.
700    1_
$a Drahota, Zdeněk, $d 1932- $u Institute of Physiology, Czech Academy of Sciences, Vídeňská 1083, Prague, 14220, Czech Republic. $7 jn20000400531
700    1_
$a Zajíčková, Pavlína $u Institute of Physiology, Czech Academy of Sciences, Vídeňská 1083, Prague, 14220, Czech Republic.
700    1_
$a Brabcová, Iveta $u Deparment of Physiology, Faculty of Science, Charles University, Viničná 7, Prague, 12800, Czech Republic.
700    1_
$a Kolář, David $u Deparment of Physiology, Faculty of Science, Charles University, Viničná 7, Prague, 12800, Czech Republic.
700    1_
$a Alánová, Petra $u Institute of Physiology, Czech Academy of Sciences, Vídeňská 1083, Prague, 14220, Czech Republic. $7 gn_A_00003295
700    1_
$a Vašinová, Jana $u Institute of Physiology, Czech Academy of Sciences, Vídeňská 1083, Prague, 14220, Czech Republic.
700    1_
$a Šilhavý, Jan $u Institute of Physiology, Czech Academy of Sciences, Vídeňská 1083, Prague, 14220, Czech Republic.
700    1_
$a Hlaváčková, Markéta $u Institute of Physiology, Czech Academy of Sciences, Vídeňská 1083, Prague, 14220, Czech Republic.
700    1_
$a Tauchmannová, Kateřina $u Institute of Physiology, Czech Academy of Sciences, Vídeňská 1083, Prague, 14220, Czech Republic.
700    1_
$a Milerová, Marie $u Institute of Physiology, Czech Academy of Sciences, Vídeňská 1083, Prague, 14220, Czech Republic.
700    1_
$a Ošťádal, Bohuslav $u Institute of Physiology, Czech Academy of Sciences, Vídeňská 1083, Prague, 14220, Czech Republic.
700    1_
$a Červenka, Luděk $u Centre for Experimental Medicine, Institute for Clinical and Experimental Medicine, Vídeňská 1958/9, Prague, 14021, Czech Republic.
700    1_
$a Žurmanová, Jitka $u Deparment of Physiology, Faculty of Science, Charles University, Viničná 7, Prague, 12800, Czech Republic.
700    1_
$a Kalous, Martin $u Department of Cell Biology, Faculty of Science, Charles Univesity, Viničná 7, Prague, 12800, Czech Republic.
700    1_
$a Nováková, Olga $u Institute of Physiology, Czech Academy of Sciences, Vídeňská 1083, Prague, 14220, Czech Republic. Deparment of Physiology, Faculty of Science, Charles University, Viničná 7, Prague, 12800, Czech Republic.
700    1_
$a Novotný, Jiří $u Deparment of Physiology, Faculty of Science, Charles University, Viničná 7, Prague, 12800, Czech Republic.
700    1_
$a Pravenec, Michal $u Institute of Physiology, Czech Academy of Sciences, Vídeňská 1083, Prague, 14220, Czech Republic.
700    1_
$a Kolář, František $u Institute of Physiology, Czech Academy of Sciences, Vídeňská 1083, Prague, 14220, Czech Republic.
773    0_
$w MED00009494 $t Clinical science (1979) $x 1470-8736 $g Roč. 131, č. 9 (2017), s. 865-881
856    41
$u https://pubmed.ncbi.nlm.nih.gov/28292971 $y Pubmed
910    __
$a ABA008 $b sig $c sign $y a $z 0
990    __
$a 20170720 $b ABA008
991    __
$a 20240314092736 $b ABA008
999    __
$a ok $b bmc $g 1238891 $s 984123
BAS    __
$a 3
BAS    __
$a PreBMC
BMC    __
$a 2017 $b 131 $c 9 $d 865-881 $e 20170314 $i 1470-8736 $m Clinical science (1979) $n Clin Sci (Lond) $x MED00009494
LZP    __
$a Pubmed-20170720

Najít záznam

Citační ukazatele

Možnosti archivace