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Abstract
We compared the Ca2+ responses to reactive oxygen species (ROS) between mouse endothelial cells derived from large-sized arteries, aortas (aortic ECs), and small-sized arteries, mesenteric arteries (MAECs). Application of hydrogen peroxide (H2O2) caused an increase in cytosolic Ca2+ levels ([Ca2+]i) in both cell types. The [Ca2+]i rises diminished in the presence of U73122, a phospholipase C inhibitor, or Xestospongin C (XeC), an inhibitor for inositol-1,4,5-trisphosphate (IP3) receptors. Removal of Ca2+ from the bath also decreased the [Ca2+]i rises in response to H2O2. In addition, treatment of endothelial cells with H2O2 reduced the [Ca2+]i responses to subsequent challenge of ATP. The decreased [Ca2+]i responses to ATP were resulted from a pre-depletion of intracellular Ca2+ stores by H2O2. Interestingly, we also found that Ca2+ store depletion was more sensitive to H2O2 treatment in endothelial cells of mesenteric arteries than those of aortas. Hypoxanthine-xanthine oxidase (HX-XO) was also found to induce [Ca2+]i rises in both types of endothelial cells, the effect of which was mediated by superoxide anions and H2O2 but not by hydroxyl radical. H2O2 contribution in HX-XO-induced [Ca2+]i rises were more significant in endothelial cells from mesenteric arteries than those from aortas. In summary, H2O2 could induce store Ca2+ release via phospholipase C-IP3 pathway in endothelial cells. Resultant emptying of intracellular Ca2+ stores contributed to the reduced [Ca2+]i responses to subsequent ATP challenge. The [Ca2+]i responses were more sensitive to H2O2 in endothelial cells of small-sized arteries than those of large-sized arteries.
Highlights
Vascular endothelial cells in vivo are constantly exposed to reactive oxygen species (ROS) that are released from neutrophils, macrophages, and vascular smooth muscle cells [1,2]
The effect of H2O2 on [Ca2+]i was investigated in aortic ECs and mesenteric artery endothelial cells (MAECs)
H2O2 at 5 mM caused marked [Ca2+]i rises in both types of cells that were bathed in normal physiological saline solution (N-PSS) containing 1 mM Ca2+ (Figure 1A–1D)
Summary
Vascular endothelial cells in vivo are constantly exposed to ROS that are released from neutrophils, macrophages, and vascular smooth muscle cells [1,2]. The [Ca2+]i rises could result from ROS actions on the plasma membrane ion channels [11], IP3 production [7,12], IP3 receptors [13,14], and/or endoplasmic reticulum Ca2+-ATPase [6] In addition to their direct action on endothelial [Ca2+]i, ROS treatment may alter the [Ca2+]i responses of endothelial cells to a variety of physiological agonists including ATP and bradykinin [7,9,12]. The role of ROS on [Ca2+]i in endothelial cells of small-sized arteries has received little attention [but see 8] It is unclear whether there is any difference in ROSinduced [Ca2+]i responses in endothelial cells from different-sized arteries. The Ca2+ store depletion was more sensitive to H2O2 in endothelial cells of small-sized arteries than those of large-sized arteries
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