TY - JOUR
T1 - Transit amplifying cells coordinate mouse incisor mesenchymal stem cell activation
AU - Walker, Jemma Victoria
AU - Zhuang, Heng
AU - Singer, Donald
AU - Illsley, Charlotte Sara
AU - Kok, Wai Ling
AU - Sivaraj, Kishor K.
AU - Gao, Yan
AU - Bolton, Chloe
AU - Liu, Yuying
AU - Zhao, Mengyuan
AU - Grayson, Portia Rebecca Clare
AU - Wang, Shuang
AU - Karbanová, Jana
AU - Lee, Tim
AU - Ardu, Stefano
AU - Lai, Qingguo
AU - Liu, Jihui
AU - Kassem, Moustapha
AU - Chen, Shuo
AU - Yang, Kai
AU - Bai, Yuxing
AU - Tredwin, Christopher
AU - Zambon, Alexander C.
AU - Corbeil, Denis
AU - Adams, Ralf
AU - Abdallah, Basem M.
AU - Hu, Bing
PY - 2019
Y1 - 2019
N2 - Stem cells (SCs) receive inductive cues from the surrounding microenvironment and cells. Limited molecular evidence has connected tissue-specific mesenchymal stem cells (MSCs) with mesenchymal transit amplifying cells (MTACs). Using mouse incisor as the model, we discover a population of MSCs neibouring to the MTACs and epithelial SCs. With Notch signaling as the key regulator, we disclose molecular proof and lineage tracing evidence showing the distinct MSCs contribute to incisor MTACs and the other mesenchymal cell lineages. MTACs can feedback and regulate the homeostasis and activation of CL-MSCs through Delta-like 1 homolog (Dlk1), which balances MSCs-MTACs number and the lineage differentiation. Dlk1’s function on SCs priming and self-renewal depends on its biological forms and its gene expression is under dynamic epigenetic control. Our findings can be validated in clinical samples and applied to accelerate tooth wound healing, providing an intriguing insight of how to direct SCs towards tissue regeneration.
AB - Stem cells (SCs) receive inductive cues from the surrounding microenvironment and cells. Limited molecular evidence has connected tissue-specific mesenchymal stem cells (MSCs) with mesenchymal transit amplifying cells (MTACs). Using mouse incisor as the model, we discover a population of MSCs neibouring to the MTACs and epithelial SCs. With Notch signaling as the key regulator, we disclose molecular proof and lineage tracing evidence showing the distinct MSCs contribute to incisor MTACs and the other mesenchymal cell lineages. MTACs can feedback and regulate the homeostasis and activation of CL-MSCs through Delta-like 1 homolog (Dlk1), which balances MSCs-MTACs number and the lineage differentiation. Dlk1’s function on SCs priming and self-renewal depends on its biological forms and its gene expression is under dynamic epigenetic control. Our findings can be validated in clinical samples and applied to accelerate tooth wound healing, providing an intriguing insight of how to direct SCs towards tissue regeneration.
U2 - 10.1038/s41467-019-11611-0
DO - 10.1038/s41467-019-11611-0
M3 - Journal article
C2 - 31399601
AN - SCOPUS:85070367007
SN - 2041-1723
VL - 10
JO - Nature Communications
JF - Nature Communications
IS - 1
M1 - 3596
ER -