Liu S, Rockey DC. Cicletanine stimulates eNOS phosphorylation and NO production via Akt and MAP kinase/Erk signaling in sinusoidal endothelial cells. Am J Physiol Gastrointest Liver Physiol 305: G163-G171, 2013. First published May 2, 2013. doi:10.1152/ajpgi.00003.2013.
In the original article, there were errors in Fig. 1A and Fig. 7B, as published. The authors selected the incorrect β-actin bands for P-eNOS and eNOS in Fig. 1A. In addition, the authors selected the incorrect β-actin bands for P-VASP in Fig. 7B (right). The authors apologize for this error and state that the changes do not alter the scientific conclusions of the article in any way. The corrected Figs. 1 and 7 with legends appear below.
Figure 1.
Effect of cicletanine on the function of endothelial isoform of nitric oxide synthase (eNOS) in sinusoidal endothelial cells. A: sinusoidal endothelial cells were isolated from rat livers and exposed to cicletanine (100 nM) for 2 h, cell lysates were harvested, and phosphor (P)-eNOS (Ser1177), total eNOS, and β-actin were detected by immunoblotting. In the graph shown on the bottom, bands corresponding to phospho-eNOS were quantified (n = 4, *P < 0.01 vs. control). B: the activity of nitric oxide synthase (NOS) in normal sinusoidal endothelial cells was examined in the same cells. NOS activity without exposure to cicletanine was arbitrarily set to 100; n = 3, *P < 0.01 vs. control (no cicletanine), **P < 0.01 vs. cicletanine. l-NAME, NG-nitro-l-arginine methyl ester. C: cells were treated with cicletanine, S-cicletanine, and R-cicletanine as indicated for 2 h, conditioned medium was harvested, and nitrite levels were measured as in materials and methods (n = 3, *P < 0.001 and **P < 0.05 vs. control).
Figure 7.
Cicletanine-induced nitric oxide (NO) production in sinusoidal endothelial cells causes protein kinase G (PKG) activation and stellate cell relaxation. A: hepatic stellate cells and sinusoidal endothelial cells were isolated separately from rat livers and cocultured (each at a density of 100,000 cells/lattice) on collagen lattices for 5 days as in materials and methods. Cells were then serum starved overnight, exposed to 50 or 100 nM cicletanine for 2 h, and then stimulated with endothelin-1 (ET-1, 10 nM). Collagen lattices were released from their substrata, and gel contraction was measured over time. A representative experiment with images of changes in gel area at the indicated time points is shown on the left. Gel areas were measured, quantified, and depicted quantitatively in the graph on the right (n = 4, *P < 0.05 and **P < 0.001 vs. control). B: hepatic stellate cells (HSC) and sinusoidal endothelial cells (EC) were isolated, and HSC were cultured alone or cocultured (HSC + EC) as in materials and methods. Cells were harvested, and cell lysates were immunoblotted to detect phospho-vasodilator-stimulated phosphoprotein (VASP) for PKG activity. HSC or HSC + EC without cicletanine served as controls. Bands corresponding to phospho-VASP were quantitated, normalized, and shown in the lower graph (n = 3, *P < 0.01 and **P < 0.001 vs. HSC + EC control). C: cells (HSC + EC) as in B were pre-exposed to l-NAME (1 μM) for 4 h and then exposed to cicletanine (100 nM) for an additional 1–2 h. Phospho-VASP, PKG, and β-actin were detected in cell lysates by immunoblotting, and representative images are shown.
