Expression of Ihh signaling pathway in condylar cartilage after bite-raising in adult rats
Temporomandibular joint osteoarthritis (TMJOA) is a complex inflammatory condition with multiple factors and degenerative processes co-occurring. However, its pathogenesis remains uncertain. The purpose of the study was to observe the expression of Indian hedgehog (Ihh) signal related molecules in T...
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| Veröffentlicht in: | Journal of molecular histology 2019-10, Vol.50 (5), p.459-470 |
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| creator | Long, Hui-qing Tian, Peng-fei Guan, Yu-xin Liu, Ling-xia Wu, Xiu-ping Li, Bing |
| description | Temporomandibular joint osteoarthritis (TMJOA) is a complex inflammatory condition with multiple factors and degenerative processes co-occurring. However, its pathogenesis remains uncertain. The purpose of the study was to observe the expression of Indian hedgehog (Ihh) signal related molecules in TMJOA induced by bite-raising and to study the effect and mechanism of Ihh signaling. Our research indicated that Ihh signaling pathway can be activated in condylar cartilage induced by bite-raising. The histological analysis showed TMJOA-like structural changes of condylar cartilage in experiment groups. Ihh, Smoothened (Smo), and Gli zinc finger transcription factors-1 (Gli-1) were activated in the experimental groups, and the expression levels increased significantly over time, whereas the sham control groups showed no fluctuation. Additionally, the expression levels of matrix metalloproteinase-13 (MMP-13) and cysteinyl aspartate specific proteinase-3 (Caspase-3) in the experiment groups increased in a time-dependent manner compared with the matched sham control groups. In conclusion, our results indicated that the Ihh signaling pathway may activate the occurrence of TMJOA by mediating the hypertrophy of chondrocytes, which may be an important regulatory mechanism and potential therapeutic target in the repair of condylar cartilage. |
| doi_str_mv | 10.1007/s10735-019-09840-0 |
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However, its pathogenesis remains uncertain. The purpose of the study was to observe the expression of Indian hedgehog (Ihh) signal related molecules in TMJOA induced by bite-raising and to study the effect and mechanism of Ihh signaling. Our research indicated that Ihh signaling pathway can be activated in condylar cartilage induced by bite-raising. The histological analysis showed TMJOA-like structural changes of condylar cartilage in experiment groups. Ihh, Smoothened (Smo), and Gli zinc finger transcription factors-1 (Gli-1) were activated in the experimental groups, and the expression levels increased significantly over time, whereas the sham control groups showed no fluctuation. Additionally, the expression levels of matrix metalloproteinase-13 (MMP-13) and cysteinyl aspartate specific proteinase-3 (Caspase-3) in the experiment groups increased in a time-dependent manner compared with the matched sham control groups. In conclusion, our results indicated that the Ihh signaling pathway may activate the occurrence of TMJOA by mediating the hypertrophy of chondrocytes, which may be an important regulatory mechanism and potential therapeutic target in the repair of condylar cartilage.</description><identifier>ISSN: 1567-2379</identifier><identifier>EISSN: 1567-2387</identifier><identifier>DOI: 10.1007/s10735-019-09840-0</identifier><identifier>PMID: 31302828</identifier><language>eng</language><publisher>Dordrecht: Springer Netherlands</publisher><subject>Aging ; Animals ; Biomedical and Life Sciences ; Biomedicine ; Bites and Stings - metabolism ; Bone and Bones ; Cartilage - metabolism ; Cartilage diseases ; Caspase ; Caspase-3 ; Cell Biology ; Chondrocytes ; Chondrocytes - pathology ; Collagenase 3 ; Developmental Biology ; Hedgehog protein ; Hedgehog Proteins - metabolism ; Hypertrophy ; Inflammation ; Life Sciences ; Matrix metalloproteinase ; Metalloproteinase ; Original Paper ; Osteoarthritis ; Osteoarthritis - etiology ; Osteoarthritis - pathology ; Proteinase ; Proteinase 3 ; Rats ; Signal Transduction ; Temporomandibular joint ; Temporomandibular Joint Disorders - etiology ; Temporomandibular Joint Disorders - pathology ; Therapeutic applications ; Transcription factors ; Zinc finger proteins</subject><ispartof>Journal of molecular histology, 2019-10, Vol.50 (5), p.459-470</ispartof><rights>Springer Nature B.V. 2019</rights><rights>Journal of Molecular Histology is a copyright of Springer, (2019). All Rights Reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-4514332f82a3323d818eb6a2f2c2a9456d17ee02f7348a17ece7a92bf3205e4c3</citedby><cites>FETCH-LOGICAL-c375t-4514332f82a3323d818eb6a2f2c2a9456d17ee02f7348a17ece7a92bf3205e4c3</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/s10735-019-09840-0$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10735-019-09840-0$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31302828$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Long, Hui-qing</creatorcontrib><creatorcontrib>Tian, Peng-fei</creatorcontrib><creatorcontrib>Guan, Yu-xin</creatorcontrib><creatorcontrib>Liu, Ling-xia</creatorcontrib><creatorcontrib>Wu, Xiu-ping</creatorcontrib><creatorcontrib>Li, Bing</creatorcontrib><title>Expression of Ihh signaling pathway in condylar cartilage after bite-raising in adult rats</title><title>Journal of molecular histology</title><addtitle>J Mol Hist</addtitle><addtitle>J Mol Histol</addtitle><description>Temporomandibular joint osteoarthritis (TMJOA) is a complex inflammatory condition with multiple factors and degenerative processes co-occurring. However, its pathogenesis remains uncertain. The purpose of the study was to observe the expression of Indian hedgehog (Ihh) signal related molecules in TMJOA induced by bite-raising and to study the effect and mechanism of Ihh signaling. Our research indicated that Ihh signaling pathway can be activated in condylar cartilage induced by bite-raising. The histological analysis showed TMJOA-like structural changes of condylar cartilage in experiment groups. Ihh, Smoothened (Smo), and Gli zinc finger transcription factors-1 (Gli-1) were activated in the experimental groups, and the expression levels increased significantly over time, whereas the sham control groups showed no fluctuation. Additionally, the expression levels of matrix metalloproteinase-13 (MMP-13) and cysteinyl aspartate specific proteinase-3 (Caspase-3) in the experiment groups increased in a time-dependent manner compared with the matched sham control groups. In conclusion, our results indicated that the Ihh signaling pathway may activate the occurrence of TMJOA by mediating the hypertrophy of chondrocytes, which may be an important regulatory mechanism and potential therapeutic target in the repair of condylar cartilage.</description><subject>Aging</subject><subject>Animals</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Bites and Stings - metabolism</subject><subject>Bone and Bones</subject><subject>Cartilage - metabolism</subject><subject>Cartilage diseases</subject><subject>Caspase</subject><subject>Caspase-3</subject><subject>Cell Biology</subject><subject>Chondrocytes</subject><subject>Chondrocytes - pathology</subject><subject>Collagenase 3</subject><subject>Developmental Biology</subject><subject>Hedgehog protein</subject><subject>Hedgehog Proteins - metabolism</subject><subject>Hypertrophy</subject><subject>Inflammation</subject><subject>Life Sciences</subject><subject>Matrix metalloproteinase</subject><subject>Metalloproteinase</subject><subject>Original Paper</subject><subject>Osteoarthritis</subject><subject>Osteoarthritis - etiology</subject><subject>Osteoarthritis - pathology</subject><subject>Proteinase</subject><subject>Proteinase 3</subject><subject>Rats</subject><subject>Signal Transduction</subject><subject>Temporomandibular joint</subject><subject>Temporomandibular Joint Disorders - etiology</subject><subject>Temporomandibular Joint Disorders - pathology</subject><subject>Therapeutic applications</subject><subject>Transcription factors</subject><subject>Zinc finger proteins</subject><issn>1567-2379</issn><issn>1567-2387</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp9kD9PwzAQxS0EolD4AgzIEgtL4GwnsTOiqkClSiywsFiXxGldpUmxE0G_Pe4fisTAdE-633une4RcMbhjAPLeM5AiiYBlEWQqhgiOyBlLUhlxoeTxQctsQM69XwBwlcbZKRkIJoLm6oy8j79Wznhv24a2FZ3M59TbWYO1bWZ0hd38E9fUNrRom3Jdo6MFus7WODMUq844mtvORA6t3xgCiGVfd9Rh5y_ISYW1N5f7OSRvj-PX0XM0fXmajB6mUSFk0kVxwmIheKU4hiFKxZTJU-QVLzhmcZKWTBoDvJIiVhh0YSRmPK8Eh8TEhRiS213uyrUfvfGdXlpfmLrGxrS915wniqVMZllAb_6gi7Z34dstJUFCAhAovqMK13rvTKVXzi7RrTUDvWle75rXoXm9bV5vTNf76D5fmvJg-ak6AGIH-LBqZsb93v4n9hs87I2N</recordid><startdate>20191001</startdate><enddate>20191001</enddate><creator>Long, Hui-qing</creator><creator>Tian, Peng-fei</creator><creator>Guan, Yu-xin</creator><creator>Liu, Ling-xia</creator><creator>Wu, Xiu-ping</creator><creator>Li, Bing</creator><general>Springer Netherlands</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>7QP</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20191001</creationdate><title>Expression of Ihh signaling pathway in condylar cartilage after bite-raising in adult rats</title><author>Long, Hui-qing ; Tian, Peng-fei ; Guan, Yu-xin ; Liu, Ling-xia ; Wu, Xiu-ping ; Li, Bing</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-4514332f82a3323d818eb6a2f2c2a9456d17ee02f7348a17ece7a92bf3205e4c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Aging</topic><topic>Animals</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Bites