• Something wrong with this record ?

Antioxidant tempol suppresses heart cytosolic phospholipase A2α stimulated by chronic intermittent hypoxia

P. Míčová, M. Klevstig, K. Holzerová, M. Vecka, J. Žurmanová, J. Neckář, F. Kolář, O. Nováková, J. Novotný, M. Hlaváčková,

. 2017 ; 95 (8) : 920-927. [pub] 20170430

Language English Country Canada

Document type Journal Article

Persistent link   https://www.medvik.cz/link/bmc18025059

Adaptation to chronic intermittent hypoxia (CIH) is associated with reactive oxygen species (ROS) generation implicated in the improved cardiac tolerance against acute ischemia-reperfusion injury. Phospholipases A2 (PLA2s) play an important role in cardiomyocyte phospholipid metabolism influencing membrane homeostasis. Here we aimed to determine the effect of CIH (7000 m, 8 h/day, 5 weeks) on the expression of cytosolic PLA2 (cPLA2α), its phosphorylated form (p-cPLA2α), calcium-independent (iPLA2), and secretory (sPLA2IIA) at protein and mRNA levels, as well as fatty acids (FA) profile in left ventricular myocardium of adult male Wistar rats. Chronic administration of antioxidant tempol was used to verify the ROS involvement in CIH effect on PLA2s expression and phospholipid FA remodeling. While CIH did not affect PLA2s mRNA levels, it increased the total cPLA2α protein in cytosol and membranes (by 191% and 38%, respectively) and p-cPLA2α (by 23%) in membranes. On the contrary, both iPLA2 and sPLA2IIA were downregulated by CIH. CIH further decreased phospholipid n-6 polyunsaturated FA (PUFA) and increased n-3 PUFA proportion. Tempol treatment prevented only CIH-induced cPLA2α up-regulation and its phosphorylation on Ser505. Our results show that CIH diversely affect myocardial PLA2s and suggest that ROS are responsible for the activation of cPLA2α under these conditions.

References provided by Crossref.org

000      
00000naa a2200000 a 4500
001      
bmc18025059
003      
CZ-PrNML
005      
20180711102708.0
007      
ta
008      
180709s2017 xxc f 000 0|eng||
009      
AR
024    7_
$a 10.1139/cjpp-2017-0022 $2 doi
035    __
$a (PubMed)28459156
040    __
$a ABA008 $b cze $d ABA008 $e AACR2
041    0_
$a eng
044    __
$a xxc
100    1_
$a Míčová, Petra $u a Department of Physiology, Faculty of Science, Charles University, Prague, Czech Republic.
245    10
$a Antioxidant tempol suppresses heart cytosolic phospholipase A2α stimulated by chronic intermittent hypoxia / $c P. Míčová, M. Klevstig, K. Holzerová, M. Vecka, J. Žurmanová, J. Neckář, F. Kolář, O. Nováková, J. Novotný, M. Hlaváčková,
520    9_
$a Adaptation to chronic intermittent hypoxia (CIH) is associated with reactive oxygen species (ROS) generation implicated in the improved cardiac tolerance against acute ischemia-reperfusion injury. Phospholipases A2 (PLA2s) play an important role in cardiomyocyte phospholipid metabolism influencing membrane homeostasis. Here we aimed to determine the effect of CIH (7000 m, 8 h/day, 5 weeks) on the expression of cytosolic PLA2 (cPLA2α), its phosphorylated form (p-cPLA2α), calcium-independent (iPLA2), and secretory (sPLA2IIA) at protein and mRNA levels, as well as fatty acids (FA) profile in left ventricular myocardium of adult male Wistar rats. Chronic administration of antioxidant tempol was used to verify the ROS involvement in CIH effect on PLA2s expression and phospholipid FA remodeling. While CIH did not affect PLA2s mRNA levels, it increased the total cPLA2α protein in cytosol and membranes (by 191% and 38%, respectively) and p-cPLA2α (by 23%) in membranes. On the contrary, both iPLA2 and sPLA2IIA were downregulated by CIH. CIH further decreased phospholipid n-6 polyunsaturated FA (PUFA) and increased n-3 PUFA proportion. Tempol treatment prevented only CIH-induced cPLA2α up-regulation and its phosphorylation on Ser505. Our results show that CIH diversely affect myocardial PLA2s and suggest that ROS are responsible for the activation of cPLA2α under these conditions.
650    _2
$a zvířata $7 D000818
650    _2
$a antioxidancia $x farmakologie $7 D000975
650    _2
$a chronická nemoc $7 D002908
650    _2
$a cyklické N-oxidy $x farmakologie $7 D003497
650    _2
$a mastné kyseliny $x metabolismus $7 D005227
650    _2
$a regulace genové exprese enzymů $x účinky léků $7 D015971
650    _2
$a fosfolipasy A2, skupina IV $x genetika $x metabolismus $7 D054513
650    _2
$a hypoxie $x enzymologie $x metabolismus $7 D000860
650    _2
$a mužské pohlaví $7 D008297
650    _2
$a fosforylace $x účinky léků $7 D010766
650    _2
$a krysa rodu Rattus $7 D051381
650    _2
$a potkani Wistar $7 D017208
650    _2
$a reaktivní formy kyslíku $x metabolismus $7 D017382
650    _2
$a spinové značení $7 D013113
655    _2
$a časopisecké články $7 D016428
700    1_
$a Klevstig, Martina $u b Institute of Physiology, Czech Academy of Sciences, Prague, Czech Republic.
700    1_
$a Holzerová, Kristýna $u a Department of Physiology, Faculty of Science, Charles University, Prague, Czech Republic. b Institute of Physiology, Czech Academy of Sciences, Prague, Czech Republic.
700    1_
$a Vecka, Marek $u c 4th Department of Internal Medicine, 1st Faculty of Medicine, Charles University and General Teaching Hospital in Prague, Czech Republic.
700    1_
$a Žurmanová, Jitka $u a Department of Physiology, Faculty of Science, Charles University, Prague, Czech Republic.
700    1_
$a Neckář, Jan $u b Institute of Physiology, Czech Academy of Sciences, Prague, Czech Republic.
700    1_
$a Kolář, František $u b Institute of Physiology, Czech Academy of Sciences, Prague, Czech Republic.
700    1_
$a Nováková, Olga $u a Department of Physiology, Faculty of Science, Charles University, Prague, Czech Republic. b Institute of Physiology, Czech Academy of Sciences, Prague, Czech Republic.
700    1_
$a Novotný, Jiří $u a Department of Physiology, Faculty of Science, Charles University, Prague, Czech Republic.
700    1_
$a Hlaváčková, Markéta $u a Department of Physiology, Faculty of Science, Charles University, Prague, Czech Republic. b Institute of Physiology, Czech Academy of Sciences, Prague, Czech Republic.
773    0_
$w MED00001020 $t Canadian journal of physiology and pharmacology $x 1205-7541 $g Roč. 95, č. 8 (2017), s. 920-927
856    41
$u https://pubmed.ncbi.nlm.nih.gov/28459156 $y Pubmed
910    __
$a ABA008 $b sig $c sign $y a $z 0
990    __
$a 20180709 $b ABA008
991    __
$a 20180711102959 $b ABA008
999    __
$a ok $b bmc $g 1317190 $s 1021980
BAS    __
$a 3
BAS    __
$a PreBMC
BMC    __
$a 2017 $b 95 $c 8 $d 920-927 $e 20170430 $i 1205-7541 $m Canadian journal of physiology and pharmacology $n Can J Physiol Pharmacol $x MED00001020
LZP    __
$a Pubmed-20180709

Find record

Citation metrics

Archiving options