Dental pulp stem cells maintain epigenetic chromatin architecture remodeling primed by the etiological stimulus of biliary atresia

Soichiro Sonoda; Liting Yu; Lisha Dai; Toshio Kukita; Koichiro Yoshimaru; Ratih Yuniartha; Ying Liu; M. Majd Sharifa; Sara Murata; Mohammed Fouad Zakaria; Hiroki Kato; Airo Tsubura; Satoshi Fukumoto; Haruyoshi Yamaza; Toshiharu Matsuura; Tomoaki Taguchi; Tatsuro Tajiri; Yamaza Takayoshi

doi:10.1186/s13287-026-04952-3

Key Points

The study aims to explore how dental pulp stem cells are affected by epigenetic changes related to biliary atresia.
Examined epigenetic memory in biliary atresia-associated dental pulp stem cells (BA-SHED)
Analyzed the dysregulation of TGFBR2 and the activation of the HNF6 promoter
Investigated the chromatin architecture in response to biliary atresia stimulus.
BA-SHED exhibited epigenetic memory that reflects bile duct deficiency
TGFBR2 was found to be dysregulated by HNF6 promoter activation
Findings suggest that BA-SHED can serve as a model for further studies in biliary atresia.

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Implication

Epigenetic mechanisms influence bile duct deficiency in biliary atresia, suggesting new research avenues.

Abstract

The present epigenetic memory in BA-SHED implies that BA-SHED imprint bile duct deficiency through TGFBR2 dysregulated by the HNF6 promoter activation epigenetically. Thus, BA-SHED are a potential model for expanding our knowledge in BA research.

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Cite This Study

Sonoda et al. (2026) studied this question.

synapsesocial.com/papers/69af94c970916d39fea4ba94 https://doi.org/10.1186/s13287-026-04952-3

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Dental pulp stem cells maintain epigenetic chromatin architecture remodeling primed by the etiological stimulus of biliary atresia

Key Points

Ask about this paper

Implication

Abstract

Discussion

Cite This Study

Dental pulp stem cells maintain epigenetic chromatin architecture remodeling primed by the etiological stimulus of biliary atresia

Key Points

Ask about this paper

Implication

Abstract

Discussion

Cite This Study

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