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

Authors
 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 
Citation
 JOURNAL OF CELLULAR PHYSIOLOGY, Vol.234(11) : 20354-20365, 2019 
Journal Title
 JOURNAL OF CELLULAR PHYSIOLOGY 
ISSN
 0021-9541 
Issue Date
2019
Keywords
ER stress ; Tmbim6 knockout ; amelogenesis ; dentinogenesis ; molar development
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.
Full Text
https://onlinelibrary.wiley.com/doi/full/10.1002/jcp.28635
DOI
10.1002/jcp.28635
Appears in Collections:
2. College of Dentistry (치과대학) > Dept. of Oral Biology (구강생물학교실) > 1. Journal Papers
Yonsei Authors
Cho, Sung Won(조성원) ORCID logo https://orcid.org/0000-0001-7505-9769
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/174703
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