Lymphocyte enhancer-binding factor 1: an essential factor in odontoblastic differentiation of dental pulp cells enzymatically isolated from rat incisors
Lymphocyte enhancer-binding factor 1 (Lef1), a HMG-domain protein, is thought to play important roles in inductive tissue interaction during tooth development. Lef1 knockdown in mice causes arrest at the bud stage in tooth development. As this gene participates in the regulation of a large and diver...
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| Veröffentlicht in: | Journal of bone and mineral metabolism 2010-11, Vol.28 (6), p.650-658 |
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| creator | Yokose, Satoshi Naka, Takahiro |
| description | Lymphocyte enhancer-binding factor 1 (Lef1), a HMG-domain protein, is thought to play important roles in inductive tissue interaction during tooth development. Lef1 knockdown in mice causes arrest at the bud stage in tooth development. As this gene participates in the regulation of a large and diverse set of peptide growth factors in ectomesenchymal cell differentiation of dental papilla, Lef1 appears to be a key factor in odontoblast differentiation. However, the relationship between Lef1 and odontoblast differentiation is still unclear. To analyze the biological roles of Lef1 in regulating odontoblast differentiation, we transiently overexpressed or suppressed Lef1 in cultured dental pulp cells. Lef1-overexpressing cells expressed higher levels of dentin sialoprotein (DSPP), osteocalcin and alkaline phosphatase (ALP) mRNA and formed larger numbers of mineralized nodules compared to control cells. However, Msx-1 expression or cell proliferation was unaffected by overexpression of Lef1. To further examine the role of Lef1 in dental pulp cells, we knocked down Lef1 expression in dental pulp cells using short interfering RNA (siRNA). Transient expression of siRNA against Lef1 markedly reduced Lef1 mRNA levels, and Lef1-suppressed cells expressed lower levels of DSPP, osteocalcin and ALP mRNA compared to control cells. Furthermore, the formation of mineralized nodules was inhibited by siRNA against Lef1; however, neither Msx-1 expression or cell proliferation was inhibited by siRNA against Lef1. These results outline the role of Lef1 in accelerating odontoblast differentiation by regulating DSP and osteocalcin mRNA expression in dental pulp cells, confirming that Lef1 is a key factor for odontoblast differentiation. |
| doi_str_mv | 10.1007/s00774-010-0185-0 |
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Lef1 knockdown in mice causes arrest at the bud stage in tooth development. As this gene participates in the regulation of a large and diverse set of peptide growth factors in ectomesenchymal cell differentiation of dental papilla, Lef1 appears to be a key factor in odontoblast differentiation. However, the relationship between Lef1 and odontoblast differentiation is still unclear. To analyze the biological roles of Lef1 in regulating odontoblast differentiation, we transiently overexpressed or suppressed Lef1 in cultured dental pulp cells. Lef1-overexpressing cells expressed higher levels of dentin sialoprotein (DSPP), osteocalcin and alkaline phosphatase (ALP) mRNA and formed larger numbers of mineralized nodules compared to control cells. However, Msx-1 expression or cell proliferation was unaffected by overexpression of Lef1. To further examine the role of Lef1 in dental pulp cells, we knocked down Lef1 expression in dental pulp cells using short interfering RNA (siRNA). Transient expression of siRNA against Lef1 markedly reduced Lef1 mRNA levels, and Lef1-suppressed cells expressed lower levels of DSPP, osteocalcin and ALP mRNA compared to control cells. Furthermore, the formation of mineralized nodules was inhibited by siRNA against Lef1; however, neither Msx-1 expression or cell proliferation was inhibited by siRNA against Lef1. These results outline the role of Lef1 in accelerating odontoblast differentiation by regulating DSP and osteocalcin mRNA expression in dental pulp cells, confirming that Lef1 is a key factor for odontoblast differentiation.