Mechanical stress stimulates phospholipase C activity and intracellular calcium ion levels in neonatal rat cardiomyocytes

Citation
C. Ruwhof et al., Mechanical stress stimulates phospholipase C activity and intracellular calcium ion levels in neonatal rat cardiomyocytes, CELL CALC, 29(2), 2001, pp. 73-83
Citations number
49
Categorie Soggetti
Cell & Developmental Biology
Journal title
CELL CALCIUM
ISSN journal
01434160 → ACNP
Volume
29
Issue
2
Year of publication
2001
Pages
73 - 83
Database
ISI
SICI code
0143-4160(200102)29:2<73:MSSPCA>2.0.ZU;2-B
Abstract
To investigate how mechanical stress is sensed by cardiomyocytes and transl ated to cardiac hypertrophy, cardiomyocytes were subjected to stretch while measuring phospholipase C (PLC) and phospholipase D (PLD) activities and l evels of intracellular calcium ions ([Ca2+](i)) and pH. In stretched cardiomyocytes, PLC activity increased 2-fold after 30 min, wh ereas PLD activity hardly increased at all. Mechanical stress induced by pr odding or by cell stretch increased [Ca2+](i) by a factor 5.2 and 4, respec tively. Gadolinium chloride (stretch-activated channel blocker) attenuated the prodding-induced and stretch-induced [Ca2+](i) rise by about 50%. Block ade of ryanodine receptors by a combination of Ruthenium Red and procaine r educed the [Ca2+](i) rise only partially. Diltiazem (L-type Ca2+ channel an tagonist) blocked the prodding-induced [Ca2+](i) rise completely, and reduc ed the stretch-induced [Ca2+](i) rise by about 50%. The stretch-induced [Ca 2+](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 ro le. The stretch-induced rise in [Ca2+](i) in cardiomyocytes is most probabl y caused by Ca2+ influx through L-type Ca2+ channels and stretch-activated channels, leading to Ca2+-induced Ca2+-release from the SR via the ryanodin e receptor. (C) 2001 Harcourt Publishers Ltd.