Store-operated calcium entry promotes shape change in pulmonary endothelial cells expressing Trp1

• Published in: American journal of physiology. Lung cellular and molecular physiology 1998-09, Vol.275 (3), p.L574
• Main Authors: Moore, Timothy M, Brough, George H, Babal, Paul, Kelly, John J, Li, Ming, Stevens, Troy
• Format: Article
• Language: English
• ISSN: 1522-1504

Activation of Ca entry is known to produce endothelial cell shape change, leading to increased permeability, leukocyte migration, and initiation of angiogenesis in conduit-vessel endothelial cells. The mode of Ca entry regulating cell shape is unknown. We hypothesized that activation of store-operated Ca channels (SOCs) is sufficient to promote cell shape change necessary for these processes. SOC activation in rat pulmonary arterial endothelial cells increased free cytosolic Ca that was dependent on a membrane current having a net inward component of 5.45 ± 0.90 pA/pF at -80 mV. Changes in endothelial cell shape accompanied SOC activation and were dependent on Ca entry-induced reconfiguration of peripheral (cortical) filamentous actin (F-actin). Because the identity of pulmonary endothelial SOCs is unknown, but mammalian homologues of the Drosophila melanogaster transient receptor potential ( trp) gene have been proposed to form Ca entry channels in nonexcitable cells, we performed RT-PCR using Trp oligonucleotide primers in both rat and human pulmonary arterial endothelial cells. Both cell types were found to express Trp1, but neither expressed Trp3 nor Trp6. Our study indicates that 1) Ca entry in pulmonary endothelial cells through SOCs produces cell shape change that is dependent on site-specific rearrangement of the microfilamentous cytoskeleton and 2) Trp1 may be a component of pulmonary endothelial SOCs.