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Departments of 2 Pathology and 1 Pharmacology, College of Medicine, University of South Alabama, Mobile, Alabama 36688
Activation of
Ca2+ 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
Ca2+ entry regulating cell shape
is unknown. We hypothesized that activation of store-operated
Ca2+ channels (SOCs) is sufficient
to promote cell shape change necessary for these processes. SOC
activation in rat pulmonary arterial endothelial cells increased free
cytosolic Ca2+ 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
Ca2+ 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 Ca2+ 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)
Ca2+ 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.
lung; inflammation; permeability; F-actin; angiogenesis
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