Regulation of the expression and function of TRPCs and Orai1 by Homer2 in mouse pancreatic acinar cells
10.11620/IJOB.2021.46.3.134
- Author:
Jung Yun KANG
1
;
Namju KANG
;
Yu-Mi YANG
Author Information
1. Department of Oral Biology, BK21 PLUS Project, Yonsei University College of Dentistry, Seoul 03722, Republic of Korea
- Publication Type:Original Article
- From:International Journal of Oral Biology
2021;46(3):134-139
- CountryRepublic of Korea
- Language:English
-
Abstract:
Under physiological conditions, calcium (Ca2+ ) regulates essential functions of polarized secretory cells by the stimulation of specific Ca2+ signaling mechanisms, such as increases in intracellular Ca2+ concentration ([Ca2+]i ) via the store-operated Ca2+ entry (SOCE) and the receptor-operated Ca2+ entry (ROCE). Homer proteins are scaffold proteins that interact with G protein-coupled receptors, inositol 1,4,5-triphosphate (IP3) receptors, Orai1-stromal interaction molecule 1, and transient receptor potential canonical (TRPC) channels. However, their role in the Ca2+ signaling in exocrine cells remains unknown. In this study, we investigated the role of Homer2 in the Ca2+ signaling and regulatory channels to mediate SOCE and ROCE in pancreatic acinar cells. Deletion of Homer2 (Homer2–/– ) markedly increased the expression of TRPC3, TRPC6, and Orai1 in pancreatic acinar cells, whereas these expressions showed no difference in whole brains of wild-type and Homer2–/– mice. Furthermore, the response of Ca2+ entry by carbachol also showed significant changes to the patterns regulated by specific blockers of SOCE and ROCE in pancreatic acinar cells of Homer2–/– mice. Thus, these results suggest that Homer2 plays a critical role in the regulatory action of the [Ca2+]i via SOCE and ROCE in mouse pancreatic acinar cells.
