Chondrogenic progenitor cells respond to cartilage injury
Objective Hypocellularity resulting from chondrocyte death in the aftermath of mechanical injury is thought to contribute to posttraumatic osteoarthritis. However, we observed that nonviable areas in cartilage injured by blunt impact were repopulated within 7–14 days by cells that appeared to migrat...
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| Veröffentlicht in: | Arthritis & rheumatology (Hoboken, N.J.) N.J.), 2012-11, Vol.64 (11), p.3626-3637 |
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| creator | Seol, Dongrim McCabe, Daniel J. Choe, Hyeonghun Zheng, Hongjun Yu, Yin Jang, Keewoong Walter, Morgan W. Lehman, Abigail D. Ding, Lei Buckwalter, Joseph A. Martin, James A. |
| description | Objective
Hypocellularity resulting from chondrocyte death in the aftermath of mechanical injury is thought to contribute to posttraumatic osteoarthritis. However, we observed that nonviable areas in cartilage injured by blunt impact were repopulated within 7–14 days by cells that appeared to migrate from the surrounding matrix. The aim of this study was to assess our hypothesis that the migrating cell population included chondrogenic progenitor cells that were drawn to injured cartilage by alarmins.
Methods
Osteochondral explants obtained from mature cattle were injured by blunt impact or scratching, resulting in localized chondrocyte death. Injured sites were serially imaged by confocal microscopy, and migrating cells were evaluated for chondrogenic progenitor characteristics. Chemotaxis assays were used to measure the responses to chemokines, injury‐conditioned medium, dead cell debris, and high mobility group box chromosomal protein 1 (HMGB‐1).
Results
Migrating cells were highly clonogenic and multipotent and expressed markers associated with chondrogenic progenitor cells. Compared with chondrocytes, these cells overexpressed genes involved in proliferation and migration and underexpressed cartilage matrix genes. They were more active than chondrocytes in chemotaxis assays and responded to cell lysates, conditioned medium, and HMGB‐1. Glycyrrhizin, a chelator of HMGB‐1 and a blocking antibody to receptor for advanced glycation end products (RAGE), inhibited responses to cell debris and conditioned medium and reduced the numbers of migrating cells on injured explants.
Conclusion
Injuries that caused chondrocyte death stimulated the emergence and homing of chondrogenic progenitor cells, in part via HMGB‐1 release and RAGE‐mediated chemotaxis. Their repopulation of the matrix could promote the repair of chondral damage that might otherwise contribute to progressive cartilage loss. |
| doi_str_mv | 10.1002/art.34613 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4950521</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1458533582</sourcerecordid><originalsourceid>FETCH-LOGICAL-c6103-bfa8c655f49d551d8834f58ad5daaadc16e80fb919f1284088846644ea709eb43</originalsourceid><addsrcrecordid>eNqFkV1rFDEUhoModm298A_IgAh6MW2-Tia5EcpoW6FYkKqXIZvJbLPOTtZkRt1_32xnu36AeJWE85z3zTkvQs8IPiYY0xMTh2PGBWEP0IwAVSUmjDxEM4wxLxkocoCepLTMT8qAPUYHlFZVJTCeIVXfhL6JYeF6b4v1dBlCLKzrulREl9a5XgyhsNnFd2bhCt8vx7g5Qo9a0yX3dHceok9n767ri_Ly6vx9fXpZWkEwK-etkVYAtFw1AKSRkvEWpGmgMcY0lggncTtXRLWESo6llFwIzp2psHJzzg7Rm0l3Pc5XrrGuH6Lp9Dr6lYkbHYzXf1Z6f6MX4bvmCjBQkgVe7QRi-Da6NOiVT9vxTO_CmDThIIExkPT_KKFAoWJqq_riL3QZxtjnTWSKgFDA7gRfT5SNIaXo2v2_Cdbb7HTeqr7LLrPPfx90T96HlYGXO8Aka7o2mt769IsTouKUqsydTNwP37nNvx316cfre-ty6vBpcD_3HSZ-1aJiFegvH851_Zm9JYLW-oLdAq4jvjk</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1115695382</pqid></control><display><type>article</type><title>Chondrogenic progenitor cells respond to cartilage injury</title><source>MEDLINE</source><source>Wiley Online Library Journals Frontfile Complete</source><creator>Seol, Dongrim ; McCabe, Daniel J. ; Choe, Hyeonghun ; Zheng, Hongjun ; Yu, Yin ; Jang, Keewoong ; Walter, Morgan W. ; Lehman, Abigail D. ; Ding, Lei ; Buckwalter, Joseph A. ; Martin, James A.</creator><creatorcontrib>Seol, Dongrim ; McCabe, Daniel J. ; Choe, Hyeonghun ; Zheng, Hongjun ; Yu, Yin ; Jang, Keewoong ; Walter, Morgan W. ; Lehman, Abigail D. ; Ding, Lei ; Buckwalter, Joseph A. ; Martin, James A.</creatorcontrib><description>Objective
