ArticleJournal of cellular and molecular medicine
Expression of phospholipase D isozymes in scar and viable tissue in congestive heart failure due to myocardial infarction.
Article in Journal of cellular and molecular medicine. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 26 citations in OpenAlex.
- PLD2 deletion ameliorates sepsis-induced cardiomyopathy by suppressing cardiomyocyte pyroptosis via the NLRP3/caspase 1/GSDMD pathway.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024Article
- Phospholipids, the Masters in the Shadows during Healing after Acute Myocardial Infarction.International journal of molecular sciences · 2023Review
- Multimodal MALDI Imaging Mass Spectrometry Reveals Spatially Correlated Lipid and Protein Changes in Mouse Heart with Acute Myocardial Infarction.Journal of the American Society for Mass Spectrometry · 2020Article
- Enhanced Integrin Activation of PLD2-Deficient Platelets Accelerates Inflammation after Myocardial Infarction.International journal of molecular sciences · 2020Article
- Phospholipase D and Its Essential Role in Cancer.Molecules and cells · 2017Review
- Physiological and pathophysiological roles for phospholipase D.Journal of lipid research · 2015Review
- Downregulation of neuronal sodium channel subunits Nav1.1 and Nav1.6 in the sinoatrial node from volume-overloaded heart failure rat.Pflugers Archiv : European journal of physiology · 2007Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The phospholipase D (PLD) associated with the cardiac sarcolemmal (SL) membrane hydrolyses phosphatidylcholine to produce phosphatidic acid, an important phospholipid signaling molecule known to influence cardiac function. The present study was undertaken to examine PLD isozyme mRNA expression, protein contents and activities in congestive heart failure (CHF) subsequent to myocardial infarction (MI). MI was induced in rats by occlusion of the left anterior descending coronary artery. At 8 weeks after the surgical procedure, hemodynamic assessment revealed that these experimental rats were at a moderate stage of CHF. Semi-quantitative reverse transcriptase-polymerase chain reaction revealed that PLD1 and PLD2 mRNA amounts were unchanged in viable left ventricular (LV) tissue of the failing heart. Furthermore, this technique demonstrated the presence of PLD1 and PLD2 mRNA in the scar tissue. While SL PLD1 and PLD2 protein contents were elevated in the viable LV tissue of the failing heart, SL PLD1 activity was significantly decreased, whereas SL PLD2 activity was significantly increased. On the other hand, although PLD1 protein was undetectable, PLD2 protein and activity were detected in the scar tissue. Our findings suggest that differential changes in PLD isozymes may contribute to the pathophysiology of CHF and may also be involved in the processes of scar remodeling.
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