Role of TGF-β1 in Fluoride-Treated Osteoblasts at Different Stages
Little attention has been paid to the tolerance of osteoblasts to fluoride in distinct differentiation stages, and the role of TGF-β1 in fluoride-treated osteoblast differentiation of progenitors and precursors was rarely mentioned in previous studies. The present study aimed to clarify how fluoride...
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| Veröffentlicht in: | Biological trace element research 2022-02, Vol.200 (2), p.740-748 |
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| creator | Jiang, Ningning Xu, Wenshu Zhang, Zhongyuan Jin, Hui Yang, Yang Zhang, Jingmin Xu, Hui |
| description | Little attention has been paid to the tolerance of osteoblasts to fluoride in distinct differentiation stages, and the role of TGF-β1 in fluoride-treated osteoblast differentiation of progenitors and precursors was rarely mentioned in previous studies. The present study aimed to clarify how fluoride affected different differentiation stages of osteoblasts, and to elucidate the role of TGF-β1 in this process. We assessed cell migration, proliferation, DNA damage, and apoptosis of early-differentiated osteoblasts derived from bone marrow stem cells (BMSCs) exposed to fluoride with or without TGF-β1. Subsequently, MC3T3-E1 cells cultured with mineral induction medium were treated with fluoride to test fluoride’s effect on late-differentiated osteoblasts. The specific fluoride concentrations and treatment times were chosen to evaluate the role of TGF-β1 in fluoride-induced osteoblastic differentiation and function. Results showed early-differentiated osteoblasts treated with a low dose of fluoride grew and moved more rapidly. TGF-β1 promoted cell proliferation and inhibited cell apoptosis in early-differentiated osteoblasts exposed to a low fluoride dose, but enhanced apoptosis at higher fluoride conditions. In the late-differentiated osteoblasts, the fluorine dose range with anabolic effects was narrowed, and the fluoride range with catabolic effects was widened. Treatment with a low fluoride dose stimulated the alkaline phosphatase (ALP) expression. TGF-β1 treatment inhibited Runx2 expression but increased RANKL expression in late-differentiated osteoblasts exposed to fluoride. Meanwhile, TGF-β1 treatments activated Smad3 phosphorylation but blocked Wnt10b expression in osteoblasts. We conclude that TGF-β1 plays an essential role in fluoride-induced differentiation and osteoblast function via activation of Smad3 instead of Wnt10 signaling. |
| doi_str_mv | 10.1007/s12011-021-02686-2 |
| format | Article |
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The present study aimed to clarify how fluoride affected different differentiation stages of osteoblasts, and to elucidate the role of TGF-β1 in this process. We assessed cell migration, proliferation, DNA damage, and apoptosis of early-differentiated osteoblasts derived from bone marrow stem cells (BMSCs) exposed to fluoride with or without TGF-β1. Subsequently, MC3T3-E1 cells cultured with mineral induction medium were treated with fluoride to test fluoride’s effect on late-differentiated osteoblasts. The specific fluoride concentrations and treatment times were chosen to evaluate the role of TGF-β1 in fluoride-induced osteoblastic differentiation and function. Results showed early-differentiated osteoblasts treated with a low dose of fluoride grew and moved more rapidly. TGF-β1 promoted cell proliferation and inhibited cell apoptosis in early-differentiated osteoblasts exposed to a low fluoride dose, but enhanced apoptosis at higher fluoride conditions. In the late-differentiated osteoblasts, the fluorine dose range with anabolic effects was narrowed, and the fluoride range with catabolic effects was widened. Treatment with a low fluoride dose stimulated the alkaline phosphatase (ALP) expression. TGF-β1 treatment inhibited Runx2 expression but increased RANKL expression in late-differentiated osteoblasts exposed to fluoride. Meanwhile, TGF-β1 treatments activated Smad3 phosphorylation but blocked Wnt10b expression in osteoblasts. We conclude that TGF-β1 plays an essential role in fluoride-induced differentiation and osteoblast function via activation of Smad3 instead of Wnt10 signaling.