Leptin reduces in vitro cementoblast mineralization and survival as well as induces PGE2 release by ERK1/2 commitment.
Identifieur interne : 000008 ( Main/Exploration ); précédent : 000007; suivant : 000009Leptin reduces in vitro cementoblast mineralization and survival as well as induces PGE2 release by ERK1/2 commitment.
Auteurs : G. Ruiz-Heiland [Allemagne] ; J W Yong [Allemagne] ; J. Von Bremen [Allemagne] ; S. Ruf [Allemagne]Source :
- Clinical oral investigations [ 1436-3771 ] ; 2021.
Descripteurs français
- KwdFr :
- MESH :
English descriptors
- KwdEn :
- MESH :
- chemical : Dinoprostone, Leptin.
- Apoptosis, Dental Cementum, Humans, MAP Kinase Signaling System, Overweight.
Abstract
OBJECTIVES
Juvenile obesity is a complex clinical condition that is present more and more frequently in the daily orthodontic practice. Over-weighted patients have an impaired bone metabolism, due in part to their increased levels of circulating adipokines. Particularly, leptin has been reported to play a key role in bone physiology. Leptin is ubiquitously present in the body, including blood, saliva, and crevicular fluid. If, and to what extent, it could influence the reaction of cementoblasts during orthodontic-induced forces is yet unknown.
MATERIAL AND METHODS
OCCM-30 cementoblasts were cultivated under compressive forces using different concentrations of leptin. The expression of ObR, Runx-2, Osteocalcin, Rank-L, Sost, Caspase 3, 8, and 9 were analyzed by RT-PCR. Western blots were employed for protein analysis. The ERK1/2 antagonist FR180204 (Calbiochem) was used and cPLA2 activation, PGE2, and cytochrome C release were further evaluated.
RESULTS
In vitro, when compressive forces are applied, leptin promotes ERK1/2 phosphorylation, as well as upregulates PGE2 and caspase 3 and caspase 9 on OCCM cells. Blockade of ERK1/2 impairs leptin-induced PGE2 secretion and reduced caspase 3 and caspase 9 expression.
CONCLUSIONS
Leptin influences the physiological effect of compressive forces on cementoblasts, exerting in vitro a pro-inflammatory and pro-apoptotic effect.
CLINICAL RELEVANCE
Our findings indicate that leptin exacerbates the physiological effect of compressive forces on cementoblasts promoting the release of PGE2 and increases the rate of cell apoptosis, and thus, increased levels of leptin may influence the inflammatory response during orthodontically induced tooth movement.
DOI: 10.1007/s00784-020-03501-3
PubMed: 32820432
PubMed Central: PMC7965856
Affiliations:
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Ruiz-Heiland</name><affiliation wicri:level="1"><nlm:affiliation>Department of Orthodontics, University of Giessen, Schlangenzahl 14, 35392, Giessen, Germany. gisela.ruiz-heiland@dentist.med.uni-giessen.de.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Department of Orthodontics, University of Giessen, Schlangenzahl 14, 35392, Giessen</wicri:regionArea><wicri:noRegion>35392, Giessen</wicri:noRegion><wicri:noRegion>35392, Giessen</wicri:noRegion><wicri:noRegion>Giessen</wicri:noRegion></affiliation></author><author><name sortKey="Yong, J W" sort="Yong, J W" uniqKey="Yong J" first="J W" last="Yong">J W Yong</name><affiliation wicri:level="1"><nlm:affiliation>Department of Orthodontics, University of Giessen, Schlangenzahl 14, 35392, Giessen, Germany.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Department of Orthodontics, University of Giessen, Schlangenzahl 14, 35392, Giessen</wicri:regionArea><wicri:noRegion>35392, Giessen</wicri:noRegion><wicri:noRegion>35392, Giessen</wicri:noRegion><wicri:noRegion>Giessen</wicri:noRegion></affiliation></author><author><name sortKey="Von Bremen, J" sort="Von Bremen, J" uniqKey="Von Bremen J" first="J" last="Von Bremen">J. 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Ruiz-Heiland</name><affiliation wicri:level="1"><nlm:affiliation>Department of Orthodontics, University of Giessen, Schlangenzahl 14, 35392, Giessen, Germany. gisela.ruiz-heiland@dentist.med.uni-giessen.de.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Department of Orthodontics, University of Giessen, Schlangenzahl 14, 35392, Giessen</wicri:regionArea><wicri:noRegion>35392, Giessen</wicri:noRegion><wicri:noRegion>35392, Giessen</wicri:noRegion><wicri:noRegion>Giessen</wicri:noRegion></affiliation></author><author><name sortKey="Yong, J W" sort="Yong, J W" uniqKey="Yong J" first="J W" last="Yong">J W Yong</name><affiliation wicri:level="1"><nlm:affiliation>Department of Orthodontics, University of Giessen, Schlangenzahl 14, 35392, Giessen, Germany.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Department of Orthodontics, University of Giessen, Schlangenzahl 14, 35392, Giessen</wicri:regionArea><wicri:noRegion>35392, Giessen</wicri:noRegion><wicri:noRegion>35392, Giessen</wicri:noRegion><wicri:noRegion>Giessen</wicri:noRegion></affiliation></author><author><name sortKey="Von Bremen, J" sort="Von Bremen, J" uniqKey="Von Bremen J" first="J" last="Von Bremen">J. Von Bremen</name><affiliation wicri:level="1"><nlm:affiliation>Department of Orthodontics, University of Giessen, Schlangenzahl 14, 35392, Giessen, Germany.