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Regulation of the expression and function of TRPCs and Orai1 by Homer2 in mouse pancreatic acinar cells

  • Kang, Jung Yun (Department of Oral Biology, BK21 PLUS Project, Yonsei University College of Dentistry) ;
  • Kang, Namju (Department of Oral Biology, BK21 PLUS Project, Yonsei University College of Dentistry) ;
  • Yang, Yu-Mi (Department of Oral Biology, BK21 PLUS Project, Yonsei University College of Dentistry)
  • Received : 2021.09.01
  • Accepted : 2021.09.07
  • Published : 2021.09.30

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.

Keywords

Acknowledgement

이 논문은 정부(과학기술정보통신부)의 재원으로 한국연구재단의 지원을 받아 수행된 연구임(NRF-2015R1D1A1A01057277, NRF-2020R1A2C1004942).

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