LncRNA TP53TG1 promotes the growth and osteo/dentinogenic differentiation of dental pulp stem cells by activating the Smad3 and JNK1/2 pathway.

IF 1.7 4区生物学 Q4 CELL BIOLOGY

In Vitro Cellular & Developmental Biology. Animal Pub Date : 2025-09-08 DOI:10.1007/s11626-025-01086-3

Tingyue Li, Zihan Dai, Zhihua Wang, Minghao Wang, Chengxiong Cai, Xiaoru Zhu, Yang Zhao, Paul Roy Cooper, Shengchao Wang, Wenxi He

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引用次数: 0

Abstract

TP53TG1 is a long non-coding RNA related to the TP53 gene, which plays an important role in various biological processes such as tumorigenesis, cell cycle regulation, and DNA damage repair. In recent years, researchers have begun to explore the role of TP53TG1 in dental pulp biology, especially its potential impact on pulpitis and other pulp-related diseases. However, the role of TP53TG1 in human dental pulp stem cells (hDPSCs) remains unclear. In this study, we obtained TP53TG1 knockdown dental pulp stem cells by plasmid transfection to determine the biological role of TP53TG1 in DPSCs. We found that the expression of TP53TG1 increased significantly during odontogenic differentiation of DPSCs. SiRNA knockdown of TP53TG1 expression resulted in inhibition of proliferation of hDPSCs. During odontogenic differentiation, downregulation of TP53TG inhibited the expression of multiple differentiation-related indices, and alkaline phosphatase activity and the formation of mineralized nodules were also inhibited. In addition, Western blot found that knockdown of TP53TG1 also weakened SMAD3 and JNK1/2 signaling in DPSCs. In conclusion, our study revealed the differentiation-inducing role of TP53TG1 in DPSCs, which plays an important role in dental pulp repair and regeneration and provides new insights and approaches for the prevention and treatment of dental pulp diseases.

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LncRNA TP53TG1通过激活Smad3和JNK1/2通路促进牙髓干细胞的生长和成骨/牙本质分化。

TP53TG1是一种与TP53基因相关的长链非编码RNA，在肿瘤发生、细胞周期调控、DNA损伤修复等多种生物学过程中发挥重要作用。近年来，研究人员开始探索TP53TG1在牙髓生物学中的作用，特别是其对牙髓炎等牙髓相关疾病的潜在影响。然而，TP53TG1在人牙髓干细胞（hDPSCs）中的作用尚不清楚。在本研究中，我们通过质粒转染获得TP53TG1敲低的牙髓干细胞，以确定TP53TG1在DPSCs中的生物学作用。我们发现TP53TG1的表达在牙源性分化过程中显著增加。SiRNA敲低TP53TG1表达可抑制hdpsc的增殖。在牙源性分化过程中，TP53TG的下调抑制了多种分化相关指标的表达，碱性磷酸酶活性和矿化结节的形成也受到抑制。此外，Western blot发现，TP53TG1的敲低也削弱了DPSCs中的SMAD3和JNK1/2信号通路。总之，我们的研究揭示了TP53TG1在DPSCs中的诱导分化作用，在牙髓修复和再生中发挥重要作用，为牙髓疾病的预防和治疗提供了新的见解和途径。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

In Vitro Cellular & Developmental Biology. Animal 生物-发育生物学

CiteScore

3.70

自引率

4.80%

发文量

审稿时长

3 months

期刊介绍： In Vitro Cellular & Developmental Biology - Animal is a journal of the Society for In Vitro Biology (SIVB). Original manuscripts reporting results of research in cellular, molecular, and developmental biology that employ or are relevant to organs, tissue, tumors, and cells in vitro will be considered for publication. Topics covered include: Biotechnology; Cell and Tissue Models; Cell Growth/Differentiation/Apoptosis; Cellular Pathology/Virology; Cytokines/Growth Factors/Adhesion Factors; Establishment of Cell Lines; Signal Transduction; Stem Cells; Toxicology/Chemical Carcinogenesis; Product Applications.