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Department of Orthodontics, University of Giessen, Schlangenzahl 14, 35392, Giessen</wicri:regionArea><wicri:noRegion>35392, Giessen</wicri:noRegion><wicri:noRegion>35392, Giessen</wicri:noRegion><wicri:noRegion>Giessen</wicri:noRegion></affiliation></author><author><name sortKey="Ruf, S" sort="Ruf, S" uniqKey="Ruf S" first="S" last="Ruf">S. Ruf</name><affiliation wicri:level="1"><nlm:affiliation>Department of Orthodontics, University of Giessen, Schlangenzahl 14, 35392, Giessen, Germany.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Department of Orthodontics, University of Giessen, Schlangenzahl 14, 35392, Giessen</wicri:regionArea><wicri:noRegion>35392, Giessen</wicri:noRegion><wicri:noRegion>35392, Giessen</wicri:noRegion><wicri:noRegion>Giessen</wicri:noRegion></affiliation></author></analytic><series><title level="j">Clinical oral investigations</title><idno type="eISSN">1436-3771</idno><imprint><date when="2021" type="published">2021</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Apoptosis (MeSH)</term><term>Dental Cementum (MeSH)</term><term>Dinoprostone (MeSH)</term><term>Humans (MeSH)</term><term>Leptin (MeSH)</term><term>MAP Kinase Signaling System (MeSH)</term><term>Overweight (MeSH)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Apoptose (MeSH)</term><term>Cément dentaire (MeSH)</term><term>Dinoprostone (MeSH)</term><term>Humains (MeSH)</term><term>Leptine (MeSH)</term><term>Surpoids (MeSH)</term><term>Système de signalisation des MAP kinases (MeSH)</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Dinoprostone</term><term>Leptin</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Apoptosis</term><term>Dental Cementum</term><term>Humans</term><term>MAP Kinase Signaling System</term><term>Overweight</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Apoptose</term><term>Cément dentaire</term><term>Dinoprostone</term><term>Humains</term><term>Leptine</term><term>Surpoids</term><term>Système de signalisation des MAP kinases</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p><b>OBJECTIVES</b></p><p>Juvenile obesity is a complex clinical condition that is present more and more frequently in the daily orthodontic practice. Over-weighted patients have an impaired bone metabolism, due in part to their increased levels of circulating adipokines. Particularly, leptin has been reported to play a key role in bone physiology. Leptin is ubiquitously present in the body, including blood, saliva, and crevicular fluid. If, and to what extent, it could influence the reaction of cementoblasts during orthodontic-induced forces is yet unknown.</p></div><div type="abstract" xml:lang="en"><p><b>MATERIAL AND METHODS</b></p><p>OCCM-30 cementoblasts were cultivated under compressive forces using different concentrations of leptin. The expression of ObR, Runx-2, Osteocalcin, Rank-L, Sost, Caspase 3, 8, and 9 were analyzed by RT-PCR. Western blots were employed for protein analysis. The ERK1/2 antagonist FR180204 (Calbiochem) was used and cPLA2 activation, PGE2, and cytochrome C release were further evaluated.</p></div><div type="abstract" xml:lang="en"><p><b>RESULTS</b></p><p>In vitro, when compressive forces are applied, leptin promotes ERK1/2 phosphorylation, as well as upregulates PGE2 and caspase 3 and caspase 9 on OCCM cells. Blockade of ERK1/2 impairs leptin-induced PGE2 secretion and reduced caspase 3 and caspase 9 expression.</p></div><div type="abstract" xml:lang="en"><p><b>CONCLUSIONS</b></p><p>Leptin influences the physiological effect of compressive forces on cementoblasts, exerting in vitro a pro-inflammatory and pro-apoptotic effect.</p></div><div type="abstract" xml:lang="en"><p><b>CLINICAL RELEVANCE</b></p><p>Our findings indicate that leptin exacerbates the physiological effect of compressive forces on cementoblasts promoting the release of PGE2 and increases the rate of cell apoptosis, and thus, increased levels of leptin may influence the inflammatory response during orthodontically induced tooth movement.</p></div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" IndexingMethod="Automated" Owner="NLM"><PMID Version="1">32820432</PMID><DateCompleted><Year>2021</Year><Month>03</Month><Day>18</Day></DateCompleted><DateRevised><Year>2021</Year><Month>06</Month><Day>28</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1436-3771</ISSN><JournalIssue CitedMedium="Internet"><Volume>25</Volume><Issue>4</Issue><PubDate><Year>2021</Year><Month>Apr</Month></PubDate></JournalIssue><Title>Clinical oral investigations</Title><ISOAbbreviation>Clin Oral Investig</ISOAbbreviation></Journal><ArticleTitle>Leptin reduces in vitro cementoblast mineralization and survival as well as induces PGE2 release by ERK1/2 commitment.