{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,3]],"date-time":"2026-10-03T08:43:28Z","timestamp":1791017008443,"version":"4.1.0"},"reference-count":52,"publisher":"BMJ","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Gut"],"published-print":{"date-parts":[[2007,6]]},"abstract":"<jats:p>\n                    <jats:bold>Background:<\/jats:bold>\n                    Neoangiogenesis is a critical component of chronic inflammatory disorders. Inhibition of angiogenesis is an effective treatment in animal models of inflammation, but has not been tested in experimental colitis.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Aim:<\/jats:bold>\n                    To investigate the effect of ATN-161, an anti-angiogenic compound, on the course of experimental murine colitis.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Method:<\/jats:bold>\n                    Interleukin 10-deficient (IL10\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    ) mice and wild-type mice were kept in ultra-barrier facilities (UBF) or conventional housing, and used for experimental conditions. Dextran sodium sulphate (DSS)-treated mice were used as a model of acute colitis. Mice were treated with ATN-161 or its scrambled peptide ATN-163. Mucosal neoangiogenesis and mean vascular density (MVD) were assessed by CD31 staining. A Disease Activity Index (DAI) was determined, and the severity of colitis was determined by a histological score. Colonic cytokine production was measured by ELISA, and lamina propria mononuclear cell proliferation by thymidine incorporation.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Result:<\/jats:bold>\n                    MVD increased in parallel with disease progression in IL10\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice kept in conventional housing, but not in IL10\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice kept in UBF. Angiogenesis also occurred in DSS-treated animals. IL10\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice with established disease treated with ATN-161, but not with ATN-163, showed a significant and progressive decrease in DAI. The histological colitis score was significantly lower in ATN-161-treated mice than in scrambled peptide-treated mice. Inhibition of angiogenesis was confirmed by a significant decrease of MVD in ATN-161-treated mice than in ATN-163-treated mice. No therapeutic effects were observed in the DSS model of colitis. ATN-161 showed no direct immunomodulatory activity in vitro.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Conclusion:<\/jats:bold>\n                    Active angiogenesis occurs in the gut of IL10\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    and DSS-treated colitic mice and parallels disease progression. ATN-161 effectively decreases angiogenesis as well as clinical severity and histological inflammation in IL10\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice but not in the DDS model of inflammatory bowel disease (IBD). The results provide the rational basis for considering anti-angiogenic strategies in the treatment of IBD in humans.\n                  <\/jats:p>","DOI":"10.1136\/gut.2006.114314","type":"journal-article","created":{"date-parts":[[2006,12,14]],"date-time":"2006-12-14T20:24:51Z","timestamp":1166127891000},"page":"855-862","source":"Crossref","is-referenced-by-count":119,"title":["Angiogenesis blockade as a new therapeutic approach to experimental colitis"],"prefix":"10.1136","volume":"56","author":[{"given":"Silvio","family":"Danese","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Miquel","family":"Sans","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David M","family":"Spencer","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ivy","family":"Beck","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fernando","family":"Do\u00f1ate","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marian L","family":"Plunkett","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Carol","family":"de la Motte","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Raymond","family":"Redline","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David E","family":"Shaw","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alan D","family":"Levine","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andrew P","family":"Mazar","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Claudio","family":"Fiocchi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"239","published-online":{"date-parts":[[2006,12,14]]},"reference":[{"key":"2025121302540466000_56.6.855.1","doi-asserted-by":"publisher","DOI":"10.1038\/nm0603-653"},{"key":"2025121302540466000_56.6.855.2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM197111182852108"},{"key":"2025121302540466000_56.6.855.3","doi-asserted-by":"publisher","DOI":"10.1038\/nm0195-27"},{"key":"2025121302540466000_56.6.855.4","doi-asserted-by":"publisher","DOI":"10.1053\/hupa.2002.130311"},{"key":"2025121302540466000_56.6.855.5","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)65648-9"},{"key":"2025121302540466000_56.6.855.6","doi-asserted-by":"publisher","DOI":"10.1038\/74651"},{"key":"2025121302540466000_56.6.855.7","first-page":"S26","volume":"3","year":"2004","journal-title":"Autoimmun Rev"},{"key":"2025121302540466000_56.6.855.8","doi-asserted-by":"publisher","DOI":"10.1172\/JCI5929"},{"key":"2025121302540466000_56.6.855.9","doi-asserted-by":"publisher","DOI":"10.1016\/S0889-857X(03)00116-9"},{"key":"2025121302540466000_56.6.855.10","doi-asserted-by":"crossref","first-page":"457","DOI":"10.1096\/fasebj.11.6.9194526","volume":"11","year":"1997","journal-title":"FASEB J"},{"key":"2025121302540466000_56.6.855.11","doi-asserted-by":"publisher","DOI":"10.1053\/j.gastro.2006.03.054"},{"key":"2025121302540466000_56.6.855.12","doi-asserted-by":"crossref","first-page":"ii96","DOI":"10.1136\/ard.61.suppl_2.ii96","volume":"61","year":"2002","journal-title":"Ann Rheum Dis"},{"key":"2025121302540466000_56.6.855.13","unstructured":"Varner JA, Cheresh DA. 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