Goblet cell LRRC26 regulates BK channel activation and protects against colitis in mice
Vivian González-Pérez, Pedro L. Martinez-Espinosa, Monica Sala‐Rabanal, Nikhil Bharadwaj, Xiaoming Xia, Albert C. Chen, David M. Alvarado, Jenny K. Gustafsson, Hongzhen Hu, Matthew A. Ciorba, Christopher J. Lingle
Abstract
Significance A primary function of goblet cells (GCs) of the intestinal epithelium is to generate a protective mucus layer lining the intestinal lumen. GC dysfunction is linked to inflammatory bowel disease (IBD). GC mucus secretion is thought to be dependent on contributions of an ensemble of anion and cation fluxes, although understanding remains limited. Here, it is shown in mouse colon that the Ca 2+ - and voltage-dependent BK-type K + channel, specifically in association with the LRRC26 regulatory subunit, plays a critical role in normal GC function, protecting mice against chemically induced colitis. The results demonstrate that normal K + fluxes mediated by LRRC26-containing BK channels are required for normal GC function, potentially providing insights into the potential role of BK channels in IBD.