Xbp1 promotes odontoblastic differentiation through modulating mitochondrial homeostasis.
Hspa9
Xbp1
MSCs
mitochondrial homeostasis
odontoblastic differentiation
Journal
FASEB journal : official publication of the Federation of American Societies for Experimental Biology
ISSN: 1530-6860
Titre abrégé: FASEB J
Pays: United States
ID NLM: 8804484
Informations de publication
Date de publication:
15 Apr 2024
15 Apr 2024
Historique:
revised:
05
03
2024
received:
23
01
2024
accepted:
25
03
2024
medline:
4
4
2024
pubmed:
4
4
2024
entrez:
4
4
2024
Statut:
ppublish
Résumé
Odontoblast differentiation depends on the orderly recruitment of transcriptional factors (TFs) in the transcriptional regulatory network. The depletion of crucial TFs disturbs dynamic alteration of the chromatin landscape and gene expression profile, leading to developmental defects. Our previous studies have revealed that the basic leucine zipper (bZIP) TF family is crucial in odontoblastic differentiation, but the function of bZIP TF family member XBP1 is still unknown. Here, we showed the stage-specific expression patterns of the spliced form Xbp1s during tooth development. Elevated Xbp1 expression and nuclear translocation of XBP1S in mesenchymal stem cells (MSCs) were induced by differentiation medium in vitro. Diminution of Xbp1 expression impaired the odontogenic differentiation potential of MSCs. The further integration of ATAC-seq and RNA-seq identified Hspa9 as a direct downstream target, an essential mitochondrial chaperonin gene that modulated mitochondrial homeostasis. The amelioration of mitochondrial dysfunction rescued the impaired odontogenic differentiation potential of MSCs caused by the diminution of Xbp1. Furthermore, the overexpression of Hspa9 rescued Xbp1-deficient defects in odontoblastic differentiation. Our study illustrates the crucial role of Xbp1 in odontoblastic differentiation via modulating mitochondrial homeostasis and brings evidence to the therapy of mitochondrial diseases caused by genetic defects.
Identifiants
pubmed: 38572599
doi: 10.1096/fj.202400186R
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
e23600Subventions
Organisme : National Natural Science Foundation of China
ID : 82230029
Organisme : National Natural Science Foundation of China
ID : 82071110
Organisme : National Natural Science Foundation of China
ID : 82071077
Organisme : National Natural Science Foundation of China
ID : 82270948
Informations de copyright
© 2024 Federation of American Societies for Experimental Biology.
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