抄録
It has been reported that ClC-2 is an apical Cl− channel which is responsible for gastric acid secretion in rabbit parietal cells (Sherry et al. 2001). However, it seems to be difficult to secrete Cl− via the apical ClC-2 channel, because the potential difference across the apical membrane is about 10 mV. Herein, we checked whether ClC-2 is really expressed in rabbit and rat parietal cells. Animals were humanely killed by overdose of urethane. Northern blot analysis showed that ClC-2 mRNA is highly expressed in rabbit parietal cells. However, Western blot analysis using two kinds of anti-ClC-2 antibodies (ACL-002 and CLC21-A) showed that ClC-2 protein is not significantly expressed in rabbit and rat parietal cells, while these antibodies clearly reacted with cloned ClC-2 expressed in HEK293 cells. Control antigen peptides for the antibodies almost completely abolished the single band of cloned ClC-2 (95 kDa), but the peptide did not affect any of non-specific bands of the membrane fraction (rich in gastric H+,K+-ATPase) from the parietal cells. Our present results suggest that ClC-2 may not directly contribute to gastric acid secretion. [Jpn J Physiol 54 Suppl:S72 (2004)]