and Stings - metabolism</topic><topic>Bone and Bones</topic><topic>Cartilage - metabolism</topic><topic>Cartilage diseases</topic><topic>Caspase</topic><topic>Caspase-3</topic><topic>Cell Biology</topic><topic>Chondrocytes</topic><topic>Chondrocytes - pathology</topic><topic>Collagenase 3</topic><topic>Developmental Biology</topic><topic>Hedgehog protein</topic><topic>Hedgehog Proteins - metabolism</topic><topic>Hypertrophy</topic><topic>Inflammation</topic><topic>Life Sciences</topic><topic>Matrix metalloproteinase</topic><topic>Metalloproteinase</topic><topic>Original Paper</topic><topic>Osteoarthritis</topic><topic>Osteoarthritis - etiology</topic><topic>Osteoarthritis - pathology</topic><topic>Proteinase</topic><topic>Proteinase 3</topic><topic>Rats</topic><topic>Signal Transduction</topic><topic>Temporomandibular joint</topic><topic>Temporomandibular Joint Disorders - etiology</topic><topic>Temporomandibular Joint Disorders - pathology</topic><topic>Therapeutic applications</topic><topic>Transcription factors</topic><topic>Zinc finger proteins</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Long, Hui-qing</creatorcontrib><creatorcontrib>Tian, Peng-fei</creatorcontrib><creatorcontrib>Guan, Yu-xin</creatorcontrib><creatorcontrib>Liu, Ling-xia</creatorcontrib><creatorcontrib>Wu, Xiu-ping</creatorcontrib><creatorcontrib>Li, Bing</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>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences 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>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 Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological 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 China</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of molecular histology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Long, Hui-qing</au><au>Tian, Peng-fei</au><au>Guan, Yu-xin</au><au>Liu, Ling-xia</au><au>Wu, Xiu-ping</au><au>Li, Bing</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Expression of Ihh signaling pathway in condylar cartilage after bite-raising in adult rats</atitle><jtitle>Journal of molecular histology</jtitle><stitle>J Mol Hist</stitle><addtitle>J Mol Histol</addtitle><date>2019-10-01</date><risdate>2019</risdate><volume>50</volume><issue>5</issue><spage>459</spage><epage>470</epage><pages>459-470</pages><issn>1567-2379</issn><eissn>1567-2387</eissn><abstract>Temporomandibular joint osteoarthritis (TMJOA) is a complex inflammatory condition with multiple factors and degenerative processes co-occurring. However, its pathogenesis remains uncertain. The purpose of the study was to observe the expression of Indian hedgehog (Ihh) signal related molecules in TMJOA induced by bite-raising and to study the effect and mechanism of Ihh signaling. Our research indicated that Ihh signaling pathway can be activated in condylar cartilage induced by bite-raising. The histological analysis showed TMJOA-like structural changes of condylar cartilage in experiment groups. Ihh, Smoothened (Smo), and Gli zinc finger transcription factors-1 (Gli-1) were activated in the experimental groups, and the expression levels increased significantly over time, whereas the sham control groups showed no fluctuation. Additionally, the expression levels of matrix metalloproteinase-13 (MMP-13) and cysteinyl aspartate specific proteinase-3 (Caspase-3) in the experiment groups increased in a time-dependent manner compared with the matched sham control groups. In conclusion, our results indicated that the Ihh signaling pathway may activate the occurrence of TMJOA by mediating the hypertrophy of chondrocytes, which may be an important regulatory mechanism and potential therapeutic target in the repair of condylar cartilage.</abstract><cop>Dordrecht</cop><pub>Springer Netherlands</pub><pmid>31302828</pmid><doi>10.1007/s10735-019-09840-0</doi><tpages>12</tpages></addata></record> |
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| subjects | Aging Animals Biomedical and Life Sciences Biomedicine Bites and Stings - metabolism Bone and Bones Cartilage - metabolism Cartilage diseases Caspase Caspase-3 Cell Biology Chondrocytes Chondrocytes - pathology Collagenase 3 Developmental Biology Hedgehog protein Hedgehog Proteins - metabolism Hypertrophy Inflammation Life Sciences Matrix metalloproteinase Metalloproteinase Original Paper Osteoarthritis Osteoarthritis - etiology Osteoarthritis - pathology Proteinase Proteinase 3 Rats Signal Transduction Temporomandibular joint Temporomandibular Joint Disorders - etiology Temporomandibular Joint Disorders - pathology Therapeutic applications Transcription factors Zinc finger proteins |
| title | Expression of Ihh signaling pathway in condylar cartilage after bite-raising in adult rats |
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