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SATB1 promotes osteogenic differentiation of diabetic rat BMSCs through MAPK signalling activation
Objective Special AT‐rich binding protein 1 (SATB1), a chromatin organizer and global transcriptional regulator, plays an important role in tumorigenesis and immune response. However, its function in the osteogenic differentiation of bone marrow‐derived mesenchymal stem cells (BMSCs) remains unknown...
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| Published in: | Oral diseases 2023-11, Vol.29 (8), p.3610-3619 |
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| Main Authors: | , , , , |
| Format: | Article |
| Language: | English |
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| cited_by | cdi_FETCH-LOGICAL-c3535-42a2d2778a2bfdbb5d562c414b201a034be684ba21850b705fe1472c231e7973 |
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| cites | cdi_FETCH-LOGICAL-c3535-42a2d2778a2bfdbb5d562c414b201a034be684ba21850b705fe1472c231e7973 |
| container_end_page | 3619 |
| container_issue | 8 |
| container_start_page | 3610 |
| container_title | Oral diseases |
| container_volume | 29 |
| creator | Guo, Jing Chen, Zhuochen Xiao, Yue Yu, Guiyuan Li, Yong |
| description | Objective
Special AT‐rich binding protein 1 (SATB1), a chromatin organizer and global transcriptional regulator, plays an important role in tumorigenesis and immune response. However, its function in the osteogenic differentiation of bone marrow‐derived mesenchymal stem cells (BMSCs) remains unknown. Therefore, this study aimed to explore the role of SATB1 in osteogenesis.
Methods
BMSCs were collected from the type 2 diabetes rat model and the protein and gene expression of SATB1 and osteospecific genes were evaluated post osteogenic induction.
Results
SATB1 protein expression significantly decreased in diabetic rat BMSCs whereas it increased in BMSCs following osteogenic induction. SATB1 knockdown significantly suppressed the expression of osteospecific genes, including alkaline phosphatase (Alp), runt‐related transcription factor 2, and osteocalcin, and reduced the number of mineral deposits and ALP activity, whereas SATB1 overexpression yielded the opposite results. Moreover, SATB1 knockdown suppressed activation of the MAPK signalling pathway (phosphorylation of p38 and ERK), and MAPK pathway inhibitors could reverse the inhibitory effect of SATB1 knockdown on osteogenic differentiation of BMSCs.
Conclusion
SATB1 plays a key role in the osteogenic differentiation of BMSCs via the p38 MAPK and ERK MAPK signalling pathways. These findings may provide a new strategy for the application of BMSCs in bone regeneration. |
| doi_str_mv | 10.1111/odi.14265 |
| format | article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2668911636</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2668911636</sourcerecordid><originalsourceid>FETCH-LOGICAL-c3535-42a2d2778a2bfdbb5d562c414b201a034be684ba21850b705fe1472c231e7973</originalsourceid><addsrcrecordid>eNp10E1PwyAcBnBiNM63g1_AkHjRQx1_3tod53yNmplsB28NtHRiuqJANX570akHE7lA4McTeBDaB3ICaQxdbU-AUynW0BZIAhkpqFhPayZ4Jih7GKDtEJ4IgXzE6CYaMCFJIYFsIT0bz08BP3u3dNEE7EI0bmE6W-HaNo3xpotWRes67Jq0pbSJ6cyriE_vZpOA46N3_eIR343vb3Cwi061re0WWFXRvn5d3EUbjWqD2fued9D84nw-ucpup5fXk_FtVjHBRMapojXN80JR3dRai1pIWnHgmhJQhHFtZMG1olAIonMiGgM8pxVlYPJRznbQ0So2_eWlNyGWSxsq07aqM64PJZWyGAFIJhM9_EOfXO_Ty5MqRgWnAPxTHa9U5V0I3jTls7dL5d9LIOVn72XqvfzqPdmD78ReL039K3-KTmC4Am-2Ne__J5XTs-tV5AcgHYrV</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2898421146</pqid></control><display><type>article</type><title>SATB1 promotes osteogenic differentiation of diabetic rat BMSCs through MAPK signalling activation</title><source>Wiley</source><creator>Guo, Jing ; Chen, Zhuochen ; Xiao, Yue ; Yu, Guiyuan ; Li, Yong</creator><creatorcontrib>Guo, Jing ; Chen, Zhuochen ; Xiao, Yue ; Yu, Guiyuan ; Li, Yong</creatorcontrib><description>Objective
Special AT‐rich binding protein 1 (SATB1), a chromatin organizer and global transcriptional regulator, plays an important role in tumorigenesis and immune response. However, its function in the osteogenic differentiation of bone marrow‐derived mesenchymal stem cells (BMSCs) remains unknown. Therefore, this study aimed to explore the role of SATB1 in osteogenesis.
