{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,29]],"date-time":"2026-04-29T08:29:37Z","timestamp":1777451377741,"version":"3.51.4"},"reference-count":0,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"4","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation"],"published-print":{"date-parts":[[1994,10]]},"abstract":"\n BACKGROUND<\/jats:title>\n Several epidemiological studies have shown an inverse relation between high-density lipoprotein (HDL) cholesterol levels and coronary heart disease. Recently, observational studies have suggested a similar inverse relation between HDL and restenosis after coronary balloon angioplasty. Despite these observations, it is unclear whether this inverse relation reflects a direct vascular protective effect of HDL or apolipoprotein (apo) A-I, the major apolipoprotein component of HDL. Therefore, to determine whether HDL directly influences neointima formation, we investigated the effect of recombinant apo A-I Milano (apo A-I M), a mutant of human apo A-I with Arg-173 to Cys substitution, on intimal thickening after balloon injury in cholesterol-fed rabbits.<\/jats:p>\n <\/jats:sec>\n \n METHODS AND RESULTS<\/jats:title>\n Cholesterol feeding was initiated 18 days before injury and continued until the time of death. Eight rabbits received intravenous injections of 40 mg of apo A-I M linked to a phospholipid carrier on alternate days, beginning 5 days before and continuing for 5 days after balloon injury of femoral and iliac arteries. Eight rabbits received the carrier alone, and four received neither apo A-I M nor the carrier. Three weeks after balloon injury, apo A-I M-treated rabbits had significantly reduced intimal thickness compared with the two control groups (mean +\/- SD): 0.49 +\/- 0.29 versus 1.14 +\/- 0.38 mm2 and 1.69 +\/- 0.43 mm2, P < .002 by ANOVA). The intima-to-media ratio was also significantly reduced by apo A-I M (0.7 +\/- 0.2 versus 1.5 +\/- 0.5 and 2.1 +\/- 0.1, P < .002 by ANOVA) compared with the two controls. The fraction of intimal lesion covered by macrophages, as identified by immunohistochemistry using macrophage-specific monoclonal antibody, was significantly less in apo A-I M-treated rabbits compared with carrier-treated animals (25.3 +\/- 17% versus 59.4 +\/- 12.3%, P < .005). Aortic cholesterol content, measured in an additional 10 rabbits, did not differ significantly between apo A-I M-treated animals (n = 5) and carrier-treated controls (n = 5).<\/jats:p>\n <\/jats:sec>\n \n CONCLUSIONS<\/jats:title>\n Apo A-I M significantly reduced intimal thickening and macrophage content after balloon injury in cholesterol-fed rabbits without a change in arterial total cholesterol content. Although the precise mechanism of action remains to be defined, these findings are consistent with a direct vascular effect of apo A-I, which could have potential therapeutic implications.<\/jats:p>\n <\/jats:sec>","DOI":"10.1161\/01.cir.90.4.1935","type":"journal-article","created":{"date-parts":[[2012,6,12]],"date-time":"2012-06-12T00:34:42Z","timestamp":1339461282000},"page":"1935-1941","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":138,"title":["Recombinant apolipoprotein A-I Milano reduces intimal thickening after balloon injury in hypercholesterolemic rabbits."],"prefix":"10.1161","volume":"90","author":[{"given":"S","family":"Ameli","sequence":"first","affiliation":[{"name":"Division of Cardiology, Cedars-Sinai Medical Center, Los Angeles, CA 90048."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"A","family":"Hultgardh-Nilsson","sequence":"additional","affiliation":[{"name":"Division of Cardiology, Cedars-Sinai Medical Center, Los Angeles, CA 90048."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"B","family":"Cercek","sequence":"additional","affiliation":[{"name":"Division of Cardiology, Cedars-Sinai Medical Center, Los Angeles, CA 90048."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"P K","family":"Shah","sequence":"additional","affiliation":[{"name":"Division of Cardiology, Cedars-Sinai Medical Center, Los Angeles, CA 90048."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"J S","family":"Forrester","sequence":"additional","affiliation":[{"name":"Division of Cardiology, Cedars-Sinai Medical Center, Los Angeles, CA 90048."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"H","family":"Ageland","sequence":"additional","affiliation":[{"name":"Division of Cardiology, Cedars-Sinai Medical Center, Los Angeles, CA 90048."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"J","family":"Nilsson","sequence":"additional","affiliation":[{"name":"Division of Cardiology, Cedars-Sinai Medical Center, Los Angeles, CA 90048."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"276","container-title":["Circulation"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/www.ahajournals.org\/doi\/pdf\/10.1161\/01.CIR.90.4.1935","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2024,5,12]],"date-time":"2024-05-12T15:42:52Z","timestamp":1715528572000},"score":1,"resource":{"primary":{"URL":"https:\/\/www.ahajournals.org\/doi\/10.1161\/01.CIR.90.4.1935"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1994,10]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1994,10]]}},"alternative-id":["10.1161\/01.CIR.90.4.1935"],"URL":"https:\/\/doi.org\/10.1161\/01.cir.90.4.1935","relation":{},"ISSN":["0009-7322","1524-4539"],"issn-type":[{"value":"0009-7322","type":"print"},{"value":"1524-4539","type":"electronic"}],"subject":[],"published":{"date-parts":[[1994,10]]},"assertion":[{"value":"1994-10-01","order":2,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]}}