</description><identifier>ISSN: 0914-8779</identifier><identifier>EISSN: 1435-5604</identifier><identifier>DOI: 10.1007/s00774-010-0185-0</identifier><identifier>PMID: 20425127</identifier><language>eng</language><publisher>Japan: Japan : Springer Japan</publisher><subject>Alkaline Phosphatase - genetics ; Alkaline Phosphatase - metabolism ; Animals ; Biological and medical sciences ; Cell Differentiation ; Cells, Cultured ; Dental Pulp - cytology ; Dental Pulp - metabolism ; Dental pulp cells ; Dentinogenesis ; Diseases of the osteoarticular system ; Extracellular Matrix Proteins - genetics ; Extracellular Matrix Proteins - metabolism ; Female ; Gene Expression Regulation ; Gene Silencing ; Genes, Reporter ; Incisor ; Lef1 ; Lymphoid Enhancer-Binding Factor 1 - biosynthesis ; Lymphoid Enhancer-Binding Factor 1 - genetics ; Lymphoid Enhancer-Binding Factor 1 - physiology ; Medical sciences ; Medicine ; Medicine & Public Health ; Metabolic Diseases ; Odontoblast differentiation ; Odontoblasts - cytology ; Odontoblasts - metabolism ; Original Article ; Orthopedics ; Osteocalcin - genetics ; Osteocalcin - metabolism ; Phosphoproteins - genetics ; Phosphoproteins - metabolism ; Proteins ; Rats ; Rats, Sprague-Dawley ; RNA, Messenger - metabolism ; RNA, Small Interfering ; Sialoglycoproteins - genetics ; Sialoglycoproteins - metabolism ; Tooth Calcification</subject><ispartof>Journal of bone and mineral metabolism, 2010-11, Vol.28 (6), p.650-658</ispartof><rights>The Japanese Society for Bone and Mineral Research and Springer 2010</rights><rights>2015 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c544t-d08a299b7ef79f33ba1a01bc3f1e4a99ebd8055304f2fc9c30dd102cc18fa5833</citedby><cites>FETCH-LOGICAL-c544t-d08a299b7ef79f33ba1a01bc3f1e4a99ebd8055304f2fc9c30dd102cc18fa5833</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00774-010-0185-0$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00774-010-0185-0$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=23367433$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20425127$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yokose, Satoshi</creatorcontrib><creatorcontrib>Naka, Takahiro</creatorcontrib><title>Lymphocyte enhancer-binding factor 1: an essential factor in odontoblastic differentiation of dental pulp cells enzymatically isolated from rat incisors</title><title>Journal of bone and mineral metabolism</title><addtitle>J Bone Miner Metab</addtitle><addtitle>J Bone Miner Metab</addtitle><description>Lymphocyte enhancer-binding factor 1 (Lef1), a HMG-domain protein, is thought to play important roles in inductive tissue interaction during tooth development. Lef1 knockdown in mice causes arrest at the bud stage in tooth development. As this gene participates in the regulation of a large and diverse set of peptide growth factors in ectomesenchymal cell differentiation of dental papilla, Lef1 appears to be a key factor in odontoblast differentiation. However, the relationship between Lef1 and odontoblast differentiation is still unclear. To analyze the biological roles of Lef1 in regulating odontoblast differentiation, we transiently overexpressed or suppressed Lef1 in cultured dental pulp cells. Lef1-overexpressing cells expressed higher levels of dentin sialoprotein (DSPP), osteocalcin and alkaline phosphatase (ALP) mRNA and formed larger numbers of mineralized nodules compared to control cells. However, Msx-1 expression or cell proliferation was unaffected by overexpression of Lef1. To further examine the role of Lef1 in dental pulp cells, we knocked down Lef1 expression in dental pulp cells using short interfering RNA (siRNA). Transient expression of siRNA against Lef1 markedly reduced Lef1 mRNA levels, and Lef1-suppressed cells expressed lower levels of DSPP, osteocalcin and ALP mRNA compared to control cells. Furthermore, the formation of mineralized nodules was inhibited by siRNA against Lef1; however, neither Msx-1 expression or cell proliferation was inhibited by siRNA against Lef1. These results outline the role of Lef1 in accelerating odontoblast differentiation by regulating DSP and osteocalcin mRNA expression in dental pulp cells, confirming that Lef1 is a key factor for odontoblast differentiation.