</ArticleTitle><Pagination><MedlinePgn>1933-1944</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1007/s00784-020-03501-3</ELocationID><Abstract><AbstractText Label="OBJECTIVES" NlmCategory="OBJECTIVE">Juvenile obesity is a complex clinical condition that is present more and more frequently in the daily orthodontic practice. Over-weighted patients have an impaired bone metabolism, due in part to their increased levels of circulating adipokines. Particularly, leptin has been reported to play a key role in bone physiology. Leptin is ubiquitously present in the body, including blood, saliva, and crevicular fluid. If, and to what extent, it could influence the reaction of cementoblasts during orthodontic-induced forces is yet unknown.</AbstractText><AbstractText Label="MATERIAL AND METHODS" NlmCategory="METHODS">OCCM-30 cementoblasts were cultivated under compressive forces using different concentrations of leptin. The expression of ObR, Runx-2, Osteocalcin, Rank-L, Sost, Caspase 3, 8, and 9 were analyzed by RT-PCR. Western blots were employed for protein analysis. The ERK1/2 antagonist FR180204 (Calbiochem) was used and cPLA2 activation, PGE2, and cytochrome C release were further evaluated.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">In vitro, when compressive forces are applied, leptin promotes ERK1/2 phosphorylation, as well as upregulates PGE2 and caspase 3 and caspase 9 on OCCM cells. Blockade of ERK1/2 impairs leptin-induced PGE2 secretion and reduced caspase 3 and caspase 9 expression.</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">Leptin influences the physiological effect of compressive forces on cementoblasts, exerting in vitro a pro-inflammatory and pro-apoptotic effect.</AbstractText><AbstractText Label="CLINICAL RELEVANCE" NlmCategory="CONCLUSIONS">Our findings indicate that leptin exacerbates the physiological effect of compressive forces on cementoblasts promoting the release of PGE2 and increases the rate of cell apoptosis, and thus, increased levels of leptin may influence the inflammatory response during orthodontically induced tooth movement.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ruiz-Heiland</LastName><ForeName>G</ForeName><Initials>G</Initials><Identifier Source="ORCID">http://orcid.org/0000-0002-1582-020X</Identifier><AffiliationInfo><Affiliation>Department of Orthodontics, University of Giessen, Schlangenzahl 14, 35392, Giessen, Germany. gisela.ruiz-heiland@dentist.med.uni-giessen.de.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yong</LastName><ForeName>J W</ForeName><Initials>JW</Initials><AffiliationInfo><Affiliation>Department of Orthodontics, University of Giessen, Schlangenzahl 14, 35392, Giessen, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>von Bremen</LastName><ForeName>J</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Orthodontics, University of Giessen, Schlangenzahl 14, 35392, Giessen, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ruf</LastName><ForeName>S</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Orthodontics, University of Giessen, Schlangenzahl 14, 35392, Giessen, Germany.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2020</Year><Month>08</Month><Day>20</Day></ArticleDate></Article><MedlineJournalInfo><Country>Germany</Country><MedlineTA>Clin Oral Investig</MedlineTA><NlmUniqueID>9707115</NlmUniqueID><ISSNLinking>1432-6981</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D020738">Leptin</NameOfSubstance></Chemical><Chemical><RegistryNumber>K7Q1JQR04M</RegistryNumber><NameOfSubstance UI="D015232">Dinoprostone</NameOfSubstance></Chemical></ChemicalList><CitationSubset>D</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D017209" MajorTopicYN="N">Apoptosis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003739" MajorTopicYN="Y">Dental Cementum</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015232" MajorTopicYN="N">Dinoprostone</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020738" MajorTopicYN="Y">Leptin</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020935" MajorTopicYN="N">MAP Kinase Signaling System</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D050177" MajorTopicYN="N">Overweight</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Cementoblasts</Keyword><Keyword MajorTopicYN="N">ERK1/2</Keyword><Keyword MajorTopicYN="N">Leptin</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2020</Year><Month>01</Month><Day>13</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2020</Year><Month>08</Month><Day>05</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2020</Year><Month>8</Month><Day>21</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2021</Year><Month>3</Month><Day>19</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2020</Year><Month>8</Month><Day>22</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">32820432</ArticleId><ArticleId IdType="doi">10.1007/s00784-020-03501-3</ArticleId><ArticleId IdType="pii">10.1007/s00784-020-03501-3</ArticleId><ArticleId IdType="pmc">PMC7965856</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>World Health Organisation (WHO). https://www.who.int/topics/obesity/en/ . 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