Hypocellularity resulting from chondrocyte death in the aftermath of mechanical injury is thought to contribute to posttraumatic osteoarthritis. However, we observed that nonviable areas in cartilage injured by blunt impact were repopulated within 7–14 days by cells that appeared to migrate from the surrounding matrix. The aim of this study was to assess our hypothesis that the migrating cell population included chondrogenic progenitor cells that were drawn to injured cartilage by alarmins.
Methods
Osteochondral explants obtained from mature cattle were injured by blunt impact or scratching, resulting in localized chondrocyte death. Injured sites were serially imaged by confocal microscopy, and migrating cells were evaluated for chondrogenic progenitor characteristics. Chemotaxis assays were used to measure the responses to chemokines, injury‐conditioned medium, dead cell debris, and high mobility group box chromosomal protein 1 (HMGB‐1).
Results
Migrating cells were highly clonogenic and multipotent and expressed markers associated with chondrogenic progenitor cells. Compared with chondrocytes, these cells overexpressed genes involved in proliferation and migration and underexpressed cartilage matrix genes. They were more active than chondrocytes in chemotaxis assays and responded to cell lysates, conditioned medium, and HMGB‐1. Glycyrrhizin, a chelator of HMGB‐1 and a blocking antibody to receptor for advanced glycation end products (RAGE), inhibited responses to cell debris and conditioned medium and reduced the numbers of migrating cells on injured explants.
Conclusion
Injuries that caused chondrocyte death stimulated the emergence and homing of chondrogenic progenitor cells, in part via HMGB‐1 release and RAGE‐mediated chemotaxis. Their repopulation of the matrix could promote the repair of chondral damage that might otherwise contribute to progressive cartilage loss.</description><identifier>ISSN: 0004-3591</identifier><identifier>ISSN: 2326-5191</identifier><identifier>EISSN: 1529-0131</identifier><identifier>EISSN: 2326-5205</identifier><identifier>DOI: 10.1002/art.34613</identifier><identifier>PMID: 22777600</identifier><identifier>CODEN: ARHEAW</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>Animals ; Apoptosis - physiology ; Biological and medical sciences ; Cartilage, Articular - injuries ; Cartilage, Articular - pathology ; Cattle ; Cell Differentiation - physiology ; Cell Movement - physiology ; Cell physiology ; Cells ; Cells, Cultured ; Chondrocytes - cytology ; Chondrocytes - physiology ; Diseases of the osteoarticular system ; Fundamental and applied biological sciences. Psychology ; Medical research ; Medical sciences ; Mineralization, calcification ; Molecular and cellular biology ; Multipotent Stem Cells - cytology ; Multipotent Stem Cells - physiology ; Osteoarthritis, Knee - etiology ; Osteoarthritis, Knee - pathology ; Proteins ; Stifle - injuries ; Stifle - pathology ; Transcriptome ; Wounds, Nonpenetrating - pathology</subject><ispartof>Arthritis & rheumatology (Hoboken, N.J.), 2012-11, Vol.64 (11), p.3626-3637</ispartof><rights>Copyright © 2012 by the American College of Rheumatology</rights><rights>2014 INIST-CNRS</rights><rights>Copyright © 2012 by the American College of Rheumatology.