</description><subject>Alkaline Phosphatase - genetics</subject><subject>Alkaline Phosphatase - metabolism</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Cell Differentiation</subject><subject>Cells, Cultured</subject><subject>Dental Pulp - cytology</subject><subject>Dental Pulp - metabolism</subject><subject>Dental pulp cells</subject><subject>Dentinogenesis</subject><subject>Diseases of the osteoarticular system</subject><subject>Extracellular Matrix Proteins - genetics</subject><subject>Extracellular Matrix Proteins - metabolism</subject><subject>Female</subject><subject>Gene Expression Regulation</subject><subject>Gene Silencing</subject><subject>Genes, Reporter</subject><subject>Incisor</subject><subject>Lef1</subject><subject>Lymphoid Enhancer-Binding Factor 1 - biosynthesis</subject><subject>Lymphoid Enhancer-Binding Factor 1 - genetics</subject><subject>Lymphoid Enhancer-Binding Factor 1 - physiology</subject><subject>Medical sciences</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Metabolic Diseases</subject><subject>Odontoblast differentiation</subject><subject>Odontoblasts - cytology</subject><subject>Odontoblasts - metabolism</subject><subject>Original Article</subject><subject>Orthopedics</subject><subject>Osteocalcin - genetics</subject><subject>Osteocalcin - metabolism</subject><subject>Phosphoproteins - genetics</subject><subject>Phosphoproteins - metabolism</subject><subject>Proteins</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>RNA, Messenger - metabolism</subject><subject>RNA, Small Interfering</subject><subject>Sialoglycoproteins - genetics</subject><subject>Sialoglycoproteins - metabolism</subject><subject>Tooth Calcification</subject><issn>0914-8779</issn><issn>1435-5604</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNp9kc9u1DAQxi0EotvCA3ABS6jiFJiJnTjpDVX8k1biAD1bjmNvUyX2YjuH8CQ8Lg7ZAuLAwbY88_tmxv4IeYbwGgHEm5g3wQtAyKupCnhAdshZVVQ18IdkBy3yohGiPSPnMd4BoKgEPiZnJfCywlLsyI_9Mh1vvV6SocbdKqdNKLrB9YM7UKt08oHiFVWOmhiNS4Ma78ODo773LvluVDENmvaDtSb8gtLgc9bSPt-y4jiPR6rNOMbc5Psy5bxW47jQIfpRJdNTG_xEg0q5qs7BEJ-QR1aN0Tw9nRfk5v27r9cfi_3nD5-u3-4LXXGeih4aVbZtJ4wVrWWsU6gAO80sGq7a1nR9A1XFgNvS6lYz6HuEUmtsrKoaxi7Iq63uMfhvs4lJTkNcR1XO-DlKUZd1I6qmzuTLf8g7PweXh5OIyDgXwFcKN0oHH2MwVh7DMKmwSAS5uiY312R2Ta6uScia56fKczeZ_rfi3qYMXJ4AFfPH2aDWX_rDMVYLztbHlBsXc8odTPhrxP90f7GJrPJSHUIufPOlBGSALYimrdlPfsC7dQ</recordid><startdate>201011</startdate><enddate>201011</enddate><creator>Yokose, Satoshi</creator><creator>Naka, Takahiro</creator><general>Japan : Springer Japan</general><general>Springer Japan</general><general>Springer</general><general>Springer Nature B.V</general><scope>FBQ</scope><scope>IQODW</scope><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>7QP</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>M1P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>201011</creationdate><title>Lymphocyte enhancer-binding factor 1: an essential factor in odontoblastic differentiation of dental pulp cells enzymatically isolated from rat incisors</title><author>Yokose, Satoshi ; Naka, Takahiro</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c544t-d08a299b7ef79f33ba1a01bc3f1e4a99ebd8055304f2fc9c30dd102cc18fa5833</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Alkaline Phosphatase - genetics</topic><topic>Alkaline Phosphatase - metabolism</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Cell Differentiation</topic><topic>Cells, Cultured</topic><topic>Dental Pulp - cytology</topic><topic>Dental Pulp - metabolism</topic><topic>Dental pulp cells</topic><topic>Dentinogenesis</topic><topic>Diseases of the osteoarticular system</topic><topic>Extracellular Matrix Proteins - genetics</topic><topic>Extracellular Matrix Proteins - metabolism</topic><topic>Female</topic><topic>Gene Expression Regulation</topic><topic>Gene Silencing</topic><topic>Genes, Reporter</topic><topic>Incisor</topic><topic>Lef1</topic><topic>Lymphoid Enhancer-Binding Factor 1 - biosynthesis</topic><topic>Lymphoid Enhancer-Binding Factor 1 - genetics</topic><topic>Lymphoid Enhancer-Binding Factor 1 - physiology</topic><topic>Medical sciences</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Metabolic Diseases</topic><topic>Odontoblast differentiation</topic><topic>Odontoblasts - cytology</topic><topic>Odontoblasts - metabolism</topic><topic>Original Article</topic><topic>Orthopedics</topic><topic>Osteocalcin - genetics</topic><topic>Osteocalcin - metabolism</topic><topic>Phosphoproteins - genetics</topic><topic>Phosphoproteins - metabolism</topic><topic>Proteins</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>RNA, Messenger - metabolism</topic><topic>RNA, Small Interfering</topic><topic>Sialoglycoproteins - genetics</topic><topic>Sialoglycoproteins - metabolism</topic><topic>Tooth