IGF-1/IGF-1R/hsa-let-7c axis regulates the committed differentiation of stem cells from apical papilla

Insulin-like growth factor-1 (IGF-1) and its receptor IGF-1R play a paramount role in tooth/bone formation while hsa-let-7c actively participates in the osteogenic differentiation of mesenchymal stem cells. However, the interaction between IGF-1/IGF-1R and hsa-let-7c on the committed differentiation...

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Main Authors: Ma, Shu, Liu, Genxia, Jin, Lin, Pang, Xiyao, Wang, Yanqiu, Wang, Zilu, Yu, Yan, Yu, Jinhua
Format: Online
Language:English
Published: Nature Publishing Group 2016
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5105129/
id pubmed-5105129
recordtype oai_dc
spelling pubmed-51051292016-11-17 IGF-1/IGF-1R/hsa-let-7c axis regulates the committed differentiation of stem cells from apical papilla Ma, Shu Liu, Genxia Jin, Lin Pang, Xiyao Wang, Yanqiu Wang, Zilu Yu, Yan Yu, Jinhua Article Insulin-like growth factor-1 (IGF-1) and its receptor IGF-1R play a paramount role in tooth/bone formation while hsa-let-7c actively participates in the osteogenic differentiation of mesenchymal stem cells. However, the interaction between IGF-1/IGF-1R and hsa-let-7c on the committed differentiation of stem cells from apical papilla (SCAPs) remains unclear. In this study, human SCAPs were isolated and treated with IGF-1 and hsa-let-7c over/low-expression viruses. The odonto/osteogenic differentiation of these stem cells and the involvement of mitogen-activated protein kinase (MAPK) pathway were subsequently investigated. Alizarin red staining showed that hsa-let-7c low-expression can significantly promote the mineralization of IGF-1 treated SCAPs, while hsa-let-7c over-expression can decrease the calcium deposition of IGF-1 treated SCAPs. Western blot assay and real-time reverse transcription polymerase chain reaction further demonstrated that the expression of odonto/osteogenic markers (ALP, RUNX2/RUNX2, OSX/OSX, OCN/OCN, COL-I/COL-I, DSPP/DSP, and DMP-1/DMP-1) in IGF-1 treated SCAPs were significantly upregulated in Let-7c-low group. On the contrary, hsa-let-7c over-expression could downregulate the expression of these odonto/osteogenic markers. Moreover, western blot assay showed that the JNK and p38 MAPK signaling pathways were activated in Let-7c-low SCAPs but inhibited in Let-7c-over SCAPs. Together, the IGF-1/IGF-1R/hsa-let-7c axis can control the odonto/osteogenic differentiation of IGF-1-treated SCAPs via the regulation of JNK and p38 MAPK signaling pathways. Nature Publishing Group 2016-11-11 /pmc/articles/PMC5105129/ /pubmed/27833148 http://dx.doi.org/10.1038/srep36922 Text en Copyright © 2016, The Author(s) http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/
repository_type Open Access Journal
institution_category Foreign Institution
institution US National Center for Biotechnology Information
building NCBI PubMed
collection Online Access
language English
format Online
author Ma, Shu
Liu, Genxia
Jin, Lin
Pang, Xiyao
Wang, Yanqiu
Wang, Zilu
Yu, Yan
Yu, Jinhua
spellingShingle Ma, Shu
Liu, Genxia
Jin, Lin
Pang, Xiyao
Wang, Yanqiu
Wang, Zilu
Yu, Yan
Yu, Jinhua
IGF-1/IGF-1R/hsa-let-7c axis regulates the committed differentiation of stem cells from apical papilla
author_facet Ma, Shu
Liu, Genxia
Jin, Lin
Pang, Xiyao
Wang, Yanqiu
Wang, Zilu
Yu, Yan
Yu, Jinhua
author_sort Ma, Shu
title IGF-1/IGF-1R/hsa-let-7c axis regulates the committed differentiation of stem cells from apical papilla
title_short IGF-1/IGF-1R/hsa-let-7c axis regulates the committed differentiation of stem cells from apical papilla
title_full IGF-1/IGF-1R/hsa-let-7c axis regulates the committed differentiation of stem cells from apical papilla
title_fullStr IGF-1/IGF-1R/hsa-let-7c axis regulates the committed differentiation of stem cells from apical papilla
title_full_unstemmed IGF-1/IGF-1R/hsa-let-7c axis regulates the committed differentiation of stem cells from apical papilla
title_sort igf-1/igf-1r/hsa-let-7c axis regulates the committed differentiation of stem cells from apical papilla
description Insulin-like growth factor-1 (IGF-1) and its receptor IGF-1R play a paramount role in tooth/bone formation while hsa-let-7c actively participates in the osteogenic differentiation of mesenchymal stem cells. However, the interaction between IGF-1/IGF-1R and hsa-let-7c on the committed differentiation of stem cells from apical papilla (SCAPs) remains unclear. In this study, human SCAPs were isolated and treated with IGF-1 and hsa-let-7c over/low-expression viruses. The odonto/osteogenic differentiation of these stem cells and the involvement of mitogen-activated protein kinase (MAPK) pathway were subsequently investigated. Alizarin red staining showed that hsa-let-7c low-expression can significantly promote the mineralization of IGF-1 treated SCAPs, while hsa-let-7c over-expression can decrease the calcium deposition of IGF-1 treated SCAPs. Western blot assay and real-time reverse transcription polymerase chain reaction further demonstrated that the expression of odonto/osteogenic markers (ALP, RUNX2/RUNX2, OSX/OSX, OCN/OCN, COL-I/COL-I, DSPP/DSP, and DMP-1/DMP-1) in IGF-1 treated SCAPs were significantly upregulated in Let-7c-low group. On the contrary, hsa-let-7c over-expression could downregulate the expression of these odonto/osteogenic markers. Moreover, western blot assay showed that the JNK and p38 MAPK signaling pathways were activated in Let-7c-low SCAPs but inhibited in Let-7c-over SCAPs. Together, the IGF-1/IGF-1R/hsa-let-7c axis can control the odonto/osteogenic differentiation of IGF-1-treated SCAPs via the regulation of JNK and p38 MAPK signaling pathways.
publisher Nature Publishing Group
publishDate 2016
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5105129/
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