Cell proliferation is associated with enhanced capacitative Ca(2+) entry in human arterial myocytes

• Published in: The American journal of physiology Vol. 277; no. 2; p. C343
• Main Author: Golovina, V A
• Format: Journal Article
• Language: English
• Published: United States 01.08.1999
• Subjects: Calcium - metabolism; Cell Division - drug effects; Cell Division - physiology; Cytoplasm - metabolism; Enzyme Inhibitors - pharmacology; Fluorescent Dyes; Fura-2; Humans; Indoles - pharmacology; Manganese - pharmacology; Muscle, Smooth, Vascular - cytology; Muscle, Smooth, Vascular - drug effects; Muscle, Smooth, Vascular - metabolism; Nickel - pharmacology; Osmolar Concentration; Potassium - pharmacology; Pulmonary Artery - cytology; Pulmonary Artery - drug effects; Pulmonary Artery - metabolism; Sarcoplasmic Reticulum - metabolism
• ISSN: 0002-9513
• DOI: 10.1152/ajpcell.1999.277.2.c343

Depletion of Ca(2+) stores in the sarcoplasmic reticulum (SR) activates extracellular Ca(2+) influx via capacitative Ca(2+) 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 Ca(2+) concentration ([Ca(2+)](cyt)) in proliferating PASMCs was twofold higher than that in growth-arrested cells. Cyclopiazonic acid (CPA; 10 microM), which inhibits SR Ca(2+)-ATPase and depletes inositol 1,4,5-trisphosphate-sensitive Ca(2+) stores, transiently increased [Ca(2+)](cyt) in the absence of extracellular Ca(2+). The addition of 1.8 mM Ca(2+) to the extracellular solution in the presence of CPA induced large increases in [Ca(2+)](cyt), indicative of CCE. The CPA-induced SR Ca(2+) release in proliferating PASMCs was twofold higher than that in growth-arrested cells, whereas the transient rise of [Ca(2+)](cyt) due to CCE was fivefold greater in proliferating cells. CCE was insensitive to nifedipine but was significantly inhibited by 50 mM K(+), which reduces the driving force for Ca(2+) influx, and by 0.5 mM Ni(2+), a putative blocker of store-operated Ca(2+) channels. These data show that augmented CCE is associated with proliferation of human PASMCs and may be involved in stimulating and maintaining cell growth.