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TMEM16A Ca2+-activated Cl channel inhibition ameliorates acute pancreatitis via the IP3R/Ca2+/NFjB/IL-6 signaling pathway

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TMEM16A Ca2+-activated Cl channels are expressed in pancreatic acinar cells and participate in inflammation-associated diseases. Whether TMEM16A contributes to the pathogenesis of acute pancreatitis (AP) remains unknown. Here, we found that increased TMEM16A expression in the pancreatic tissue was correlated with the interleukin-6 (IL-6) level in the pancreatic tissue and in the serum of a cerulein-induced AP mouse model. IL-6 treatment promoted TMEM16A expression in AR42J pancreatic acinar cells via the IL-6 receptor (IL-6R)/signal transducers and activators of transcription 3 (STAT3) signaling pathway. In addition, TMEM16A was co-immunoprecipitated with the inositol 1,4,5-trisphosphate receptor (IP3R) and was activated by IP3R-mediated Ca2+ release. | TMEM16A Ca2 -activated Cl channel inhibition ameliorates acute pancreatitis via the IP3R Ca2 NFjB IL-6 signaling pathway