CpG ODN‐induced matrix metalloproteinase‐13 expression is mediated via activation of the ERK and NF‐κB signalling pathways in odontoblast cells
Identifieur interne : 001232 ( Main/Exploration ); précédent : 001231; suivant : 001233CpG ODN‐induced matrix metalloproteinase‐13 expression is mediated via activation of the ERK and NF‐κB signalling pathways in odontoblast cells
Auteurs : J. Zhang ; Q. L. Zhu ; P. Huang [République populaire de Chine] ; Q. Yu ; Z. H. Wang ; P. R. Cooper [Royaume-Uni] ; A. J. Smith [Royaume-Uni] ; W. He [République populaire de Chine]Source :
- International Endodontic Journal [ 0143-2885 ] ; 2013-07.
English descriptors
- Teeft :
- Chemical biology, Chondrocytes, Control peptide, Critical reviews, Dental pulp, Elisa, Elisa analyses, Endodontic, Fresh medium, Hard tissues, Human chondrocytes, Ijbasr plasmids, Immune response, Independent experiments, Inhibitor, Inhibitory, Inhibitory peptide, International endodontic journal, John wiley sons, Kinase, Life technologies, Luciferase, Luciferase activity, Mapk, Mapk pathways, Matrix, Matrix metalloproteinase, Matrix metalloproteinases, Medical university, Metalloproteinase, Mouse olcs, Mrna, Mrna level, Murine cell line, Negative control, Odontoblast cell line, Odontoblast cells, Odontoblasts, Odontoblasts zhang, Olcs, Operative dentistry endodontics, Oral biology, Oral biology medicine, Other groups, Pathway, Peptide, Plasmid, Present study, Previous studies, Protein expression, Protein kinase, Pulp tissue, Remodelling, Reporter plasmid, Room temperature, Santa cruz biotechnology, Separate experiment, Tissue remodelling, Tlr9, Transient transfection, Untreated control, Western blot, Zhang.
Abstract
Aim: To investigate the effects of CpG ODN (CpG oligodeoxynucleotides) to model the action of bacterial challenge on pulpal matrix metalloproteinase‐13 (MMP‐13) expression and elucidate the associated intracellular signalling pathways. Methodology: Real‐time PCR was used to detect the effects of CpG ODN on MMP‐13 mRNA expression levels in a murine odontoblast‐lineage cell line (OLCs). The possible involvement of TLR9/MyD88, NF‐κB or MAPK pathways involved in the CpG ODN‐induced MMP‐13 expression was examined by real‐time PCR, transient transfection, luciferase activity assay and ELISA. Western blotting was performed to assay the phosphorylation of ERK at a range of time points. Results: MMP‐13 was constitutively expressed in OLCs, and their exposure to CpG ODN significantly increased MMP‐13 expression. Pre‐treatment of OLCs with the inhibitory peptide MyD88, or chloroquine, attenuated the CpG ODN‐induced expression of MMP‐13. Treatment of the OLCs with CpG ODN increased NF‐κB‐luciferase activity. This activity was decreased by the over‐expression of a nondegrading mutant of IκBα (IκBαSR), although enhanced by the over‐expression of NF‐κB p65. MMP‐13 expression induced by CpG ODN was markedly suppressed by NF‐κB inhibitors (pyrrolidine dithiocarbamate, PDTC), IκBα phosphorylation inhibitors (Bay 117082) or IκB protease inhibitor (L‐1‐tosylamido‐2‐phenylethyl chloromethyl ketone, TPCK). The inhibitor of ERK1/2, U0126, but not inhibitors of p38 MAPK and JNK, SB203580 and SP600125, decreased CpG ODN‐mediated MMP‐13 expression. Conclusion: The CpG ODN‐induced MMP‐13 expression in OLCs is mediated through TLR9, NF‐κB and the ERK pathway indicating that potentially the recognition of CpG ODN by TLR9 on odontoblasts may regulate the remodelling of injured dental pulp and hard tissues by inducing MMP‐13 expression.
