Endothelial sulfonylurea receptor 1–regulated NC_Ca-ATP channels mediate progressive hemorrhagic necrosis following spinal cord injury
J. Clin. Invest. J. Marc Simard, et al. 117:2105 doi:10.1172/JCI32041 [Go to this article.]

Figure 2
The SUR1-regulated NC_Ca-ATP channel is upregulated in endothelial cells by hypoxia. (A) Immunolabeling (scale bar: 50 μm) and Western blots for SUR1 in human aortic endothelial cells (ENDO) cultured under normoxic (N) or hypoxic (H) conditions as indicated, as well as Western blots for SUR1 of rat insulinoma RIN-m5F cells (INSUL) cultured under normoxic or hypoxic condition, with β-actin also shown. (B and C) Whole-cell currents during ramp pulses (4 per minute; holding potential [HP], –50 mV) or at the holding potential of –50 mV, before and after application of diazoxide (B) or Na azide (C), in endothelial cells exposed to normoxic or hypoxic conditions; the difference currents are also shown in red. E_rev, reversal potential; GLIB, glibenclamide. Data are representative of 7–15 recordings from human aortic endothelial cells (B) or bEnd.3 cells (C) for each condition. (D) Single-channel recordings of inside-out patches with Cs⁺ as the principal cation, with channel openings inhibited by ATP on the cytoplasmic side; channel amplitude at various potentials indicated a slope conductance of 37 pS (data from 7 patches) from human brain microvascular endothelial cells. Error bars indicate SEM.