Carbon dots enhance extracellular matrix secretion for dentin-pulp complex regeneration through PI3K/Akt/mTOR pathway-mediated activation of autophagy.
Carbon dots enhance extracellular matrix secretion for dentin-pulp complex regeneration through PI3K/Akt/mTOR pathway-mediated activation of autophagy.
复制标题
碳点通过 PI3K/Akt/mTOR 通路介导的自噬激活增强细胞外基质分泌,促进牙本质牙髓复合体再生
DOI:
10.1016/j.mtbio.2022.100344
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发表时间:
2022-12
影响因子:
8.2
通讯作者:
Sun, Hongchen
中科院分区:
文献类型:
--
作者:
Liu, Lili;Li, Xianjing;Bu, Wenhuan;Jin, Nianqiang;Meng, Yuan;Wang, Yi;Wang, Duan;Xu, Xiaowei;Zhou, Ding;Sun, Hongchen
关键词:
Pulp injury is one of the most common clinical diseases, and severe cases are usually associated with the functional loss of the tooth, while the current clinical treatment modality is only a cavity filling procedure without the regeneration of the dentin-pulp complex, thus leading to a devitalized and brittle tooth. In this study, carbon dots (CDots) with excellent biocompatibility are prepared from ascorbic acid and polyethyleneimine via a hydrothermal method. The as-prepared CDots can enhance extracellular matrix (ECM) secretion of human dental pulp stem cells (DPSCs), giving rise to increased cell adhesion on ECM and a stronger osteogenic/odontogenic differentiation capacity of DPSCs. Further, the mechanism underlying CDots-enhanced ECM secretion is revealed by the transcriptome analysis, Western blot assay and molecular dynamics simulation, identifying that the pharmacological activities of CDots are originated from a reasonable activation of the autophagy, which is mediated by regulating phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin signaling pathway. Based on the abundant CDots-induced ECM and thereby the reinforcement of the cell-ECM adhesion, an intact dental pulp stem cell sheet can be achieved, which in return promote in vivo the efficient regeneration of dentin-pulp complex as well as blood vessels.
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影响因子:
18.9
作者:
Li Z;Du T;Ruan C;Niu X
通讯作者:
Niu X
DOI:
10.1016/j.msec.2010.01.013
发表时间:
2010-05-10
影响因子:
7.9
作者:
Brammer, Karla S.;Oh, Seunghan;Jin, Sungho
通讯作者:
Jin, Sungho
影响因子:
--
作者:
LINDE, A
通讯作者:
LINDE, A
影响因子:
4.1
作者:
Liu S;Quan T;Yang L;Deng L;Kang X;Gao M;Xia Z;Li X;Gao D
通讯作者:
Gao D
DOI:
10.1126/science.1176009
发表时间:
2009-11-27
期刊:
Science (New York, N.Y.)
影响因子:
--
作者:
Hynes RO
通讯作者:
Hynes RO