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c6103-bfa8c655f49d551d8834f58ad5daaadc16e80fb919f1284088846644ea709eb43</citedby><cites>FETCH-LOGICAL-c6103-bfa8c655f49d551d8834f58ad5daaadc16e80fb919f1284088846644ea709eb43</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fart.34613$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fart.34613$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>230,314,776,780,881,1411,27903,27904,45553,45554</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=26674229$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22777600$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Seol, Dongrim</creatorcontrib><creatorcontrib>McCabe, Daniel J.</creatorcontrib><creatorcontrib>Choe, Hyeonghun</creatorcontrib><creatorcontrib>Zheng, Hongjun</creatorcontrib><creatorcontrib>Yu, Yin</creatorcontrib><creatorcontrib>Jang, Keewoong</creatorcontrib><creatorcontrib>Walter, Morgan W.</creatorcontrib><creatorcontrib>Lehman, Abigail D.</creatorcontrib><creatorcontrib>Ding, Lei</creatorcontrib><creatorcontrib>Buckwalter, Joseph A.</creatorcontrib><creatorcontrib>Martin, James A.</creatorcontrib><title>Chondrogenic progenitor cells respond to cartilage injury</title><title>Arthritis & rheumatology (Hoboken, N.J.)</title><addtitle>Arthritis & Rheumatism</addtitle><description>Objective
Hypocellularity resulting from chondrocyte death in the aftermath of mechanical injury is thought to contribute to posttraumatic osteoarthritis. However, we observed that nonviable areas in cartilage injured by blunt impact were repopulated within 7–14 days by cells that appeared to migrate from the surrounding matrix. The aim of this study was to assess our hypothesis that the migrating cell population included chondrogenic progenitor cells that were drawn to injured cartilage by alarmins.
Methods
Osteochondral explants obtained from mature cattle were injured by blunt impact or scratching, resulting in localized chondrocyte death. Injured sites were serially imaged by confocal microscopy, and migrating cells were evaluated for chondrogenic progenitor characteristics. Chemotaxis assays were used to measure the responses to chemokines, injury‐conditioned medium, dead cell debris, and high mobility group box chromosomal protein 1 (HMGB‐1).
Results
Migrating cells were highly clonogenic and multipotent and expressed markers associated with chondrogenic progenitor cells. Compared with chondrocytes, these cells overexpressed genes involved in proliferation and migration and underexpressed cartilage matrix genes. They were more active than chondrocytes in chemotaxis assays and responded to cell lysates, conditioned medium, and HMGB‐1. Glycyrrhizin, a chelator of HMGB‐1 and a blocking antibody to receptor for advanced glycation end products (RAGE), inhibited responses to cell debris and conditioned medium and reduced the numbers of migrating cells on injured explants.
Conclusion
Injuries that caused chondrocyte death stimulated the emergence and homing of chondrogenic progenitor cells, in part via HMGB‐1 release and RAGE‐mediated chemotaxis. Their repopulation of the matrix could promote the repair of chondral damage that might otherwise contribute to progressive cartilage loss.</description><subject>Animals</subject><subject>Apoptosis - physiology</subject><subject>Biological and medical sciences</subject><subject>Cartilage, Articular - injuries</subject><subject>Cartilage, Articular - pathology</subject><subject>Cattle</subject><subject>Cell Differentiation - physiology</subject><subject>Cell Movement - physiology</subject><subject>Cell physiology</subject><subject>Cells</subject><subject>Cells, Cultured</subject><subject>Chondrocytes - cytology</subject><subject>Chondrocytes - physiology</subject><subject>Diseases of the osteoarticular system</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Medical research</subject><subject>Medical sciences</subject><subject>Mineralization, calcification</subject><subject>Molecular and cellular biology</subject><subject>Multipotent Stem Cells - cytology</subject><subject>Multipotent Stem Cells - physiology</subject><subject>Osteoarthritis, Knee - etiology</subject><subject>Osteoarthritis, Knee - pathology</subject><subject>Proteins</subject><subject>Stifle - injuries</subject><subject>Stifle - pathology</subject><subject>Transcriptome</subject><subject>Wounds, Nonpenetrating - pathology</subject><issn>0004-3591</issn><issn>2326-5191</issn><issn>1529-0131</issn><issn>2326-5205</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkV1rFDEUhoModm298A_IgAh6MW2-Tia5EcpoW6FYkKqXIZvJbLPOTtZkRt1_32xnu36AeJWE85z3zTkvQs8IPiYY0xMTh2PGBWEP0IwAVSUmjDxEM4wxLxkocoCepLTMT8qAPUYHlFZVJTCeIVXfhL6JYeF6b4v1dBlCLKzrulREl9a5XgyhsNnFd2bhCt8vx7g5Qo9a0yX3dHceok9n767ri_Ly6vx9fXpZWkEwK-etkVYAtFw1AKSRkvEWpGmgMcY0lggncTtXRLWESo6llFwIzp2psHJzzg7Rm0l3Pc5XrrGuH6Lp9Dr6lYkbHYzXf1Z6f6MX4bvmCjBQkgVe7QRi-Da6NOiVT9vxTO_CmDThIIExkPT_KKFAoWJqq_riL3QZxtjnTWSKgFDA7gRfT5SNIaXo2v2_Cdbb7HTeqr7LLrPPfx90T96HlYGXO8Aka7o2mt769IsTouKUqsydTNwP37nNvx316cfre-ty6vBpcD_3HSZ-1aJiFegvH851_Zm9JYLW-oLdAq4jvjk</recordid><startdate>201211</startdate><enddate>201211</enddate><creator>Seol, Dongrim</creator><creator>McCabe, Daniel J.</creator><creator>Choe, Hyeonghun</creator><creator>Zheng, Hongjun</creator><creator>Yu, Yin</creator><creator>Jang, Keewoong</creator><creator>Walter, Morgan W.</creator><creator>Lehman, Abigail D.</creator><creator>Ding, Lei</creator><creator>Buckwalter, Joseph A.</creator><creator>Martin, James A.</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><general>Wiley</general><general>Wiley Subscription Services, Inc</general><scope>BSCLL</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>7QL</scope><scope>7QP</scope><scope>7T5</scope><scope>7TM</scope><scope>7U7</scope><scope>C1K</scope><scope>H94</scope><scope>K9.</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>201211</creationdate><title>Chondrogenic progenitor cells respond to cartilage injury</title><author>Seol, Dongrim ; McCabe, Daniel J. ; Choe, Hyeonghun ; Zheng, Hongjun ; Yu, Yin ; Jang, Keewoong ; Walter, Morgan W. ; Lehman, Abigail D. ; Ding, Lei ; Buckwalter, Joseph A. ; Martin, James A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c6103-bfa8c655f49d551d8834f58ad5daaadc16e80fb919f1284088846644ea709eb43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Animals</topic><topic>Apoptosis - physiology</topic><topic>Biological and medical sciences</topic><topic>Cartilage, Articular - injuries</topic><topic>Cartilage, Articular - pathology</topic><topic>Cattle</topic><topic>Cell Differentiation - physiology</topic><topic>Cell Movement - physiology</topic><topic>Cell physiology</topic><topic>Cells</topic><topic>Cells, Cultured</topic><topic>Chondrocytes - cytology</topic><topic>Chondrocytes - physiology</topic><topic>Diseases of the osteoarticular system</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Medical research</topic><topic>Medical sciences</topic><topic>Mineralization, calcification</topic><topic>Molecular and cellular biology</topic><topic>Multipotent Stem Cells - cytology</topic><topic>Multipotent Stem Cells - physiology</topic><topic>Osteoarthritis, Knee - etiology</topic><topic>Osteoarthritis, Knee - pathology</topic><topic>Proteins</topic><topic>Stifle - injuries</topic><topic>Stifle - pathology</topic><topic>Transcriptome</topic><topic>Wounds, Nonpenetrating - pathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Seol, Dongrim</creatorcontrib><creatorcontrib>McCabe, Daniel J.</creatorcontrib><creatorcontrib>Choe, Hyeonghun</creatorcontrib><creatorcontrib>Zheng, Hongjun</creatorcontrib><creatorcontrib>Yu, Yin</creatorcontrib><creatorcontrib>Jang, Keewoong</creatorcontrib><creatorcontrib>Walter, Morgan W.</creatorcontrib><creatorcontrib>Lehman, Abigail D.</creatorcontrib><creatorcontrib>Ding, Lei</creatorcontrib><creatorcontrib>Buckwalter, Joseph A.</creatorcontrib><creatorcontrib>Martin, James A.