In the article “Localization of the Endothelium System in Aldosterone-Producing Adenomas” by Egidy et al (Hypertension 2001;38:1137–1142), the figures and legends were mismatched. Following is the correct match of the figures⇓⇓⇓⇓ and legends.
Figure 1. Components of the ET system in APAs. ETA and ETB receptors, ECE-1, PPET-1, and GAPDH mRNAs were detected by RT-PCR using the specific primers described previously22 and total RNA from the 20 frozen adrenal cortex samples. Only 5 samples are shown in Figure 2. Thirty cycles of amplification gave each gene at the expected size: 675 bp (ETA), 400 bp (ETB), 341 bp (PPET-1), 622 bp (ECE-1), and 649 bp (GAPDH). The molecular weight markers shown on the right are λ/HindIII, φX174 DNA/HaeIII.
Figure 2. Localization of the ET system in APAs. ISH was performed on sections of adrenal cortex from the 20 patients with the antisense probes for ETA (a and b), ETB (c and d), ECE-1 (e and f), and PPET-1 (g and h). Photographs representative of the 20 samples studied are shown in dark-field illumination (left) and in bright-field illumination (right). ETA mRNA was found in compact cells of the zona glomerulosa (arrow, a) and ETB mRNA in vascular structures (arrow, c). ECE-1 mRNA labeling was ubiquitous and intense, and no specific signal for PPET-1 mRNA was detected. Scale bar 50 μm.
Figure 3. Cellular distribution of ETA and ETB receptor mRNAs in APAs. ISH with the antisense probe for ETA (a) and ETB (b) receptors. Microphotographs representative of the 20 samples studied are shown in bright-field illumination. Immunohistochemistry was performed with anti-αSMA (c) (smooth muscle cell marker) and anti-CD31 (d) (endothelial cell marker) antibodies to identify the cells labeled with the ETA and ETB probes. ETA mRNA labeling was found in secretory cells (arrow) and smooth muscle cells (arrowhead), and ETB mRNA labeling was found mainly in endothelial cells (arrow) and smooth muscle cells (arrowhead). Scale bar 20 μm.
Figure 4. ET-1 immunoreactivity. ET-1 immunohistochemistry was performed in paraffin-embedded specimens of stable transfected CHO/PPET-1/ECE-1 cells (a), CHO/ETB cells (b), CHO/ETB cells incubated with ET-1 for 30 minutes at 4°C (c), and untransfected CHO cells (d). CHO/PPET-1/ECE-1 cells contained ET-1 that was recognized by the antibody (arrow, a). No immunoreactivity was detected in CHO/ETB cells (b) or in untransfected CHO cells (d). In contrast, ET-1 incubated with CHO/ETB and bound to ETB receptors was recognized by the anti–ET-1 antibody (arrow, c).
Figure 5. Cellular distribution of PPET-1 and ECE-1 mRNAs in APAs. ISH with the antisense probes for ECE-1 (a) and PPET-1 (c and e). Microphotographs representative of the 20 APA samples studied are shown in bright-field illumination. Immunohistochemistry was performed with the anti–ECE-1 (b) and anti–ET-1 (d and f) antibodies. There was intense ubiquitous labeling for ECE-1 mRNA and protein, whereas no specific labeling was detected for PPET-1 mRNA (c). However, strong ET-1 immunoreactivity was found in endothelial cells (arrow, d). Thickened precapillary arterioles were found in 6 of the 20 samples and contained PPET-1 mRNA (arrow, e) and ET-1 (arrow, f). Scale bar 20 μm.