Url:
DOI: 10.1111/iej.12043
Affiliations:
- Royaume-Uni, République populaire de Chine
- Angleterre, Midlands de l'Ouest
- Birmingham
- Université de Birmingham
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He</name><affiliation></affiliation><affiliation wicri:level="1"><country wicri:rule="url">République populaire de Chine</country></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">International Endodontic Journal</title><title level="j" type="alt">INTERNATIONAL ENDODONTIC JOURNAL</title><idno type="ISSN">0143-2885</idno><idno type="eISSN">1365-2591</idno><imprint><biblScope unit="vol">46</biblScope><biblScope unit="issue">7</biblScope><biblScope unit="page" from="666">666</biblScope><biblScope unit="page" to="674">674</biblScope><biblScope unit="page-count">9</biblScope><date type="published" when="2013-07">2013-07</date></imprint><idno type="ISSN">0143-2885</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0143-2885</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Chemical biology</term><term>Chondrocytes</term><term>Control peptide</term><term>Critical reviews</term><term>Dental pulp</term><term>Elisa</term><term>Elisa analyses</term><term>Endodontic</term><term>Fresh medium</term><term>Hard tissues</term><term>Human chondrocytes</term><term>Ijbasr plasmids</term><term>Immune response</term><term>Independent experiments</term><term>Inhibitor</term><term>Inhibitory</term><term>Inhibitory peptide</term><term>International endodontic journal</term><term>John wiley sons</term><term>Kinase</term><term>Life technologies</term><term>Luciferase</term><term>Luciferase activity</term><term>Mapk</term><term>Mapk pathways</term><term>Matrix</term><term>Matrix metalloproteinase</term><term>Matrix metalloproteinases</term><term>Medical university</term><term>Metalloproteinase</term><term>Mouse olcs</term><term>Mrna</term><term>Mrna level</term><term>Murine cell line</term><term>Negative control</term><term>Odontoblast cell line</term><term>Odontoblast cells</term><term>Odontoblasts</term><term>Odontoblasts zhang</term><term>Olcs</term><term>Operative dentistry endodontics</term><term>Oral biology</term><term>Oral biology medicine</term><term>Other groups</term><term>Pathway</term><term>Peptide</term><term>Plasmid</term><term>Present study</term><term>Previous studies</term><term>Protein expression</term><term>Protein kinase</term><term>Pulp tissue</term><term>Remodelling</term><term>Reporter plasmid</term><term>Room temperature</term><term>Santa cruz biotechnology</term><term>Separate experiment</term><term>Tissue remodelling</term><term>Tlr9</term><term>Transient transfection</term><term>Untreated control</term><term>Western blot</term><term>Zhang</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Aim: To investigate the effects of CpG ODN (CpG oligodeoxynucleotides) to model the action of bacterial challenge on pulpal matrix metalloproteinase‐13 (MMP‐13) expression and elucidate the associated intracellular signalling pathways. Methodology: Real‐time PCR was used to detect the effects of CpG ODN on MMP‐13 mRNA expression levels in a murine odontoblast‐lineage cell line (OLCs). The possible involvement of TLR9/MyD88, NF‐κB or MAPK pathways involved in the CpG ODN‐induced MMP‐13 expression was examined by real‐time PCR, transient transfection, luciferase activity assay and ELISA. Western blotting was performed to assay the phosphorylation of ERK at a range of time points. Results: MMP‐13 was constitutively expressed in OLCs, and their exposure to CpG ODN significantly increased MMP‐13 expression. Pre‐treatment of OLCs with the inhibitory peptide MyD88, or chloroquine, attenuated the CpG ODN‐induced expression of MMP‐13. Treatment of the OLCs with CpG ODN increased NF‐κB‐luciferase activity. This activity was decreased by the over‐expression of a nondegrading mutant of IκBα (IκBαSR), although enhanced by the over‐expression of NF‐κB p65. MMP‐13 expression induced by CpG ODN was markedly suppressed by NF‐κB inhibitors (pyrrolidine dithiocarbamate, PDTC), IκBα phosphorylation inhibitors (Bay 117082) or IκB protease inhibitor (L‐1‐tosylamido‐2‐phenylethyl chloromethyl ketone, TPCK). The inhibitor of ERK1/2, U0126, but not inhibitors of p38 MAPK and JNK, SB203580 and SP600125, decreased CpG ODN‐mediated MMP‐13 expression. Conclusion: The CpG ODN‐induced MMP‐13 expression in OLCs is mediated through TLR9, NF‐κB and the ERK pathway indicating that potentially the recognition of CpG ODN by TLR9 on odontoblasts may regulate the remodelling of injured dental pulp and hard tissues by inducing MMP‐13 expression.</div></front></TEI><affiliations><list><country><li>Royaume-Uni</li><li>République populaire de Chine</li></country><region><li>Angleterre</li><li>Midlands de l'Ouest</li></region><settlement><li>Birmingham</li></settlement><orgName><li>Université de Birmingham</li></orgName></list><tree><noCountry><name sortKey="Wang, Z H" sort="Wang, Z H" uniqKey="Wang Z" first="Z. H." last="Wang">Z. H. Wang</name><name sortKey="Yu, Q" sort="Yu, Q" uniqKey="Yu Q" first="Q." last="Yu">Q. Yu</name><name sortKey="Zhang, J" sort="Zhang, J" uniqKey="Zhang J" first="J." last="Zhang">J. Zhang</name><name sortKey="Zhu, Q L" sort="Zhu, Q L" uniqKey="Zhu Q" first="Q. L." last="Zhu">Q. L. Zhu</name></noCountry><country name="République populaire de Chine"><noRegion><name sortKey="Huang, P" sort="Huang, P" uniqKey="Huang P" first="P." last="Huang">P. Huang</name></noRegion><name sortKey="He, W" sort="He, W" uniqKey="He W" first="W." last="He">W. He</name></country><country name="Royaume-Uni"><region name="Angleterre"><name sortKey="Cooper, P R" sort="Cooper, P R" uniqKey="Cooper P" first="P. R." last="Cooper">P. R. Cooper</name></region><name sortKey="Smith, A J" sort="Smith, A J" uniqKey="Smith A" first="A. J." last="Smith">A. J. Smith</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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