Interleukin‑Iβ promotes cartilage degeneration by regulating forkhead box protein O4 and type Ⅱ collagen
Osteoarthritis (OA) is one of the most prevalent pain‑inducing and disabling diseases globally. Aging is a primary contributing factor to the progression of OA. Forkhead box protein O4 (FOXO4) is known to be involved in the cell cycle and apoptosis regulation. The aim of the present study was to inv...
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description | Osteoarthritis (OA) is one of the most prevalent pain‑inducing and disabling diseases globally. Aging is a primary contributing factor to the progression of OA. Forkhead box protein O4 (FOXO4) is known to be involved in the cell cycle and apoptosis regulation. The aim of the present study was to investigate the association between FOXO4 expression and chondrocyte degeneration in rats. Chondrocytes were assigned to the control (4‑week‑old rats), natural degeneration (16‑week‑old rats) or induced degeneration (IL‑1β‑treated chondrocytes from 4‑week‑old rats) groups. Immunocytochemical analysis with β‑galactosidase staining revealed a greater number of stained cells present in the natural and induced degeneration groups than in the control group. PCR analysis indicated lower mRNA expression levels of collagen type II α1 chain (Col2α) and higher levels of FOXO4, and western blotting revealed reduced Col2α protein expression levels and significantly elevated FOXO4 levels in the natural and induced degeneration groups, compared with those in the control group. The results of the present study revealed that FOXO4 expression was altered in the natural and induced degeneration groups, and further research and exploration are needed to clarify the underlying mechanism. |
doi_str_mv | 10.3892/mmr.2021.12453 |
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Aging is a primary contributing factor to the progression of OA. Forkhead box protein O4 (FOXO4) is known to be involved in the cell cycle and apoptosis regulation. The aim of the present study was to investigate the association between FOXO4 expression and chondrocyte degeneration in rats. Chondrocytes were assigned to the control (4‑week‑old rats), natural degeneration (16‑week‑old rats) or induced degeneration (IL‑1β‑treated chondrocytes from 4‑week‑old rats) groups. Immunocytochemical analysis with β‑galactosidase staining revealed a greater number of stained cells present in the natural and induced degeneration groups than in the control group. PCR analysis indicated lower mRNA expression levels of collagen type II α1 chain (Col2α) and higher levels of FOXO4, and western blotting revealed reduced Col2α protein expression levels and significantly elevated FOXO4 levels in the natural and induced degeneration groups, compared with those in the control group. The results of the present study revealed that FOXO4 expression was altered in the natural and induced degeneration groups, and further research and exploration are needed to clarify the underlying mechanism.</description><identifier>ISSN: 1791-2997</identifier><identifier>EISSN: 1791-3004</identifier><identifier>DOI: 10.3892/mmr.2021.12453</identifier><identifier>PMID: 34549304</identifier><language>eng</language><publisher>Greece: Spandidos Publications UK Ltd</publisher><subject>Aging ; Animals ; Apoptosis ; Arthritis ; Biomarkers ; Cartilage ; Cartilage diseases ; Cartilage, Articular - metabolism ; Cartilage, Articular - pathology ; Cell cycle ; Cells, Cultured ; Chondrocytes ; Chondrocytes - metabolism ; Collagen (type II) ; Collagen Type II - genetics ; Collagen Type II - metabolism ; Degeneration ; Disease Susceptibility ; Experiments ; Forkhead protein ; Forkhead Transcription Factors - genetics ; Forkhead Transcription Factors - metabolism ; FOXO4 protein ; Gene expression ; Gene Expression Regulation ; IL-1β ; Interleukin-1beta - metabolism ; Laboratory animals ; Life sciences ; Male ; Morphology ; Osteoarthritis ; Osteoarthritis - etiology ; Osteoarthritis - metabolism ; Osteoarthritis - pathology ; Prostheses ; Proteins ; Rats ; RNA, Messenger - genetics ; RNA, Messenger - metabolism ; Western blotting ; β-Galactosidase</subject><ispartof>Molecular medicine reports, 2021-11, Vol.24 (5), Article 813</ispartof><rights>Copyright Spandidos Publications UK Ltd. 2021</rights><rights>Copyright: © Wu et al. 2021</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c418t-1b1b724b787fb2b233beabeb640a85852d0e06b8d09bd84fc10540e508b5a6b83</citedby><cites>FETCH-LOGICAL-c418t-1b1b724b787fb2b233beabeb640a85852d0e06b8d09bd84fc10540e508b5a6b83</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,777,781,882,27905,27906</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34549304$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wu, Jianxiong</creatorcontrib><creatorcontrib>Zhang, Hongjun</creatorcontrib><creatorcontrib>Deng, Rulin</creatorcontrib><creatorcontrib>Xing, Lifeng</creatorcontrib><creatorcontrib>Hu, Mingwu</creatorcontrib><creatorcontrib>Fu, Xiaoling</creatorcontrib><title>Interleukin‑Iβ promotes cartilage degeneration by regulating forkhead box protein O4 and type Ⅱ collagen</title><title>Molecular medicine reports</title><addtitle>Mol Med Rep</addtitle><description>Osteoarthritis (OA) is one of the most prevalent pain‑inducing and disabling diseases globally. Aging is a primary contributing factor to the progression of OA. Forkhead box protein O4 (FOXO4) is known to be involved in the cell cycle and apoptosis regulation. The aim of the present study was to investigate the association between FOXO4 expression and chondrocyte degeneration in rats. Chondrocytes were assigned to the control (4‑week‑old rats), natural degeneration (16‑week‑old rats) or induced degeneration (IL‑1β‑treated chondrocytes from 4‑week‑old rats) groups. Immunocytochemical analysis with β‑galactosidase staining revealed a greater number of stained cells present in the natural and induced degeneration groups than in the control group. PCR analysis indicated lower mRNA expression levels of collagen type II α1 chain (Col2α) and higher levels of FOXO4, and western blotting revealed reduced Col2α protein expression levels and significantly elevated FOXO4 levels in the natural and induced degeneration groups, compared with those in the control group. The results of the present study revealed that FOXO4 expression was altered in the natural and induced degeneration groups, and further research and exploration are needed to clarify the underlying mechanism.</description><subject>Aging</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Arthritis</subject><subject>Biomarkers</subject><subject>Cartilage</subject><subject>Cartilage diseases</subject><subject>Cartilage, Articular - metabolism</subject><subject>Cartilage, Articular - pathology</subject><subject>Cell cycle</subject><subject>Cells, Cultured</subject><subject>Chondrocytes</subject><subject>Chondrocytes - metabolism</subject><subject>Collagen (type II)</subject><subject>Collagen Type II - genetics</subject><subject>Collagen Type II - metabolism</subject><subject>Degeneration</subject><subject>Disease Susceptibility</subject><subject>Experiments</subject><subject>Forkhead protein</subject><subject>Forkhead Transcription Factors - genetics</subject><subject>Forkhead Transcription Factors - metabolism</subject><subject>FOXO4 protein</subject><subject>Gene expression</subject><subject>Gene Expression Regulation</subject><subject>IL-1β</subject><subject>Interleukin-1beta - metabolism</subject><subject>Laboratory animals</subject><subject>Life sciences</subject><subject>Male</subject><subject>Morphology</subject><subject>Osteoarthritis</subject><subject>Osteoarthritis - etiology</subject><subject>Osteoarthritis - metabolism</subject><subject>Osteoarthritis - pathology</subject><subject>Prostheses</subject><subject>Proteins</subject><subject>Rats</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Messenger - metabolism</subject><subject>Western blotting</subject><subject>β-Galactosidase</subject><issn>1791-2997</issn><issn>1791-3004</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</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>eNpdkT1uFDEYhi0EIiHQUiJLNDS78e_abpBQBGGlSGmgtuyZbyaTzNiLPROxHU0OkBuQK3AEDsAhchI8yRIBlf-e75VfPQi9pGTJtWGHw5CWjDC6pExI_gjtU2XoghMiHu_2zBi1h57lfE7ISjJpnqI9LqQwnIh9FNZhhNTDdNGF22_X618_8CbFIY6QceXS2PWuBVxDCwGSG7sYsN_iBO3Ul1NocRPTxRm4Gvv4dR4doQv4VGAXajxuN_Dz--3VDa5iPweF5-hJ4_oML3brAfr84f2no4-Lk9Pj9dG7k0UlqB4X1FOvmPBKq8Yzzzj34Dz4lSBOSy1ZTYCsvK6J8bUWTUWJFAQk0V66cs8P0Nv73M3kB6grCGNyvd2kbnBpa6Pr7L8voTuzbby0WihFlSgBb3YBKX6ZII926HIFpUWAOGXLpJJcMaJMQV__h57HKYVSb6a04YxRVajlPVWlmHOC5uEzlNhZpS0q7azS3qksA6_-rvCA_3HHfwMcRZ-6</recordid><startdate>20211101</startdate><enddate>20211101</enddate><creator>Wu, Jianxiong</creator><creator>Zhang, Hongjun</creator><creator>Deng, Rulin</creator><creator>Xing, Lifeng</creator><creator>Hu, Mingwu</creator><creator>Fu, Xiaoling</creator><general>Spandidos Publications UK Ltd</general><general>D.A. Spandidos</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>7X7</scope><scope>7XB</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>AN0</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><scope>5PM</scope></search><sort><creationdate>20211101</creationdate><title>Interleukin‑Iβ promotes cartilage degeneration by regulating forkhead box protein O4 and type Ⅱ collagen</title><author>Wu, Jianxiong ; Zhang, Hongjun ; Deng, Rulin ; Xing, Lifeng ; Hu, Mingwu ; Fu, Xiaoling</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c418t-1b1b724b787fb2b233beabeb640a85852d0e06b8d09bd84fc10540e508b5a6b83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Aging</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Arthritis</topic><topic>Biomarkers</topic><topic>Cartilage</topic><topic>Cartilage