|Cardiac vulnerability to ischemia/reperfusion injury drastically increases in late pregnancy.|
|PMID: 22648276 Owner: NLM Status: MEDLINE|
|Although the murine late pregnant (LP) heart is speculated to be a better functioning heart during physiological conditions, the susceptibility of LP hearts to I/R injury is still unknown. The aims of this study were to investigate the cardiac vulnerability of LP rodents to ischemia/reperfusion (I/R) injury and to explore its underlying mechanisms. In vivo female rat hearts [non-pregnant (NP) or LP] or ex vivo Langendorff-perfused mouse hearts were subjected to I/R. The infarct size was approximately fourfold larger in LP animals compared with NP both in vivo and ex vivo. The heart functional recovery was extremely poor in LP mice compared with NP (~10% recovery in LP vs. 80% recovery in NP at the end of reperfusion, P < 0.01). Interestingly, the poor functional recovery and the larger infarct size in LP were partially restored one day post-partum and almost fully restored 1 week post-partum to their corresponding NP levels. Mitochondrial respiratory function and the threshold for opening of the mitochondrial permeability transition pore were significantly lower in LP compared with NP when they both were subjected to myocardial I/R injury [Respiratory control ratio = 1.9 ± 0.1 vs. 4.0 ± 0.5 in NP, P < 0.05; calcium retention capacity (CRC) = 167 ± 10 vs. 233 ± 18 nmol/mg protein in NP, P < 0.01]. Cardiac reactive oxygen species (ROS) generation, as well mitochondrial superoxide production, was approximately twofold higher in LP compared with NP following I/R. The phosphorylation levels of Akt, ERK1/2, and STAT3, but not GSK3β, were significantly reduced in the hearts from LP subjected to I/R. In conclusion, increased mitochondrial ROS generation, decreased CRC as well as impaired activation of Akt/ERK/STAT3 at reperfusion are the possible underlying mechanisms for higher vulnerability of LP hearts to I/R.|
|Jingyuan Li; Soban Umar; Andrea Iorga; Ji-Youn Youn; Yibin Wang; Vera Regitz-Zagrosek; Hua Cai; Mansoureh Eghbali|
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|Type: Journal Article; Research Support, N.I.H., Extramural Date: 2012-05-31|
|Title: Basic research in cardiology Volume: 107 ISSN: 1435-1803 ISO Abbreviation: Basic Res. Cardiol. Publication Date: 2012 Jul|
|Created Date: 2012-05-31 Completed Date: 2012-08-27 Revised Date: 2014-03-05|
Medline Journal Info:
|Nlm Unique ID: 0360342 Medline TA: Basic Res Cardiol Country: Germany|
|Languages: eng Pagination: 271 Citation Subset: IM|
|APA/MLA Format Download EndNote Download BibTex|
Calcium / metabolism
Disease Models, Animal
Glycogen Synthase Kinase 3 / metabolism
Mice, Inbred C57BL
Mitochondria, Heart / metabolism
Mitochondrial Membrane Transport Proteins / metabolism
Mitogen-Activated Protein Kinase 1 / metabolism
Mitogen-Activated Protein Kinase 3 / metabolism
Myocardial Infarction / etiology*, metabolism, pathology, physiopathology
Myocardial Reperfusion Injury / etiology*, metabolism, pathology, physiopathology
Myocardium / metabolism*, pathology
Pregnancy Complications, Cardiovascular / etiology*, metabolism, pathology, physiopathology
Proto-Oncogene Proteins c-akt / metabolism
Reactive Oxygen Species / metabolism
Recovery of Function
STAT3 Transcription Factor / metabolism
Ventricular Function, Left
|HL077440/HL/NHLBI NIH HHS; HL088975/HL/NHLBI NIH HHS; HL089876/HL/NHLBI NIH HHS; HL089876S1/HL/NHLBI NIH HHS; R01 HL077440/HL/NHLBI NIH HHS; R01 HL088975/HL/NHLBI NIH HHS; R01 HL089876/HL/NHLBI NIH HHS; R01 HL103205/HL/NHLBI NIH HHS; T32 GM065823/GM/NIGMS NIH HHS|
|0/Mitochondrial Membrane Transport Proteins; 0/Reactive Oxygen Species; 0/STAT3 Transcription Factor; 0/mitochondrial permeability transition pore; EC 184.108.40.206/Proto-Oncogene Proteins c-akt; EC 220.127.116.11/glycogen synthase kinase 3 beta; EC 18.104.22.168/Mitogen-Activated Protein Kinase 1; EC 22.214.171.124/Mitogen-Activated Protein Kinase 3; EC 126.96.36.199/Glycogen Synthase Kinase 3; SY7Q814VUP/Calcium|
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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