Calcification</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yokose, Satoshi</creatorcontrib><creatorcontrib>Naka, Takahiro</creatorcontrib><collection>AGRIS</collection><collection>Pascal-Francis</collection><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>Calcium & Calcified Tissue Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma 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 Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Nursing & Allied Health Premium</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 China</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of bone and mineral metabolism</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yokose, Satoshi</au><au>Naka, Takahiro</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Lymphocyte enhancer-binding factor 1: an essential factor in odontoblastic differentiation of dental pulp cells enzymatically isolated from rat incisors</atitle><jtitle>Journal of bone and mineral metabolism</jtitle><stitle>J Bone Miner Metab</stitle><addtitle>J Bone Miner Metab</addtitle><date>2010-11</date><risdate>2010</risdate><volume>28</volume><issue>6</issue><spage>650</spage><epage>658</epage><pages>650-658</pages><issn>0914-8779</issn><eissn>1435-5604</eissn><abstract>Lymphocyte enhancer-binding factor 1 (Lef1), a HMG-domain protein, is thought to play important roles in inductive tissue interaction during tooth development. Lef1 knockdown in mice causes arrest at the bud stage in tooth development. As this gene participates in the regulation of a large and diverse set of peptide growth factors in ectomesenchymal cell differentiation of dental papilla, Lef1 appears to be a key factor in odontoblast differentiation. However, the relationship between Lef1 and odontoblast differentiation is still unclear. To analyze the biological roles of Lef1 in regulating odontoblast differentiation, we transiently overexpressed or suppressed Lef1 in cultured dental pulp cells. Lef1-overexpressing cells expressed higher levels of dentin sialoprotein (DSPP), osteocalcin and alkaline phosphatase (ALP) mRNA and formed larger numbers of mineralized nodules compared to control cells. However, Msx-1 expression or cell proliferation was unaffected by overexpression of Lef1. To further examine the role of Lef1 in dental pulp cells, we knocked down Lef1 expression in dental pulp cells using short interfering RNA (siRNA). Transient expression of siRNA against Lef1 markedly reduced Lef1 mRNA levels, and Lef1-suppressed cells expressed lower levels of DSPP, osteocalcin and ALP mRNA compared to control cells. Furthermore, the formation of mineralized nodules was inhibited by siRNA against Lef1; however, neither Msx-1 expression or cell proliferation was inhibited by siRNA against Lef1. These results outline the role of Lef1 in accelerating odontoblast differentiation by regulating DSP and osteocalcin mRNA expression in dental pulp cells, confirming that Lef1 is a key factor for odontoblast differentiation.</abstract><cop>Japan</cop><pub>Japan : Springer Japan</pub><pmid>20425127</pmid><doi>10.1007/s00774-010-0185-0</doi><tpages>9</tpages></addata></record> |
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| subjects | Alkaline Phosphatase - genetics Alkaline Phosphatase - metabolism Animals Biological and medical sciences Cell Differentiation Cells, Cultured Dental Pulp - cytology Dental Pulp - metabolism Dental pulp cells Dentinogenesis Diseases of the osteoarticular system Extracellular Matrix Proteins - genetics Extracellular Matrix Proteins - metabolism Female Gene Expression Regulation Gene Silencing Genes, Reporter Incisor Lef1 Lymphoid Enhancer-Binding Factor 1 - biosynthesis Lymphoid Enhancer-Binding Factor 1 - genetics Lymphoid Enhancer-Binding Factor 1 - physiology Medical sciences Medicine Medicine & Public Health Metabolic Diseases Odontoblast differentiation Odontoblasts - cytology Odontoblasts - metabolism Original Article Orthopedics Osteocalcin - genetics Osteocalcin - metabolism Phosphoproteins - genetics Phosphoproteins - metabolism Proteins Rats Rats, Sprague-Dawley RNA, Messenger - metabolism RNA, Small Interfering Sialoglycoproteins - genetics Sialoglycoproteins - metabolism Tooth Calcification |
| title | Lymphocyte enhancer-binding factor 1: an essential factor in odontoblastic differentiation of dental pulp cells enzymatically isolated from rat incisors |
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