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Cited by 44Cardiac Ischemia and ReperfusionEicosanoids and Hypertension PharmacologyFatty Acid Research and Health

Group V secretory phospholipase A2 plays a pathogenic role in myocardial ischaemia–reperfusion injury

Yano, Toshiaki, Fujioka, Daisuke, Saito, Yukio, Kobayashi, Tsuyoshi, Nakamura, Takamitsu, Obata, Jun-ei, Kawabata, Kenichi, Watanabe, Kazuhiro +4 more·2011·Cardiovascular Research
DOI 10.1093/cvr/cvq399
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Abstract

AIMS: Group V secretory phospholipase A(2) (sPLA(2)-V) is highly expressed in the heart. This study examined (i) the role of sPLA(2)-V in myocardial ischaemia-reperfusion (I/R) injury and (ii) the cooperative action of sPLA(2)-V and cytosolic PLA(2) (cPLA(2)) in myocardial I/R injury, using sPLA(2)-V knockout (sPLA(2)V(-/-)) mice. METHODS AND RESULTS: Myocardial I/R injury was created by 1 h ligation of the left anterior descending coronary artery, followed by 24 h of reperfusion. The sPLA(2)V(-/-) mice had a 44% decrease in myocardial infarct size, a preservation of echocardiographic LV function (%fractional shortening: 40 ± 3.5 vs. 21 ± 4.6, respectively), and lower content of leucotriene B(4) (LTB(4)) and thromboxane B(2) (TXB(2)) (40 and 37% lower, respectively) in the ischaemic myocardium after I/R compared with wild-type (WT) mice. Intraperitoneal administration of AACOCF3 or MAFP, inhibitors of cPLA(2) activity, decreased myocardial infarct size and myocardial content of LTB(4) and TXB(2) in both genotyped mice. The decrease in myocardial infarct size and content of LTB(4) and TXB(2) after cPLA(2) inhibitor administration was greater in WT mice than in sPLA(2)V(-/-) mice. I/R increased phosphorylation of extracellular signal-related kinase 1/2, c-Jun N-terminal kinase, and p38 mitogen-activated protein kinases in the ischaemic myocardium in association with cPLA(2) phosphorylation. The I/R-induced increase in the phosphorylation of p38 and cPLA(2) was less in sPLA(2)-V(-/-) mice than in WT mice. Pretreatment with the p38 inhibitor SB202190 suppressed an increase in cPLA(2) phosphorylation after I/R in WT mice. CONCLUSION: sPLA(2)-V plays an important role in the pathogenesis of myocardial I/R injury partly in concert with the activation of cPLA(2).

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  • A few kinases participate in phosphorylation of TBX3, such as AKT3 at S720, cyclin A-CDK2 at either S190 or S354, p38 MAP kinase at S692, and AKT1 is also involved.

    “Moreover, a few kinases participate in phosphorylation of TBX3, such as AKT3 at S720, cyclin A-CDK2 at either S190 or S354, p38 MAP kinase at S692, and AKT1 is also involved54,59–61.”

    From Proteostatic reactivation of the developmental transcription factor TBX3 drives BRAF/MAPK-mediated tumorigenesis (2024) · cites this paper as [60]

    Section 3.7 discusses phosphorylation of p38 and cPLA2 in ischaemic myocardium, not phosphorylation of TBX3. Searches for TBX3 and the specified kinases and phosphorylation sites found no passage addressing the claim in our copy; no page number was provided for the section. (LLM, conf=0.77)

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Cited by

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Authors
Yano, T., Fujioka, D., Saito, Y., Kobayashi, T., Nakamura, T., Obata, J.-E., Kawabata, K., Watanabe, K., Watanabe, Y., Mishina, H., Tamaru, S., & Kugiyama, K.
Affiliations
University of Yamanashi (JP)
Corresponding author
Kugiyama, Kiyotaka
ORCID
Venue
Cardiovascular Research
Publisher
Oxford University Press (OUP)
Published
2010-12-17
Volume
90
Issue
2
Pages
335-343
ISSN
  • 0008-6363 (ISSN-L)
  • 1755-3245
DOI
10.1093/cvr/cvq399
OpenAlex
W2081762160
Cited by
44
References
0
Citations by year
2026: 1 · 2025: 3 · 2024: 1 · 2023: 6 · 2022: 2 · 2021: 1 · 2020: 3 · 2019: 1 · 2018: 2 · 2017: 3 · 2016: 2 · 2015: 3 · 2014: 4 · 2013: 4 · 2012: 7
FWCI
2.61
Type
journal article
Language
en
Open access
closed
Locations
  • Cardiovascular Research (publishedVersion)
  • PubMed (publishedVersion)
Funders
Japan Society for the Promotion of Science (15012222, 19390209, 22390158)
Topics
  • Health Sciences › Medicine › Pathology and Forensic Medicine › Cardiac Ischemia and Reperfusion
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Eicosanoids and Hypertension Pharmacology
  • Health Sciences › Nursing › Nutrition and Dietetics › Fatty Acid Research and Health
Keywords
myocardial ischemia-reperfusion injury, cytosolic phospholipase A2, myocardial infarct size, thromboxane B2, p38 MAPK, c-Jun N-terminal kinase, AACOCF3
MeSH terms
Animals, Cells, Cultured, Echocardiography, Enzyme Inhibitors, Leukotriene B4, Male, Mice, Inbred C57BL, Myocardial Infarction, Myocardium, Thromboxane B2, Myocardial Reperfusion Injury, Arachidonic Acid, Mice, Knockout, In Situ Nick-End Labeling, Myocytes, Cardiac, Mice, Caspase 3, Caspase 8, Group V Phospholipases A2, Group IV Phospholipases A2

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