Methods
BMSCs were collected from the type 2 diabetes rat model and the protein and gene expression of SATB1 and osteospecific genes were evaluated post osteogenic induction.
Results
SATB1 protein expression significantly decreased in diabetic rat BMSCs whereas it increased in BMSCs following osteogenic induction. SATB1 knockdown significantly suppressed the expression of osteospecific genes, including alkaline phosphatase (Alp), runt‐related transcription factor 2, and osteocalcin, and reduced the number of mineral deposits and ALP activity, whereas SATB1 overexpression yielded the opposite results. Moreover, SATB1 knockdown suppressed activation of the MAPK signalling pathway (phosphorylation of p38 and ERK), and MAPK pathway inhibitors could reverse the inhibitory effect of SATB1 knockdown on osteogenic differentiation of BMSCs.
Conclusion
SATB1 plays a key role in the osteogenic differentiation of BMSCs via the p38 MAPK and ERK MAPK signalling pathways. These findings may provide a new strategy for the application of BMSCs in bone regeneration.</description><identifier>ISSN: 1354-523X</identifier><identifier>EISSN: 1601-0825</identifier><identifier>DOI: 10.1111/odi.14265</identifier><identifier>PMID: 35608610</identifier><language>eng</language><publisher>Denmark: Wiley Subscription Services, Inc</publisher><subject>Alkaline phosphatase ; BMSCs ; Bone growth ; Chromatin ; Diabetes ; Diabetes mellitus (non-insulin dependent) ; Gene expression ; Immune response ; MAP kinase ; MAPK signalling pathway ; Mesenchymal stem cells ; Osteocalcin ; Osteogenesis ; osteogenic differentiation ; Phosphorylation ; Proteins ; Regeneration ; SATB1 ; Signal transduction ; Tumorigenesis</subject><ispartof>Oral diseases, 2023-11, Vol.29 (8), p.3610-3619</ispartof><rights>2022 Wiley Periodicals LLC.</rights><rights>This article is protected by copyright. All rights reserved.</rights><rights>2023 Wiley Periodicals LLC</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3535-42a2d2778a2bfdbb5d562c414b201a034be684ba21850b705fe1472c231e7973</citedby><cites>FETCH-LOGICAL-c3535-42a2d2778a2bfdbb5d562c414b201a034be684ba21850b705fe1472c231e7973</cites><orcidid>0000-0002-5761-1000 ; 0000-0002-4108-0989</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,778,782,27911,27912</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35608610$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Guo, Jing</creatorcontrib><creatorcontrib>Chen, Zhuochen</creatorcontrib><creatorcontrib>Xiao, Yue</creatorcontrib><creatorcontrib>Yu, Guiyuan</creatorcontrib><creatorcontrib>Li, Yong</creatorcontrib><title>SATB1 promotes osteogenic differentiation of diabetic rat BMSCs through MAPK signalling activation</title><title>Oral diseases</title><addtitle>Oral Dis</addtitle><description>Objective
Special AT‐rich binding protein 1 (SATB1), a chromatin organizer and global transcriptional regulator, plays an important role in tumorigenesis and immune response. However, its function in the osteogenic differentiation of bone marrow‐derived mesenchymal stem cells (BMSCs) remains unknown. Therefore, this study aimed to explore the role of SATB1 in osteogenesis.