</description><identifier>ISSN: 0163-4984</identifier><identifier>EISSN: 1559-0720</identifier><identifier>DOI: 10.1007/s12011-021-02686-2</identifier><identifier>PMID: 34031801</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>3T3 Cells ; Alkaline phosphatase ; Anabolism ; Animals ; Apoptosis ; Biochemistry ; Biomedical and Life Sciences ; Biomedical materials ; Biotechnology ; Bone marrow ; Cbfa-1 protein ; Cell Differentiation ; Cell migration ; cell movement ; Cell proliferation ; Differentiation ; DNA damage ; Exposure ; Fluorides ; Fluorides - pharmacology ; Fluorine ; Life Sciences ; Mice ; Nutrition ; Oncology ; Osteoblastogenesis ; Osteoblasts ; Osteoblasts - drug effects ; Osteogenesis ; Osteoprogenitor cells ; Phosphatase ; Phosphorylation ; Progenitor cells ; Proliferation ; Signal Transduction ; Smad3 protein ; Stem cells ; TRANCE protein ; Transforming Growth Factor beta1 ; Transforming growth factor-b1 ; wnt proteins</subject><ispartof>Biological trace element research, 2022-02, Vol.200 (2), p.740-748</ispartof><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2021</rights><rights>2021. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.</rights><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2021.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3232-7d3a5bb8ef713656e26b2eef16778319455a872801e7461d7e9c27142901d5ad3</citedby><cites>FETCH-LOGICAL-c3232-7d3a5bb8ef713656e26b2eef16778319455a872801e7461d7e9c27142901d5ad3</cites><orcidid>0000-0002-7072-1706</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s12011-021-02686-2$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12011-021-02686-2$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,778,782,27907,27908,41471,42540,51302</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34031801$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Jiang, Ningning</creatorcontrib><creatorcontrib>Xu, Wenshu</creatorcontrib><creatorcontrib>Zhang, Zhongyuan</creatorcontrib><creatorcontrib>Jin, Hui</creatorcontrib><creatorcontrib>Yang, Yang</creatorcontrib><creatorcontrib>Zhang, Jingmin</creatorcontrib><creatorcontrib>Xu, Hui</creatorcontrib><title>Role of TGF-β1 in Fluoride-Treated Osteoblasts at Different Stages</title><title>Biological trace element research</title><addtitle>Biol Trace Elem Res</addtitle><addtitle>Biol Trace Elem Res</addtitle><description>Little attention has been paid to the tolerance of osteoblasts to fluoride in distinct differentiation stages, and the role of TGF-β1 in fluoride-treated osteoblast differentiation of progenitors and precursors was rarely mentioned in previous studies. The present study aimed to clarify how fluoride affected different differentiation stages of osteoblasts, and to elucidate the role of TGF-β1 in this process. We assessed cell migration, proliferation, DNA damage, and apoptosis of early-differentiated osteoblasts derived from bone marrow stem cells (BMSCs) exposed to fluoride with or without TGF-β1. Subsequently, MC3T3-E1 cells cultured with mineral induction medium were treated with fluoride to test fluoride’s effect on late-differentiated osteoblasts. The specific fluoride concentrations and treatment times were chosen to evaluate the role of TGF-β1 in fluoride-induced osteoblastic differentiation and function. Results showed early-differentiated osteoblasts treated with a low dose of fluoride grew and moved more rapidly. TGF-β1 promoted cell proliferation and inhibited cell apoptosis in early-differentiated osteoblasts exposed to a low fluoride dose, but enhanced apoptosis at higher fluoride conditions. In the late-differentiated osteoblasts, the fluorine dose range with anabolic effects was narrowed, and the fluoride range with catabolic effects was widened. Treatment with a low fluoride dose stimulated the alkaline phosphatase (ALP) expression. TGF-β1 treatment inhibited Runx2 expression but increased RANKL expression in late-differentiated osteoblasts exposed to fluoride. Meanwhile, TGF-β1 treatments activated Smad3 phosphorylation but blocked Wnt10b expression in osteoblasts. We conclude that TGF-β1 plays an essential role in fluoride-induced differentiation and osteoblast function via activation of Smad3 instead of Wnt10 signaling.