Journal
AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY
Volume 297, Issue 1, Pages C169-C178Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpcell.00674.2008
Keywords
paracellular transport; ascorbate transport; anion channels; endothelial permeability
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Funding
- National Institute of Diabetes and Digestive and Kidney Diseases [DK-050435]
- Cell Culture Core of the Vanderbilt Diabetes Research and Training Center [DK-020593]
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May JM, Qu Z, Qiao H. Transfer of ascorbic acid across the vascular endothelium: mechanism and self-regulation. Am J Physiol Cell Physiol 297: C169-C178, 2009. First published May 6, 2009; doi:10.1152/ajpcell.00674.2008.-To determine how ascorbic acid moves from the bloodstream into tissues, we assessed transfer of the vitamin across the barrier generated by EA. hy926 endothelial cells when these were cultured on semipermeable filter supports. Ascorbate transfer from the luminal to the abluminal compartment was time dependent, inhibited by anion channel blockers and by activation of protein kinase A, but was increased by thrombin. Ascorbate transfer occurred by a paracellular route, since it did not correlate with intracellular ascorbate contents and was not rectified or saturable. Nonetheless, intracellular ascorbate inhibited the transfer of both ascorbate and radiolabeled inulin across the endothelial barrier. The increase in barrier function due to ascorbate was dependent on its intracellular concentration, significant by 15 min of incubation, prevented by the cytoskeletal inhibitor colchicine, associated with F-actin stress fiber formation, and not due to collagen deposition. These results show that ascorbate traverses the endothelial barrier by a paracellular route that is regulated by cell metabolism, ion channels, and ascorbate itself. Since the latter effect occurred over the physiological range of ascorbate plasma concentrations, it could reflect a role for the vitamin in control of endothelial barrier function in vivo.
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