Methods
BMSCs were collected from the type 2 diabetes rat model and the protein and gene expression of SATB1 and osteospecific genes were evaluated post osteogenic induction.
Results
SATB1 protein expression significantly decreased in diabetic rat BMSCs whereas it increased in BMSCs following osteogenic induction. SATB1 knockdown significantly suppressed the expression of osteospecific genes, including alkaline phosphatase (Alp), runt‐related transcription factor 2, and osteocalcin, and reduced the number of mineral deposits and ALP activity, whereas SATB1 overexpression yielded the opposite results. Moreover, SATB1 knockdown suppressed activation of the MAPK signalling pathway (phosphorylation of p38 and ERK), and MAPK pathway inhibitors could reverse the inhibitory effect of SATB1 knockdown on osteogenic differentiation of BMSCs.
Conclusion
SATB1 plays a key role in the osteogenic differentiation of BMSCs via the p38 MAPK and ERK MAPK signalling pathways. These findings may provide a new strategy for the application of BMSCs in bone regeneration.</description><subject>Alkaline phosphatase</subject><subject>BMSCs</subject><subject>Bone growth</subject><subject>Chromatin</subject><subject>Diabetes</subject><subject>Diabetes mellitus (non-insulin dependent)</subject><subject>Gene expression</subject><subject>Immune response</subject><subject>MAP kinase</subject><subject>MAPK signalling pathway</subject><subject>Mesenchymal stem cells</subject><subject>Osteocalcin</subject><subject>Osteogenesis</subject><subject>osteogenic differentiation</subject><subject>Phosphorylation</subject><subject>Proteins</subject><subject>Regeneration</subject><subject>SATB1</subject><subject>Signal transduction</subject><subject>Tumorigenesis</subject><issn>1354-523X</issn><issn>1601-0825</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><recordid>eNp10E1PwyAcBnBiNM63g1_AkHjRQx1_3tod53yNmplsB28NtHRiuqJANX570akHE7lA4McTeBDaB3ICaQxdbU-AUynW0BZIAhkpqFhPayZ4Jih7GKDtEJ4IgXzE6CYaMCFJIYFsIT0bz08BP3u3dNEE7EI0bmE6W-HaNo3xpotWRes67Jq0pbSJ6cyriE_vZpOA46N3_eIR343vb3Cwi061re0WWFXRvn5d3EUbjWqD2fued9D84nw-ucpup5fXk_FtVjHBRMapojXN80JR3dRai1pIWnHgmhJQhHFtZMG1olAIonMiGgM8pxVlYPJRznbQ0So2_eWlNyGWSxsq07aqM64PJZWyGAFIJhM9_EOfXO_Ty5MqRgWnAPxTHa9U5V0I3jTls7dL5d9LIOVn72XqvfzqPdmD78ReL039K3-KTmC4Am-2Ne__J5XTs-tV5AcgHYrV</recordid><startdate>202311</startdate><enddate>202311</enddate><creator>Guo, Jing</creator><creator>Chen, Zhuochen</creator><creator>Xiao, Yue</creator><creator>Yu, Guiyuan</creator><creator>Li, Yong</creator><general>Wiley Subscription Services, Inc</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QP</scope><scope>K9.</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-5761-1000</orcidid><orcidid>https://orcid.org/0000-0002-4108-0989</orcidid></search><sort><creationdate>202311</creationdate><title>SATB1 promotes osteogenic differentiation of diabetic rat BMSCs through MAPK signalling activation</title><author>Guo, Jing ; Chen, Zhuochen ; Xiao, Yue ; Yu, Guiyuan ; Li, Yong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3535-42a2d2778a2bfdbb5d562c414b201a034be684ba21850b705fe1472c231e7973</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Alkaline phosphatase</topic><topic>BMSCs</topic><topic>Bone growth</topic><topic>Chromatin</topic><topic>Diabetes</topic><topic>Diabetes mellitus (non-insulin dependent)</topic><topic>Gene expression</topic><topic>Immune response</topic><topic>MAP kinase</topic><topic>MAPK signalling pathway</topic><topic>Mesenchymal stem