</description><subject>3T3 Cells</subject><subject>Alkaline phosphatase</subject><subject>Anabolism</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedical materials</subject><subject>Biotechnology</subject><subject>Bone marrow</subject><subject>Cbfa-1 protein</subject><subject>Cell Differentiation</subject><subject>Cell migration</subject><subject>cell movement</subject><subject>Cell proliferation</subject><subject>Differentiation</subject><subject>DNA damage</subject><subject>Exposure</subject><subject>Fluorides</subject><subject>Fluorides - pharmacology</subject><subject>Fluorine</subject><subject>Life Sciences</subject><subject>Mice</subject><subject>Nutrition</subject><subject>Oncology</subject><subject>Osteoblastogenesis</subject><subject>Osteoblasts</subject><subject>Osteoblasts - drug effects</subject><subject>Osteogenesis</subject><subject>Osteoprogenitor cells</subject><subject>Phosphatase</subject><subject>Phosphorylation</subject><subject>Progenitor cells</subject><subject>Proliferation</subject><subject>Signal Transduction</subject><subject>Smad3 protein</subject><subject>Stem cells</subject><subject>TRANCE protein</subject><subject>Transforming Growth Factor beta1</subject><subject>Transforming growth factor-b1</subject><subject>wnt proteins</subject><issn>0163-4984</issn><issn>1559-0720</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqFkb9OwzAQhy0EglJ4AQYUiYXF4DvHdjKiQgsSEhKU2XKaCwpKE7CTgdfiQXgmXMofiQEGy4O_-3x3P8YOQJyAEOY0AAoALnB1dKY5brARKJVzYVBsspEALXmaZ-kO2w3hUQgwmMtttiNTISETMGKT266hpKuS-WzK314hqdtk2gydr0vic0-upzK5CT11ReNCHxLXJ-d1VZGntk_uevdAYY9tVa4JtP95j9n99GI-ueTXN7Orydk1X0iUyE0pnSqKjCoDUitNqAskqkAbk0nIU6VcZjC2RSbVUBrKF2ggxVxAqVwpx-x47X3y3fNAobfLOiyoaVxL3RAsaqm1kivbv6iSiKnCuIcxO_qFPnaDb-MgUQgGALLURArX1MJ3IXiq7JOvl86_WBB2lYZdp2FjGvYjDYux6PBTPRRLKr9LvtYfAbkGQnxqH8j__P2H9h103pEH</recordid><startdate>20220201</startdate><enddate>20220201</enddate><creator>Jiang, Ningning</creator><creator>Xu, Wenshu</creator><creator>Zhang, Zhongyuan</creator><creator>Jin, Hui</creator><creator>Yang, Yang</creator><creator>Zhang, Jingmin</creator><creator>Xu, Hui</creator><general>Springer US</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QH</scope><scope>7QP</scope><scope>7TN</scope><scope>7U7</scope><scope>7UA</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>BKSAR</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>F1W</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H97</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>L.G</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>PCBAR</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope><scope>7S9</scope><scope>L.6</scope><orcidid>https://orcid.org/0000-0002-7072-1706</orcidid></search><sort><creationdate>20220201</creationdate><title>Role of TGF-β1 in Fluoride-Treated Osteoblasts at Different Stages</title><author>Jiang, Ningning ; Xu, Wenshu ; Zhang, Zhongyuan ; Jin, Hui ; Yang, Yang ; Zhang, Jingmin ; Xu, Hui</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3232-7d3a5bb8ef713656e26b2eef16778319455a872801e7461d7e9c27142901d5ad3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>3T3 Cells</topic><topic>Alkaline phosphatase</topic><topic>Anabolism</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedical materials</topic><topic>Biotechnology</topic><topic>Bone marrow</topic><topic>Cbfa-1 protein</topic><topic>Cell Differentiation</topic><topic>Cell migration</topic><topic>cell movement</topic><topic>Cell proliferation</topic><topic>Differentiation</topic><topic>DNA damage</topic><topic>Exposure</topic><topic>Fluorides</topic><topic>Fluorides - pharmacology</topic><topic>Fluorine</topic><topic>Life Sciences</topic><topic>Mice</topic><topic>Nutrition</topic><topic>Oncology</topic><topic>Osteoblastogenesis</topic><topic>Osteoblasts</topic><topic>Osteoblasts - drug effects</topic><topic>Osteogenesis</topic><topic>Osteoprogenitor cells</topic><topic>Phosphatase</topic><topic>Phosphorylation</topic><topic>Progenitor cells</topic><topic>Proliferation</topic><topic>Signal Transduction</topic><topic>Smad3 protein</topic><topic>Stem cells</topic><topic>TRANCE protein</topic><topic>Transforming Growth Factor beta1</topic><topic>Transforming growth factor-b1</topic><topic>wnt proteins</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Jiang, Ningning</creatorcontrib><creatorcontrib>Xu, Wenshu</creatorcontrib><creatorcontrib>Zhang, Zhongyuan</creatorcontrib><creatorcontrib>Jin, Hui</creatorcontrib><creatorcontrib>Yang, Yang</creatorcontrib><creatorcontrib>Zhang, Jingmin</creatorcontrib><creatorcontrib>Xu, Hui</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Aqualine</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Oceanic Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Water