Skip to main content
. 2003 Sep 1;198(5):783–796. doi: 10.1084/jem.20030891

Figure 2.

Figure 2.

Activated PMN rapidly release ATP. (A) Chromatographic identification of ATP in supernatants derived from activated PMN. Shown here is a representative overlay chromatogram of activated PMN supernatant (bold line) and authentic ATP (narrow line). Inset represents an overlay UV spectra derived from fraction #2 (see Fig. 1) and of authentic ATP with one dominant peak at 260 nm. (B) Time course of ATP release from activated PMN (107 PMN/ml activated with 10−6 M FMLP). PMN were activated for indicated periods of time and supernatant ATP was quantified by luciferase assay. Data represent mean ± SD ATP/107 PMN for three separate experiments. (C) Authentic ATP selectively promotes endothelial barrier function in posthypoxic endothelia. Indicated concentrations of ATP were added to HMEC-1 preexposed to normoxia or hypoxia. As indicated, ATP influenced endothelial permeability only in posthypoxic endothelial cells (*, P < 0.025 compared with no ATP). In contrast, the addition of adenosine (Ado, 100 μM) was associated with an increase in barrier function in both normoxic and posthypoxic endothelial cells (#, P < 0.01 compared with buffer alone). The addition of 8-phenyl-theophylline (8-PT at 10 μM, a nonselective adenosine receptor antagonist) obviated the barrier effect of 100 μM ATP in posthypoxic endothelial cells. Data are derived from six monolayers in each condition. Data are expressed as mean ± SD of percent control flux with HBSS only.