ACELL August 46/2
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چکیده
Golovina, Vera A. Cell proliferation is associated with enhanced capacitative Ca21 entry in human arterial myocytes. Am. J. Physiol. 277 (Cell Physiol. 46): C343–C349, 1999.—Depletion of Ca21 stores in the sarcoplasmic reticulum (SR) activates extracellular Ca21 influx via capacitative Ca21 entry (CCE). Here, CCE levels in proliferating and growth-arrested human pulmonary artery smooth muscle cells (PASMCs) were compared by digital imaging fluorescence microscopy. Resting cytosolic free Ca21 concentration ([Ca]cyt) in proliferating PASMCs was twofold higher than that in growth-arrested cells. Cyclopiazonic acid (CPA; 10 μM), which inhibits SR Ca21-ATPase and depletes inositol 1,4,5-trisphosphate-sensitive Ca21 stores, transiently increased [Ca]cyt in the absence of extracellular Ca21. The addition of 1.8 mM Ca21 to the extracellular solution in the presence of CPA induced large increases in [Ca]cyt, indicative of CCE. The CPA-induced SR Ca21 release in proliferating PASMCs was twofold higher than that in growth-arrested cells, whereas the transient rise of [Ca]cyt due to CCE was fivefold greater in proliferating cells. CCE was insensitive to nifedipine but was significantly inhibited by 50 mM K1, which reduces the driving force for Ca21 influx, and by 0.5 mM Ni21, a putative blocker of store-operated Ca21 channels. These data show that augmented CCE is associated with proliferation of human PASMCs and may be involved in stimulating and maintaining cell growth.
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ACELL August 46/2
JOHN M. PARK,1 ROSALYN M. ADAM,1 CRAIG A. PETERS,1 PAUL D. GUTHRIE,1 ZIJIE SUN,2 MICHAEL KLAGSBRUN,3 AND MICHAEL R. FREEMAN3 1Urologic Laboratory, Department of Urology, 3Laboratory for Surgical Research, Children’s Hospital, and Department of Surgery, Harvard Medical School, Boston, Massachusetts 02115; and 2Departments of Surgery and Genetics, Stanford University School of Medicine, Stanford,...
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ESTHER TITOS,1 NAN CHIANG,2 CHARLES N. SERHAN,2 MARIO ROMANO,3 JOAN GAYA,4 GLORIA PUEYO,5 AND JOAN CLÀRIA1 1DNA Unit and 4Hormonal Laboratory, Institut d’Investigacions Biomèdiques August Pi i Sunyer, Hospital Clı́nic and 5Quı́mica Farmacéutica Bayer (Consumer Care Division), Barcelona 08036, Spain; 2Center for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Periop...
متن کاملACELL October 46/4
NABENDU S. CHATTERJEE,1 CHANDIRA K. KUMAR,1 ALVARO ORTIZ,1 STANLEY A. RUBIN,2 AND HAMID M. SAID1 1Medical Research Service, Veterans Affairs Medical Center, Long Beach 90822, and Department of Medicine and Physiology/Biophysics, University of California School of Medicine, Irvine 92697; and 2Veterans Affairs West Los Angeles, Los Angeles 90073, and Department of Medicine, University of Californ...
متن کاملACELL August 46/2
Tonkonogi, M., and K. Sahlin. Actively phosphorylating mitochondria are more resistant to lactic acidosis than inactive mitochondria. Am. J. Physiol. 277 (Cell Physiol. 46): C288–C293, 1999.—Oxidative phosphorylation of isolated rat skeletal muscle mitochondria after exposure to lactic acidosis in either phosphorylating or nonphosphorylating states has been evaluated. Mitochondrial respiration ...
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