Erratum: Expression of the <b><i>Slc12a1</i></b> Gene in Pancreatic β-cells: Molecular Characterization and <b><i>in silico</i></b> Analysis

The solute carrier protein family 12 group A, member one (<i>Slc12a1</i>) and two (<i>Slc12a2</i>) encode several splice variants of the kidney-specific and the ubiquitous isoforms, respectively, of the bumetanide (BTD)-sensitive Na-dependent K2Cl co-transporter. The <i>Slc12a2 </i>co-transporter is involved in the maintenance of a high intracellular chloride concentration [Cl^–]_iin β-cells and its inhibition with BTD blocks glucose-induced insulin secretion. In β-cells, [Cl^–]_iplays an important role in glucose-induced depolarization and insulin secretion. Glucose promotes electrogenic efflux of Cl^–contributing to β-cell's electrical and secretory activity. To identify the expression pattern of <i>Slc12a1 </i>and <i>Slc12a2 </i>genes in β-cells we have used RT-PCR, Western blotting and immunolocalization studies in mouse pancreatic islets, β-cell lines and rat tissues. Our results demonstrate expression of specific splice variants of <i>Slc12a1 </i>and <i>Slc12a2 </i>transcripts in β-cells <i>i.e.</i>, variants 1 of <i>Slc12a1 </i>(NKCC2A) and S<i>lc12a2 </i>(NKCC1<i>a</i>). Molecular cloning and characterization of <i>Slc12a1 </i>variant 1 transcripts from β-cells revealed an alternative splicing event involving the 5'-UTR region. NKCC2A expression at the protein level in islets and β-cells was confirmed by immunoblotting and immunolocalization. Further, NKCC2A, NKCC1<i>a </i>and pro-insulin co-localized in β-cells but not in the exocrine pancreas. Therefore, our results provide for the first time evidence of NKCC2A expression in pancreatic β-cells where it may play a role in insulin secretion.