{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,18]],"date-time":"2026-06-18T13:08:44Z","timestamp":1781788124178,"version":"3.54.5"},"reference-count":20,"publisher":"SAGE Publications","license":[{"start":{"date-parts":[[2011,1,1]],"date-time":"2011-01-01T00:00:00Z","timestamp":1293840000000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Biomark\ufffdInsights"],"published-print":{"date-parts":[[2011,1]]},"abstract":"<jats:sec>\n                    <jats:title>Background and Aim<\/jats:title>\n                    <jats:p>\n                      The current study utilized a carbon tetrachloride (CCl\n                      <jats:sub>4<\/jats:sub>\n                      )-induced liver fibrosis model to measure levels of the MMP9-mediated collagen type III degradation fragment CO3-610 (site of cleavage: KNGETGPQGP), during disease progression and regression, and to investigate a potential prognostic role of the biomarker.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Materials and Methods<\/jats:title>\n                    <jats:p>\n                      72 female Sprague-Dawley rats aged 6 months old were injected with CCl\n                      <jats:sub>4<\/jats:sub>\n                      twice a week over different periods of time to induce varying degrees of liver fibrosis. After 4, 6 and 8 weeks of treatment, administration of CCl\n                      <jats:sub>4<\/jats:sub>\n                      was stopped. The 6- and 8-week treatment groups were left to regress for a further 6 or 12 weeks at which point they were sacrificed and livers removed and sectioned. Liver fibrosis was quantified using Visiopharm software to analyse Sirius red-stained sections. Serum levels of CO3-610 were measured in all animals using an ELISA assay as described by Barascuk et al.\n                      <jats:sup>1<\/jats:sup>\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Quantitative histology revealed total collagen deposition in the liver increased as fibrosis progressed. In animals treated with CCl\n                      <jats:sub>4<\/jats:sub>\n                      for 4 weeks, collagen comprised on average 4.94% of the total tissue in liver sections, while after 6 weeks the mean was 8.25%, and after 8 weeks, 9.11%. During the regression phase, the total collagen deposition gradually decreased to a mean of 6.9% and 5.09% for animals regressing 6 and 12 weeks respectively after 6 weeks treatment, and 6.27% for animals regressed 12 weeks after 8 weeks treatment. CO3-610 values increased progressively in rats treated for 4 weeks (by a mean of 55.0 ng\/ml), 6 weeks (mean 61.1 ng\/ml) and 8 weeks (mean 70.2 ng\/ml). During the regression phase, CO3-610 values rapidly decreased by a mean of 28.9 ng\/ml at 6 weeks and 21.6 ng\/ml at 12 weeks in animals previously treated for 6 weeks, and by a mean of 19.52 ng\/ml in animals treated for 8 weeks and regressed for 12 weeks. CO3-610 levels were statistically significantly correlated with total collagen during disease progression ( r = 0.5701, P &lt; 0.0001). No statistically significant correlation was observed during regression ( r = 0.2081, P = 0.1138).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>\n                      Levels of the MMP-9 generated fragment of collagen type III, CO3-610, correlated with the degree of liver fibrosis in rats during the progression phase, but were not correlated with total collagen levels during regression. CO3-610 seems to be produced only under the CCL\n                      <jats:sub>4<\/jats:sub>\n                      stimulus, and signifies CO3-610 as a potential marker of progression rather than regression. The corresponding steep elevations in levels of CO3-610 total collagen and collagen type III during liver fibrosis progression underline a potential prognostic capacity of the biomarker.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.4137\/bmi.s6347","type":"journal-article","created":{"date-parts":[[2011,3,24]],"date-time":"2011-03-24T16:45:31Z","timestamp":1300985131000},"page":"BMI.S6347","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":42,"title":["Measurement of CO3-610, a Potential Liver Biomarker Derived from Matrix Metalloproteinase-9 Degradation of Collagen Type III, in a Rat Model of Reversible Carbon-Tetrachloride-Induced Fibrosis"],"prefix":"10.4137","volume":"6","author":[{"given":"Efstathios","family":"Vassiliadis","sequence":"first","affiliation":[{"name":"Nordic Bioscience, Herlev, Denmark."},{"name":"University of Southern Denmark, Odense, Denmark."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dorthe","family":"Vang Larsen","sequence":"additional","affiliation":[{"name":"Nordic Bioscience, Herlev, Denmark."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rikke Elgaard","family":"Clausen","sequence":"additional","affiliation":[{"name":"Nordic Bioscience, Herlev, Denmark."},{"name":"University of Copenhagen, Denmark."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sanne Skovg\u00e5rd","family":"Veidal","sequence":"additional","affiliation":[{"name":"Nordic Bioscience, Herlev, Denmark."},{"name":"University of Southern Denmark, Odense, Denmark."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Natasha","family":"Barascuk","sequence":"additional","affiliation":[{"name":"Nordic Bioscience, Herlev, Denmark."},{"name":"University of Southern Denmark, Odense, Denmark."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lise","family":"Larsen","sequence":"additional","affiliation":[{"name":"Nordic Bioscience, Herlev, Denmark."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Henrik","family":"Simonsen","sequence":"additional","affiliation":[{"name":"Nordic Bioscience, Herlev, Denmark."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Toni Segovia","family":"Silvestre","sequence":"additional","affiliation":[{"name":"Nordic Bioscience, Herlev, Denmark."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christina","family":"Hansen","sequence":"additional","affiliation":[{"name":"Nordic Bioscience, Herlev, Denmark."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Trine","family":"Overgaard","sequence":"additional","affiliation":[{"name":"Nordic Bioscience, Herlev, Denmark."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Diana Julie","family":"Leeming","sequence":"additional","affiliation":[{"name":"Nordic Bioscience, Herlev, Denmark."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Morten A","family":"Karsdal","sequence":"additional","affiliation":[{"name":"Nordic Bioscience, Herlev, Denmark."},{"name":"University of Southern Denmark, Odense, Denmark."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","published-online":{"date-parts":[[2011,3,24]]},"reference":[{"key":"bibr1-BMI.S6347","doi-asserted-by":"publisher","DOI":"10.1016\/j.clinbiochem.2010.03.012"},{"key":"bibr2-BMI.S6347","doi-asserted-by":"publisher","DOI":"10.1172\/JCI24282"},{"key":"bibr3-BMI.S6347","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M006577200"},{"key":"bibr4-BMI.S6347","author":"Jarcuska P.","year":"2010","journal-title":"Clin Chim 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