Mechanical stress stimulates phospholipase C activity and intracellular calcium ion levels in neonatal rat cardiomyocytes |
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Authors: | Ruwhof C van Wamel J T Noordzij L A Aydin S Harper J C van der Laarse A |
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Affiliation: | Department of Cardiology, Leiden University Medical Center, Leiden, The Netherlands. |
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Abstract: | To investigate how mechanical stress is sensed by cardiomyocytes and translated to cardiac hypertrophy, cardiomyocytes were subjected to stretch while measuring phospholipase C (PLC) and phospholipase D (PLD) activities and levels of intracellular calcium ions ([Ca2+]i) and pH.In stretched cardiomyocytes, PLC activity increased 2-fold after 30 min, whereas PLD activity hardly increased at all. Mechanical stress induced by prodding or by cell stretch increased [Ca2+](i)by a factor 5.2 and 4, respectively. Gadolinium chloride (stretch-activated channel blocker) attenuated the prodding-induced and stretch-induced [Ca2+](i)rise by about 50%. Blockade of ryanodine receptors by a combination of Ruthenium Red and procaine reduced the [Ca2+](i)rise only partially. Diltiazem (L-type Ca2+ channel antagonist) blocked the prodding-induced [Ca2+](i)rise completely, and reduced the stretch-induced [Ca2+](i)rise by about 50%. The stretch-induced [Ca2+](i)rise was unaffected by U73122, an inhibitor of PLC activity. Stretch did not cause cellular alkalinization.In conclusion, in cardiomyocytes, PLC and [Ca2+](i)levels are involved in the stretch-induced signal transduction, whereas PLD plays apparently no role. The stretch-induced rise in [Ca2+](i)in cardiomyocytes is most probably caused by [Ca2+](i)influx through L-type Ca2+ channels and stretch-activated channels, leading to Ca2+-induced Ca2+ -release from the SR via the ryanodine receptor. |
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