cells</topic><topic>Osteocalcin</topic><topic>Osteogenesis</topic><topic>osteogenic differentiation</topic><topic>Phosphorylation</topic><topic>Proteins</topic><topic>Regeneration</topic><topic>SATB1</topic><topic>Signal transduction</topic><topic>Tumorigenesis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Guo, Jing</creatorcontrib><creatorcontrib>Chen, Zhuochen</creatorcontrib><creatorcontrib>Xiao, Yue</creatorcontrib><creatorcontrib>Yu, Guiyuan</creatorcontrib><creatorcontrib>Li, Yong</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>Oral diseases</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Guo, Jing</au><au>Chen, Zhuochen</au><au>Xiao, Yue</au><au>Yu, Guiyuan</au><au>Li, Yong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>SATB1 promotes osteogenic differentiation of diabetic rat BMSCs through MAPK signalling activation</atitle><jtitle>Oral diseases</jtitle><addtitle>Oral Dis</addtitle><date>2023-11</date><risdate>2023</risdate><volume>29</volume><issue>8</issue><spage>3610</spage><epage>3619</epage><pages>3610-3619</pages><issn>1354-523X</issn><eissn>1601-0825</eissn><abstract>Objective
Special AT‐rich binding protein 1 (SATB1), a chromatin organizer and global transcriptional regulator, plays an important role in tumorigenesis and immune response. However, its function in the osteogenic differentiation of bone marrow‐derived mesenchymal stem cells (BMSCs) remains unknown. Therefore, this study aimed to explore the role of SATB1 in osteogenesis.
Methods
BMSCs were collected from the type 2 diabetes rat model and the protein and gene expression of SATB1 and osteospecific genes were evaluated post osteogenic induction.
Results
SATB1 protein expression significantly decreased in diabetic rat BMSCs whereas it increased in BMSCs following osteogenic induction. SATB1 knockdown significantly suppressed the expression of osteospecific genes, including alkaline phosphatase (Alp), runt‐related transcription factor 2, and osteocalcin, and reduced the number of mineral deposits and ALP activity, whereas SATB1 overexpression yielded the opposite results. Moreover, SATB1 knockdown suppressed activation of the MAPK signalling pathway (phosphorylation of p38 and ERK), and MAPK pathway inhibitors could reverse the inhibitory effect of SATB1 knockdown on osteogenic differentiation of BMSCs.
Conclusion
SATB1 plays a key role in the osteogenic differentiation of BMSCs via the p38 MAPK and ERK MAPK signalling pathways. These findings may provide a new strategy for the application of BMSCs in bone regeneration.</abstract><cop>Denmark</cop><pub>Wiley Subscription Services, Inc</pub><pmid>35608610</pmid><doi>10.1111/odi.14265</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0002-5761-1000</orcidid><orcidid>https://orcid.org/0000-0002-4108-0989</orcidid></addata></record> |
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| ispartof | Oral diseases, 2023-11, Vol.29 (8), p.3610-3619 |
| issn | 1354-523X 1601-0825 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_2668911636 |
| source | Wiley |
| subjects | Alkaline phosphatase BMSCs Bone growth Chromatin Diabetes Diabetes mellitus (non-insulin dependent) Gene expression Immune response MAP kinase MAPK signalling pathway Mesenchymal stem cells Osteocalcin Osteogenesis osteogenic differentiation Phosphorylation Proteins Regeneration SATB1 Signal transduction Tumorigenesis |
| title | SATB1 promotes osteogenic differentiation of diabetic rat BMSCs through MAPK signalling activation |
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