Resources Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection (ProQuest)</collection><collection>Earth, Atmospheric & Aquatic Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>ASFA: Aquatic Sciences and Fisheries Abstracts</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Aquatic Science & Fisheries Abstracts (ASFA) 3: Aquatic Pollution & Environmental Quality</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Aquatic Science & Fisheries Abstracts (ASFA) Professional</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database (ProQuest)</collection><collection>Biological Science Database</collection><collection>Earth, Atmospheric & Aquatic Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>AGRICOLA</collection><collection>AGRICOLA - Academic</collection><jtitle>Biological trace element research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jiang, Ningning</au><au>Xu, Wenshu</au><au>Zhang, Zhongyuan</au><au>Jin, Hui</au><au>Yang, Yang</au><au>Zhang, Jingmin</au><au>Xu, Hui</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Role of TGF-β1 in Fluoride-Treated Osteoblasts at Different Stages</atitle><jtitle>Biological trace element research</jtitle><stitle>Biol Trace Elem Res</stitle><addtitle>Biol Trace Elem Res</addtitle><date>2022-02-01</date><risdate>2022</risdate><volume>200</volume><issue>2</issue><spage>740</spage><epage>748</epage><pages>740-748</pages><issn>0163-4984</issn><eissn>1559-0720</eissn><abstract>Little attention has been paid to the tolerance of osteoblasts to fluoride in distinct differentiation stages, and the role of TGF-β1 in fluoride-treated osteoblast differentiation of progenitors and precursors was rarely mentioned in previous studies. The present study aimed to clarify how fluoride affected different differentiation stages of osteoblasts, and to elucidate the role of TGF-β1 in this process. We assessed cell migration, proliferation, DNA damage, and apoptosis of early-differentiated osteoblasts derived from bone marrow stem cells (BMSCs) exposed to fluoride with or without TGF-β1. Subsequently, MC3T3-E1 cells cultured with mineral induction medium were treated with fluoride to test fluoride’s effect on late-differentiated osteoblasts. The specific fluoride concentrations and treatment times were chosen to evaluate the role of TGF-β1 in fluoride-induced osteoblastic differentiation and function. Results showed early-differentiated osteoblasts treated with a low dose of fluoride grew and moved more rapidly. TGF-β1 promoted cell proliferation and inhibited cell apoptosis in early-differentiated osteoblasts exposed to a low fluoride dose, but enhanced apoptosis at higher fluoride conditions. In the late-differentiated osteoblasts, the fluorine dose range with anabolic effects was narrowed, and the fluoride range with catabolic effects was widened. Treatment with a low fluoride dose stimulated the alkaline phosphatase (ALP) expression. TGF-β1 treatment inhibited Runx2 expression but increased RANKL expression in late-differentiated osteoblasts exposed to fluoride. Meanwhile, TGF-β1 treatments activated Smad3 phosphorylation but blocked Wnt10b expression in osteoblasts. We conclude that TGF-β1 plays an essential role in fluoride-induced differentiation and osteoblast function via activation of Smad3 instead of Wnt10 signaling.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>34031801</pmid><doi>10.1007/s12011-021-02686-2</doi><tpages>9</tpages><orcidid>https://orcid.org/0000-0002-7072-1706</orcidid></addata></record> |
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| subjects | 3T3 Cells Alkaline phosphatase Anabolism Animals Apoptosis Biochemistry Biomedical and Life Sciences Biomedical materials Biotechnology Bone marrow Cbfa-1 protein Cell Differentiation Cell migration cell movement Cell proliferation Differentiation DNA damage Exposure Fluorides Fluorides - pharmacology Fluorine Life Sciences Mice Nutrition Oncology Osteoblastogenesis Osteoblasts Osteoblasts - drug effects Osteogenesis Osteoprogenitor cells Phosphatase Phosphorylation Progenitor cells Proliferation Signal Transduction Smad3 protein Stem cells TRANCE protein Transforming Growth Factor beta1 Transforming growth factor-b1 wnt proteins |
| title | Role of TGF-β1 in Fluoride-Treated Osteoblasts at Different Stages |
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