Suppressing STAT3 activation impairs bone formation during maxillary expansion and relapse
Autor(a) principal: | |
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Data de Publicação: | 2023 |
Outros Autores: | , , , , , |
Tipo de documento: | Conjunto de dados |
Título da fonte: | SciELO Data |
Texto Completo: | https://doi.org/10.48331/scielodata.37EU59 |
Resumo: | Objectives: The mid-palatal expansion technique is commonly used to correct maxilla constriction in dental clinics. There is, however, a tendency for it to relapse, and the key molecules responsible for modulating bone formation remain elusive. Thus, this study aimed to investigate whether signal transducer and activator of transcription 3 (STAT3) activation contributes to osteoblast-mediated bone formation during palatal expansion and relapse. Methodology: Thirty male Wistar rats were randomly allocated into Ctrl (control), E (expansion only), and E+Stattic (expansion plus STAT3-inhibitor, Stattic) groups. Micro-computed tomography, micromorphology staining, and immunohistochemistry of the mid-palatal suture were performed on days 7 and 14. In vitro cyclic tensile stress (10% magnitude, 0.5 Hz frequency, and 24 h duration) was applied to rat primary osteoblasts and Stattic was administered for STAT3 inhibition. The role of STAT3 in mechanical loading-induced osteoblasts was confirmed by alkaline phosphatase (ALP), alizarin red staining, and western blots. Results: The E group manifested a greater arch width than the E+Stattic group after expansion, and the differences between the two groups remained significant after relapse. Active bone formation was detected in the E group with increased expression of ALP, COL-I, and Runx2, whereas the expression of osteogenesis-related factors was downregulated in the E+stattic group. After STAT3 inhibition, expansive force-induced bone resorption was attenuated, as demonstrated by TRAP staining. Furthermore, the administration of Stattic in vitro partially suppressed tensile stress-enhanced osteogenic markers in osteoblasts. Conclusions: Overall, STAT3 inactivation reduced osteoblast-mediated bone formation during palatal expansion and post-expansion relapse, suggesting that it may be a potential therapeutic target to treat force-induced bone formation. |
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https://doi.org/10.48331/scielodata.37EU59Wang, SiXiao, XiaoyueChen, JianweiZhai, QimingXin, LiangjingZheng, XinhuiSong, JinlinSuppressing STAT3 activation impairs bone formation during maxillary expansion and relapseSciELO DataObjectives: The mid-palatal expansion technique is commonly used to correct maxilla constriction in dental clinics. There is, however, a tendency for it to relapse, and the key molecules responsible for modulating bone formation remain elusive. Thus, this study aimed to investigate whether signal transducer and activator of transcription 3 (STAT3) activation contributes to osteoblast-mediated bone formation during palatal expansion and relapse. Methodology: Thirty male Wistar rats were randomly allocated into Ctrl (control), E (expansion only), and E+Stattic (expansion plus STAT3-inhibitor, Stattic) groups. Micro-computed tomography, micromorphology staining, and immunohistochemistry of the mid-palatal suture were performed on days 7 and 14. In vitro cyclic tensile stress (10% magnitude, 0.5 Hz frequency, and 24 h duration) was applied to rat primary osteoblasts and Stattic was administered for STAT3 inhibition. The role of STAT3 in mechanical loading-induced osteoblasts was confirmed by alkaline phosphatase (ALP), alizarin red staining, and western blots. Results: The E group manifested a greater arch width than the E+Stattic group after expansion, and the differences between the two groups remained significant after relapse. Active bone formation was detected in the E group with increased expression of ALP, COL-I, and Runx2, whereas the expression of osteogenesis-related factors was downregulated in the E+stattic group. After STAT3 inhibition, expansive force-induced bone resorption was attenuated, as demonstrated by TRAP staining. Furthermore, the administration of Stattic in vitro partially suppressed tensile stress-enhanced osteogenic markers in osteoblasts. Conclusions: Overall, STAT3 inactivation reduced osteoblast-mediated bone formation during palatal expansion and post-expansion relapse, suggesting that it may be a potential therapeutic target to treat force-induced bone formation.2023-03-28info:eu-repo/semantics/openAccesshttp://creativecommons.org/licenses/by/4.0Medicine, Health and Life SciencesOsteogenesisPalatal Expansion TechniqueSTAT3 Transcription Factorinfo:eu-repo/semantics/datasetinfo:eu-repo/semantics/datasetinfo:eu-repo/semantics/publishedVersionDatasetreponame:SciELO Datainstname:Scientific Electronic Library Online (SCIELO)instacron:SCIRepositório de Dados de PesquisaONGhttps://data.scielo.org/oai/requestdata@scielo.orgopendoar:2024-04-11T06:12:08SciELO Data - Scientific Electronic Library Online (SCIELO)falsedoi:10.48331/scielodata.37EU59 |
