Phospholipase A2is not responsible for lysophosphatidylcholine-induced damage in cardiomyocytes
| Autor: | Hiroko Hashizume, Yasushi Abiko, Chun-Yang Xiao, Min Chen |
|---|---|
| Rok vydání: | 1998 |
| Předmět: |
Male
Phosphodiesterase Inhibitors Physiology Phospholipases A Calcium in biology Rats Sprague-Dawley chemistry.chemical_compound Phospholipase A2 Physiology (medical) medicine Animals Myocyte Cell damage Cells Cultured Unsaturated fatty acid Cell Size biology Myocardium Lysophosphatidylcholines medicine.disease Rats Cell biology Phospholipases A2 Lysophosphatidylcholine Biochemistry chemistry Enzyme inhibitor Fatty Acids Unsaturated biology.protein Calcium lipids (amino acids peptides and proteins) Cardiology and Cardiovascular Medicine Intracellular Signal Transduction |
| Zdroj: | American Journal of Physiology-Heart and Circulatory Physiology. 275:H1782-H1787 |
| ISSN: | 1522-1539 0363-6135 |
| DOI: | 10.1152/ajpheart.1998.275.5.h1782 |
| Popis: | Lysophosphatidylcholine (LPC) is known to increase the intracellular concentration of Ca2+([Ca2+]i), leading to cell damage. In the present study we examined whether LPC activates phospholipase A2(PLA2) and whether the activation of PLA2is responsible for the LPC-induced cell damage in isolated rat cardiomyocytes. LPC (15 μM) produced an increase in [Ca2+]i, a change in cell shape from rod to round, and the release of creatine kinase (CK) accompanied by a significant elevation of the cellular level of nonesterified fatty acids (NEFA), especially arachidonic acid. Three PLA2inhibitors, 7,7-dimethyl-(5 Z,8 Z)-eicosadienoic acid (DEDA), 3-(4-octadecylbenzoyl)acrylic acid (OBAA), and manoalide, attenuated the LPC-induced accumulation of unsaturated NEFA to a similar degree. Nevertheless, whereas both DEDA and OBAA attenuated the LPC-induced increase in [Ca2+]i, change in cell shape, and release of CK, manoalide attenuated none of them. In the Ca2+-free solution, LPC did not increase [Ca2+]iwith significantly less accumulation of NEFA, but it changed the cell shape from rod to round and increased the release of CK. These results suggest that exogenous LPC increases the PLA2activity, which, however, may not be responsible for the LPC-induced damage in cardiomyocytes. |
| Databáze: | OpenAIRE |
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