diseases</topic><topic>Cartilage, Articular - metabolism</topic><topic>Cartilage, Articular - pathology</topic><topic>Cell cycle</topic><topic>Cells, Cultured</topic><topic>Chondrocytes</topic><topic>Chondrocytes - metabolism</topic><topic>Collagen (type II)</topic><topic>Collagen Type II - genetics</topic><topic>Collagen Type II - metabolism</topic><topic>Degeneration</topic><topic>Disease Susceptibility</topic><topic>Experiments</topic><topic>Forkhead protein</topic><topic>Forkhead Transcription Factors - genetics</topic><topic>Forkhead Transcription Factors - metabolism</topic><topic>FOXO4 protein</topic><topic>Gene expression</topic><topic>Gene Expression Regulation</topic><topic>IL-1β</topic><topic>Interleukin-1beta - metabolism</topic><topic>Laboratory animals</topic><topic>Life sciences</topic><topic>Male</topic><topic>Morphology</topic><topic>Osteoarthritis</topic><topic>Osteoarthritis - etiology</topic><topic>Osteoarthritis - metabolism</topic><topic>Osteoarthritis - pathology</topic><topic>Prostheses</topic><topic>Proteins</topic><topic>Rats</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Messenger - metabolism</topic><topic>Western blotting</topic><topic>β-Galactosidase</topic><toplevel>online_resources</toplevel><creatorcontrib>Wu, Jianxiong</creatorcontrib><creatorcontrib>Zhang, Hongjun</creatorcontrib><creatorcontrib>Deng, Rulin</creatorcontrib><creatorcontrib>Xing, Lifeng</creatorcontrib><creatorcontrib>Hu, Mingwu</creatorcontrib><creatorcontrib>Fu, Xiaoling</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>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</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>British Nursing Database</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><collection>PubMed Central (Full Participant titles)</collection><jtitle>Molecular medicine reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wu, Jianxiong</au><au>Zhang, Hongjun</au><au>Deng, Rulin</au><au>Xing, Lifeng</au><au>Hu, Mingwu</au><au>Fu, Xiaoling</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Interleukin‑Iβ promotes cartilage degeneration by regulating forkhead box protein O4 and type Ⅱ collagen</atitle><jtitle>Molecular medicine reports</jtitle><addtitle>Mol Med Rep</addtitle><date>2021-11-01</date><risdate>2021</risdate><volume>24</volume><issue>5</issue><artnum>813</artnum><issn>1791-2997</issn><eissn>1791-3004</eissn><abstract>Osteoarthritis (OA) is one of the most prevalent pain‑inducing and disabling diseases globally. Aging is a primary contributing factor to the progression of OA. Forkhead box protein O4 (FOXO4) is known to be involved in the cell cycle and apoptosis regulation. The aim of the present study was to investigate the association between FOXO4 expression and chondrocyte degeneration in rats. Chondrocytes were assigned to the control (4‑week‑old rats), natural degeneration (16‑week‑old rats) or induced degeneration (IL‑1β‑treated chondrocytes from 4‑week‑old rats) groups. Immunocytochemical analysis with β‑galactosidase staining revealed a greater number of stained cells present in the natural and induced degeneration groups than in the control group. PCR analysis indicated lower mRNA expression levels of collagen type II α1 chain (Col2α) and higher levels of FOXO4, and western blotting revealed reduced Col2α protein expression levels and significantly elevated FOXO4 levels in the natural and induced degeneration groups, compared with those in the control group. The results of the present study revealed that FOXO4 expression was altered in the natural and induced degeneration groups, and further research and exploration are needed to clarify the underlying mechanism.</abstract><cop>Greece</cop><pub>Spandidos Publications UK Ltd</pub><pmid>34549304</pmid><doi>10.3892/mmr.2021.12453</doi><oa>free_for_read</oa></addata></record> |
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subjects | Aging Animals Apoptosis Arthritis Biomarkers Cartilage Cartilage diseases Cartilage, Articular - metabolism Cartilage, Articular - pathology Cell cycle Cells, Cultured Chondrocytes Chondrocytes - metabolism Collagen (type II) Collagen Type II - genetics Collagen Type II - metabolism Degeneration Disease Susceptibility Experiments Forkhead protein Forkhead Transcription Factors - genetics Forkhead Transcription Factors - metabolism FOXO4 protein Gene expression Gene Expression Regulation IL-1β Interleukin-1beta - metabolism Laboratory animals Life sciences Male Morphology Osteoarthritis Osteoarthritis - etiology Osteoarthritis - metabolism Osteoarthritis - pathology Prostheses Proteins Rats RNA, Messenger - genetics RNA, Messenger - metabolism Western blotting β-Galactosidase |
title | Interleukin‑Iβ promotes cartilage degeneration by regulating forkhead box protein O4 and type Ⅱ collagen |
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