dc.title.none.fl_str_mv |
Suppressing STAT3 activation impairs bone formation during maxillary expansion and relapse |
title |
Suppressing STAT3 activation impairs bone formation during maxillary expansion and relapse |
spellingShingle |
Suppressing STAT3 activation impairs bone formation during maxillary expansion and relapse Wang, Si Medicine, Health and Life Sciences Osteogenesis Palatal Expansion Technique STAT3 Transcription Factor |
title_short |
Suppressing STAT3 activation impairs bone formation during maxillary expansion and relapse |
title_full |
Suppressing STAT3 activation impairs bone formation during maxillary expansion and relapse |
title_fullStr |
Suppressing STAT3 activation impairs bone formation during maxillary expansion and relapse |
title_full_unstemmed |
Suppressing STAT3 activation impairs bone formation during maxillary expansion and relapse |
title_sort |
Suppressing STAT3 activation impairs bone formation during maxillary expansion and relapse |
author |
Wang, Si |
author_facet |
Wang, Si Xiao, Xiaoyue Chen, Jianwei Zhai, Qiming Xin, Liangjing Zheng, Xinhui Song, Jinlin |
author_role |
author |
author2 |
Xiao, Xiaoyue Chen, Jianwei Zhai, Qiming Xin, Liangjing Zheng, Xinhui Song, Jinlin |
author2_role |
author author author author author author |
dc.contributor.author.fl_str_mv |
Wang, Si Xiao, Xiaoyue Chen, Jianwei Zhai, Qiming Xin, Liangjing Zheng, Xinhui Song, Jinlin |
dc.subject.none.fl_str_mv |
Medicine, Health and Life Sciences Osteogenesis Palatal Expansion Technique STAT3 Transcription Factor |
topic |
Medicine, Health and Life Sciences Osteogenesis Palatal Expansion Technique STAT3 Transcription Factor |
description |
Objectives: The mid-palatal expansion technique is commonly used to correct maxilla constriction in dental clinics. There is, however, a tendency for it to relapse, and the key molecules responsible for modulating bone formation remain elusive. Thus, this study aimed to investigate whether signal transducer and activator of transcription 3 (STAT3) activation contributes to osteoblast-mediated bone formation during palatal expansion and relapse. Methodology: Thirty male Wistar rats were randomly allocated into Ctrl (control), E (expansion only), and E+Stattic (expansion plus STAT3-inhibitor, Stattic) groups. Micro-computed tomography, micromorphology staining, and immunohistochemistry of the mid-palatal suture were performed on days 7 and 14. In vitro cyclic tensile stress (10% magnitude, 0.5 Hz frequency, and 24 h duration) was applied to rat primary osteoblasts and Stattic was administered for STAT3 inhibition. The role of STAT3 in mechanical loading-induced osteoblasts was confirmed by alkaline phosphatase (ALP), alizarin red staining, and western blots. Results: The E group manifested a greater arch width than the E+Stattic group after expansion, and the differences between the two groups remained significant after relapse. Active bone formation was detected in the E group with increased expression of ALP, COL-I, and Runx2, whereas the expression of osteogenesis-related factors was downregulated in the E+stattic group. After STAT3 inhibition, expansive force-induced bone resorption was attenuated, as demonstrated by TRAP staining. Furthermore, the administration of Stattic in vitro partially suppressed tensile stress-enhanced osteogenic markers in osteoblasts. Conclusions: Overall, STAT3 inactivation reduced osteoblast-mediated bone formation during palatal expansion and post-expansion relapse, suggesting that it may be a potential therapeutic target to treat force-induced bone formation. |
publishDate |
2023 |
dc.date.issued.fl_str_mv |
2023-03-28 |
dc.type.openaire.fl_str_mv |
info:eu-repo/semantics/dataset |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
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info:eu-repo/semantics/dataset |
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dataset |
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publishedVersion |
dc.identifier.url.fl_str_mv |
https://doi.org/10.48331/scielodata.37EU59 |
url |
https://doi.org/10.48331/scielodata.37EU59 |
dc.rights.openaire.fl_str_mv |
info:eu-repo/semantics/openAccess http://creativecommons.org/licenses/by/4.0 |
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openAccess |
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http://creativecommons.org/licenses/by/4.0 |
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SciELO Data |
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SciELO Data - Scientific Electronic Library Online (SCIELO) |
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