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Autophagy mediates cementoblast mineralization under compression through periostin/β-catenin axis.

Yuhui YangHao LiuRuoxi WangYi ZhaoYunfei ZhengYiping HuangWeiran Li
Published in: Journal of cellular physiology (2023)
Repair of orthodontic external root resorption and periodontal tissue dysfunction induced by mechanical force remains a clinical challenge. Cementoblasts are vital in cementum mineralization, a process important for restoring damaged cementum. Despite autophagy plays a role in mineralization under various environmental stimuli, the underlying mechanism of autophagy in mediating cementoblast mineralization remains unclear. Here we verified that murine cementoblasts exhibit compromised mineralization under compressive force. Autophagy was indispensable for cementoblast mineralization, and autophagic activation markedly reversed cementoblast mineralization and prevented cementum damage in mice during tooth movement. Subsequently, messenger RNA sequencing analyses identified periostin (Postn) as a mediator of autophagy and mineralization in cementoblasts. Cementoblast mineralization was significantly inhibited following the knockdown of Postn. Furthermore, Postn silencing suppressed Wnt signaling by modulating the stability of β-catenin. Together our results highlight the role of autophagy in cementoblast mineralization via Postn/β-catenin signaling under compressive force and may provide a new strategy for the remineralization of cementum and regeneration of periodontal tissue.
Keyphrases
  • cell death
  • oxidative stress
  • endoplasmic reticulum stress
  • signaling pathway
  • stem cells
  • cell proliferation
  • single molecule
  • type diabetes
  • single cell
  • high fat diet induced
  • bone loss