</creatorcontrib><collection>Istex</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>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Immunology Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Arthritis & rheumatology (Hoboken, N.J.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Seol, Dongrim</au><au>McCabe, Daniel J.</au><au>Choe, Hyeonghun</au><au>Zheng, Hongjun</au><au>Yu, Yin</au><au>Jang, Keewoong</au><au>Walter, Morgan W.</au><au>Lehman, Abigail D.</au><au>Ding, Lei</au><au>Buckwalter, Joseph A.</au><au>Martin, James A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Chondrogenic progenitor cells respond to cartilage injury</atitle><jtitle>Arthritis & rheumatology (Hoboken, N.J.)</jtitle><addtitle>Arthritis & Rheumatism</addtitle><date>2012-11</date><risdate>2012</risdate><volume>64</volume><issue>11</issue><spage>3626</spage><epage>3637</epage><pages>3626-3637</pages><issn>0004-3591</issn><issn>2326-5191</issn><eissn>1529-0131</eissn><eissn>2326-5205</eissn><coden>ARHEAW</coden><abstract>Objective
Hypocellularity resulting from chondrocyte death in the aftermath of mechanical injury is thought to contribute to posttraumatic osteoarthritis. However, we observed that nonviable areas in cartilage injured by blunt impact were repopulated within 7–14 days by cells that appeared to migrate from the surrounding matrix. The aim of this study was to assess our hypothesis that the migrating cell population included chondrogenic progenitor cells that were drawn to injured cartilage by alarmins.
Methods
Osteochondral explants obtained from mature cattle were injured by blunt impact or scratching, resulting in localized chondrocyte death. Injured sites were serially imaged by confocal microscopy, and migrating cells were evaluated for chondrogenic progenitor characteristics. Chemotaxis assays were used to measure the responses to chemokines, injury‐conditioned medium, dead cell debris, and high mobility group box chromosomal protein 1 (HMGB‐1).
Results
Migrating cells were highly clonogenic and multipotent and expressed markers associated with chondrogenic progenitor cells. Compared with chondrocytes, these cells overexpressed genes involved in proliferation and migration and underexpressed cartilage matrix genes. They were more active than chondrocytes in chemotaxis assays and responded to cell lysates, conditioned medium, and HMGB‐1. Glycyrrhizin, a chelator of HMGB‐1 and a blocking antibody to receptor for advanced glycation end products (RAGE), inhibited responses to cell debris and conditioned medium and reduced the numbers of migrating cells on injured explants.
Conclusion
Injuries that caused chondrocyte death stimulated the emergence and homing of chondrogenic progenitor cells, in part via HMGB‐1 release and RAGE‐mediated chemotaxis. Their repopulation of the matrix could promote the repair of chondral damage that might otherwise contribute to progressive cartilage loss.</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>22777600</pmid><doi>10.1002/art.34613</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Wiley Online Library Journals Frontfile Complete |
| subjects | Animals Apoptosis - physiology Biological and medical sciences Cartilage, Articular - injuries Cartilage, Articular - pathology Cattle Cell Differentiation - physiology Cell Movement - physiology Cell physiology Cells Cells, Cultured Chondrocytes - cytology Chondrocytes - physiology Diseases of the osteoarticular system Fundamental and applied biological sciences. Psychology Medical research Medical sciences Mineralization, calcification Molecular and cellular biology Multipotent Stem Cells - cytology Multipotent Stem Cells - physiology Osteoarthritis, Knee - etiology Osteoarthritis, Knee - pathology Proteins Stifle - injuries Stifle - pathology Transcriptome Wounds, Nonpenetrating - pathology |
| title | Chondrogenic progenitor cells respond to cartilage injury |
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