EID3 inhibits the osteogenic differentiation of periodontal ligament stem cells and mediates the signal transduction of TAZ-EID3-AKT/MTOR/ERK
Copyright © 2024 Elsevier B.V. All rights reserved..
Exploring the molecular mechanisms of cell behaviors is beneficial for promoting periodontal ligament stem cell (PDLSC)-mediated tissue regeneration. This study intends to explore the regulatory effects of EID3 on cell proliferation, apoptosis, and osteogenic differentiation and to preliminarily explore the regulatory mechanism of EID3. Here, EID3 was overexpressed or knocked down in PDLSCs by recombinant lentivirus. Then, cell proliferation activity was analyzed by colony-forming assay, EdU assay, and cell cycle assay. Cell apoptosis was detected by flow cytometry. The osteo-differentiation potential was analyzed using ALP activity assay, ALP staining, alizarin red staining, and mRNA and protein assay of osteo-differentiation related genes. The results showed that when EID3 was knocked down, the proliferation activity and osteogenic differentiation potential of PDLSCs decreased, while they increased when EID3 was overexpressed. The cell apoptosis rate decreased in PDLSCs with EID3 knockdown but increased in PDLSCs with EID3 overexpression. Moreover, EID3 inhibited the transduction of the AKT/MTOR and ERK signaling pathway. In addition, TAZ negatively regulated the expression of EID3, and the overexpression of EID3 partially reversed the promotive effects of TAZ on the osteogenic differentiation of PDLSCs. Taken together, EID3 inhibits the proliferation and osteogenic differentiation while promoting the apoptosis of PDLSCs. EID3 inhibits the transduction of the AKT/MTOR and ERK signaling pathways and mediates the regulatory effect of TAZ on PDLSC osteogenic differentiation.
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2024 |
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| Erschienen: |
2024 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:1871 |
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| Enthalten in: |
Biochimica et biophysica acta. Molecular cell research - 1871(2024), 3 vom: 27. März, Seite 119662 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Jia, Linglu [VerfasserIn] |
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| Links: |
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| Anmerkungen: |
Date Completed 04.03.2024 Date Revised 26.03.2024 published: Print-Electronic Citation Status MEDLINE |
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| doi: |
10.1016/j.bbamcr.2024.119662 |
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| funding: |
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| Förderinstitution / Projekttitel: |
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| 245 | 1 | 0 | |a EID3 inhibits the osteogenic differentiation of periodontal ligament stem cells and mediates the signal transduction of TAZ-EID3-AKT/MTOR/ERK |
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| 520 | |a Copyright © 2024 Elsevier B.V. All rights reserved. | ||
| 520 | |a Exploring the molecular mechanisms of cell behaviors is beneficial for promoting periodontal ligament stem cell (PDLSC)-mediated tissue regeneration. This study intends to explore the regulatory effects of EID3 on cell proliferation, apoptosis, and osteogenic differentiation and to preliminarily explore the regulatory mechanism of EID3. Here, EID3 was overexpressed or knocked down in PDLSCs by recombinant lentivirus. Then, cell proliferation activity was analyzed by colony-forming assay, EdU assay, and cell cycle assay. Cell apoptosis was detected by flow cytometry. The osteo-differentiation potential was analyzed using ALP activity assay, ALP staining, alizarin red staining, and mRNA and protein assay of osteo-differentiation related genes. The results showed that when EID3 was knocked down, the proliferation activity and osteogenic differentiation potential of PDLSCs decreased, while they increased when EID3 was overexpressed. The cell apoptosis rate decreased in PDLSCs with EID3 knockdown but increased in PDLSCs with EID3 overexpression. Moreover, EID3 inhibited the transduction of the AKT/MTOR and ERK signaling pathway. In addition, TAZ negatively regulated the expression of EID3, and the overexpression of EID3 partially reversed the promotive effects of TAZ on the osteogenic differentiation of PDLSCs. Taken together, EID3 inhibits the proliferation and osteogenic differentiation while promoting the apoptosis of PDLSCs. EID3 inhibits the transduction of the AKT/MTOR and ERK signaling pathways and mediates the regulatory effect of TAZ on PDLSC osteogenic differentiation | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a Apoptosis | |
| 650 | 4 | |a EID3 | |
| 650 | 4 | |a Osteogenic differentiation | |
| 650 | 4 | |a Periodontal ligament stem cells | |
| 650 | 4 | |a Proliferation | |
| 650 | 4 | |a TAZ | |
| 650 | 7 | |a Proto-Oncogene Proteins c-akt |2 NLM | |
| 650 | 7 | |a EC 2.7.11.1 |2 NLM | |
| 650 | 7 | |a TOR Serine-Threonine Kinases |2 NLM | |
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| 650 | 7 | |a WWTR1 protein, human |2 NLM | |
| 650 | 7 | |a EID3 protein, human |2 NLM | |
| 650 | 7 | |a Transcriptional Coactivator with PDZ-Binding Motif Proteins |2 NLM | |
| 700 | 1 | |a Tian, Hui |e verfasserin |4 aut | |
| 700 | 1 | |a Sun, Shaoqing |e verfasserin |4 aut | |
| 700 | 1 | |a Hao, Xingyao |e verfasserin |4 aut | |
| 700 | 1 | |a Wen, Yong |e verfasserin |4 aut | |
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