An endoplasmic reticulum stress regulator, Tmbim6, modulates secretory stage of mice molar

Yam Prasad Aryal, Sanjiv Neupane, Nirpesh Adhikari, Chang Hyeon An, Jung Hong Ha, Tae Yub Kwon, Hitoshi Yamamoto, Jae Kwang Jung, Eui Kyun Park, Ji Youn Kim, Sung Won Cho, Wern Joo Sohn, Youngkyun Lee, Han Jung Chae, Hyung Ryong Kim, Jae Young Kim

Research output: Contribution to journalArticlepeer-review

4 Citations (Scopus)

Abstract

To understand the role of endoplasmic reticulum (ER)-stress in mice molar development, we studied Tmbim6 that antagonizes the unfolded protein response, using Tmbim6 knockout (KO) mice and in vitro organ cultivation with knocking down using small interfering RNA. During molar development, Tmbim6 is expressed in developing tooth at E14–E16, postnatal0 (PN0), and PN6. Mineral content in Tmbim6 KO enamel was reduced while dentin was slightly increased revealing ultrastructural changes in pattern formation of both enamel and dentin. Moreover, odontoblast differentiation was altered with increased Dspp expression at PN0 followed by altered AMELX localizations at PN5. These results were confirmed by in vitro organ cultivation and showed altered Bmp signaling, proliferation, and actin rearrangement in the presumptive ameloblast and odontoblasts that followed the altered expression of differentiation and ER stress-related signaling molecules at E16.5. Overall, ER stress modulated by Tmbim6 would play important roles in patterned dental hard tissue formation in mice molar within a limited period of development.

Original languageEnglish
Pages (from-to)20354-20365
Number of pages12
JournalJournal of Cellular Physiology
Volume234
Issue number11
DOIs
Publication statusPublished - 2019 Nov

Bibliographical note

Funding Information:
This study was supported by the Bio & Medical Technology Development Program of the National Research Foundation (NRF-2017M3A9E4047243), funded by the Ministry of Science & ICT and Future Planning, Republic of Korea.

Funding Information:
This study was supported by the Bio & Medical Technology Development Program of the National Research Foundation (NRF‐ 2017M3A9E4047243), funded by the Ministry of Science & ICT and Future Planning, Republic of Korea.

Funding Information:
National Research Foundation of Korea, Grant/Award Number: NRF‐ 2017M3A9E404724; Bio & Medical Tech; nology Development Program of the ; National Research Foundation, Grant/Award Number: 2017M3A9E4047243; Ministry of Science & ICT and Future Planning, Republic of Korea

Publisher Copyright:
© 2019 Wiley Periodicals, Inc.

All Science Journal Classification (ASJC) codes

  • Physiology
  • Clinical Biochemistry
  • Cell Biology

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