ArticleJournal of clinical laboratory analysis2021
Upregulated microRNA-126 induces apoptosis of dental pulp stem cell via mediating PTEN-regulated Akt activation.
Article in Journal of clinical laboratory analysis, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The trial behind it
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- Potential of Dental Pulp Stem Cell Exosomes: Unveiling miRNA-Driven Regenerative Mechanisms.International dental journal · 2025Review
- Effects of sEV derived from SHED and DPSC on the proliferation, migration and osteogenesis of PDLSC.Regenerative therapy · 2023Article
- Current concepts of microRNA-mediated regulatory mechanisms in human pulp tissue-derived stem cells: a snapshot in the regenerative dentistry.Cell and tissue research · 2023Review
- microRNA-126 inhibits vascular cell adhesion molecule-1 and interleukin-1beta in human dental pulp cells.Journal of clinical laboratory analysis · 2022Article
- Micro-RNAs: A safety net to protect hematopoietic stem cell self-renewal.Wiley interdisciplinary reviews. RNA · 2022Review
- Challenges and strategy in treatment with exosomes for cell-free-based tissue engineering in dentistry.Future science OA · 2021Review
- Upregulated microRNA-126 induces apoptosis of dental pulp stem cell via mediating PTEN-regulated Akt activation.Journal of clinical laboratory analysis · 2021Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
introductionHuman dental pulp stem cells (DPSCs) have potential applications in regenerative medicine. The molecular mechanisms underlying DPSCs viability and apoptosis are not completely understood. Here, we investigated the role of miR-126 in DPSCs viability and apoptosis. MATERIAL AND
methodsSenescent DPSCs were compared with early passage DPSCs. real-time PCR and microARRAY were performed to identify the differential expression of miR-126, and western blot was performed to detect the expression of PTEN. MTT assay was utilized to reveal the proliferative rate of both senescent and early passage DPSCs. Flow cytometry was used to examine the apoptotic rate of DPSCs. Dual-luciferase reporter assay was carried out to detect the interaction of miR-126 and PTEN.
resultsSenescent DPSCs showed a high level of apoptosis. Further study showed that miR-126 is upregulated in senescent DPSCs and its overexpression in early passaged DPSCs induced apoptosis. Phosphatase and tensin homolog gene (PTEN) was identified as a target of miR-126. PTEN was downregulated in senescent DPSCs, whereas miR-126 inhibition upregulated PTEN level, and subsequently activated Akt pathway and suppressed the apoptotic phenotype of senescent DPSCs. In addition, PTEN overexpression rescued apoptosis of DPSCs at later stage.
conclusionOur results demonstrate that the miR-126-PTEN-Akt axis plays a key role in the regulation of DPSCs apoptosis and provide a candidate target to improve the functional and therapeutic potential of DPSCs.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.