{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,11,2]],"date-time":"2025-11-02T16:12:16Z","timestamp":1762099936632},"reference-count":35,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"3","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["ATVB"],"published-print":{"date-parts":[[2002,3]]},"abstract":"<jats:p>\n            In this study, we investigated the role of T and B lymphocytes in neointimal hyperplasia after endothelial denudation. Catheter-induced endothelial denudation of wild-type mice resulted in rapid infiltration of lymphocytes to the site of injury. Mice defective in recombination-activating gene 2 (\n            <jats:italic>RAG2<\/jats:italic>\n            <jats:sup>\u2212\/\u2212<\/jats:sup>\n            ) showed increased neointimal formation 14 days after vascular injury in comparison to their wild-type immune-competent littermates. Immunohistochemical studies revealed the preponderance of smooth muscle cells and a significantly higher number of proliferating cells in the neointima of the\n            <jats:italic>RAG2<\/jats:italic>\n            <jats:sup>\u2212\/\u2212<\/jats:sup>\n            mice. The neointima size and the number of proliferating smooth muscle cells in the injured vessel of\n            <jats:italic>RAG2<\/jats:italic>\n            <jats:sup>\u2212\/\u2212<\/jats:sup>\n            mice were similar to those observed in the injured arteries of apolipoprotein E (apoE)-deficient (\n            <jats:italic>apoE<\/jats:italic>\n            <jats:sup>\u2212\/\u2212<\/jats:sup>\n            ) mice. Interestingly, mice with double\n            <jats:italic>apoE<\/jats:italic>\n            and\n            <jats:italic>RAG2<\/jats:italic>\n            gene mutations (\n            <jats:italic>apoE<\/jats:italic>\n            <jats:sup>\u2212\/\u2212<\/jats:sup>\n            <jats:italic>RAG2<\/jats:italic>\n            <jats:sup>\u2212\/\u2212<\/jats:sup>\n            ) displayed similar neointimal characteristics as mice with a single gene defect, suggesting a similar mechanism for apoE and lymphocyte protection against injury-induced neointimal formation. The protective role of lymphocytes against neointimal formation after vascular injury directly contrasts to their reported role in the promotion of atherosclerosis, which was observed in both\n            <jats:italic>apoE<\/jats:italic>\n            <jats:sup>+\/+<\/jats:sup>\n            and\n            <jats:italic>apoE<\/jats:italic>\n            <jats:sup>\u2212\/\u2212<\/jats:sup>\n            mice. Thus, these results support the hypothesis of different etiology between hyperlipidemia-induced atherosclerosis and injury-induced vascular occlusion.\n          <\/jats:p>","DOI":"10.1161\/hq0302.105377","type":"journal-article","created":{"date-parts":[[2002,7,28]],"date-time":"2002-07-28T23:16:47Z","timestamp":1027898207000},"page":"450-455","update-policy":"http:\/\/dx.doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":25,"title":["Both Apolipoprotein E and Immune Deficiency Exacerbate Neointimal Hyperplasia After Vascular Injury in Mice"],"prefix":"10.1161","volume":"22","author":[{"given":"Binghua","family":"Zhu","sequence":"first","affiliation":[{"name":"From the Department of Pathology and Laboratory Medicine (B.Z., D.Y.H.), University of Cincinnati College of Medicine, Cincinnati, Ohio, and the Department of Pathology (C.A.R., G.S.G.), University of Chicago, Chicago, Illinois."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Catherine A.","family":"Reardon","sequence":"additional","affiliation":[{"name":"From the Department of Pathology and Laboratory Medicine (B.Z., D.Y.H.), University of Cincinnati College of Medicine, Cincinnati, Ohio, and the Department of Pathology (C.A.R., G.S.G.), University of Chicago, Chicago, Illinois."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Godfrey S.","family":"Getz","sequence":"additional","affiliation":[{"name":"From the Department of Pathology and Laboratory Medicine (B.Z., D.Y.H.), University of Cincinnati College of Medicine, Cincinnati, Ohio, and the Department of Pathology (C.A.R., G.S.G.), University of Chicago, Chicago, Illinois."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"David Y.","family":"Hui","sequence":"additional","affiliation":[{"name":"From the Department of Pathology and Laboratory Medicine (B.Z., D.Y.H.), University of Cincinnati College of Medicine, Cincinnati, Ohio, and the Department of Pathology (C.A.R., G.S.G.), University of Chicago, Chicago, Illinois."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"276","reference":[{"key":"e_1_3_3_1_2","first-page":"351","volume":"149","year":"1996","unstructured":"Lichtman AH, Cybulsky M, Luscinskas FW. Immunology of atherosclerosis: the promise of mouse models. Am J Pathol. 1996; 149: 351\u2013357.","journal-title":"Am J Pathol"},{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1097\/00041433-199710000-00009"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-2796.2000.00654.x"},{"key":"e_1_3_3_4_2","doi-asserted-by":"publisher","DOI":"10.1038\/28204"},{"key":"e_1_3_3_5_2","first-page":"675","volume":"149","year":"1996","unstructured":"Emeson EE, Shen ML, Bell CGH, Qureshi A. Inhibition of atherosclerosis in CD4 T-cell-ablated and nude (nu\/nu) C57BL\/6 hyperlipidemic mice. Am J Pathol. 1996; 149: 675\u2013685.","journal-title":"Am J Pathol"},{"key":"e_1_3_3_6_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.94.9.4642"},{"key":"e_1_3_3_7_2","doi-asserted-by":"publisher","DOI":"10.1161\/atvb.21.6.1011"},{"key":"e_1_3_3_8_2","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119681"},{"key":"e_1_3_3_9_2","doi-asserted-by":"publisher","DOI":"10.1172\/JCI200111380"},{"key":"e_1_3_3_10_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.88.23.10530"},{"key":"e_1_3_3_11_2","first-page":"1045","volume":"138","year":"1991","unstructured":"Ferns GA, Reidy MA, Ross R. Balloon catheter de-endothelialization of the nude rat carotid: response to injury in the absence of functional T lymphocytes. Am J Pathol. 1991; 138: 1045\u20131057.","journal-title":"Am J Pathol"},{"key":"e_1_3_3_12_2","doi-asserted-by":"publisher","DOI":"10.1161\/circ.84.3.1909221"},{"key":"e_1_3_3_13_2","doi-asserted-by":"publisher","DOI":"10.1161\/atvb.19.7.1687"},{"key":"e_1_3_3_14_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)64823-7"},{"key":"e_1_3_3_15_2","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.32.20156"},{"key":"e_1_3_3_16_2","doi-asserted-by":"publisher","DOI":"10.1161\/atvb.20.4.1020"},{"key":"e_1_3_3_17_2","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M102357200"},{"key":"e_1_3_3_18_2","doi-asserted-by":"publisher","DOI":"10.1161\/atvb.20.8.1852"},{"key":"e_1_3_3_19_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0021-9258(19)70201-4"},{"key":"e_1_3_3_20_2","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(92)90029-C"},{"key":"e_1_3_3_21_2","doi-asserted-by":"publisher","DOI":"10.1210\/endo.142.8.8331"},{"key":"e_1_3_3_22_2","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.1.89"},{"key":"e_1_3_3_23_2","doi-asserted-by":"publisher","DOI":"10.1016\/0049-3848(96)87301-4"},{"key":"e_1_3_3_24_2","doi-asserted-by":"crossref","first-page":"1008","DOI":"10.4049\/jimmunol.126.3.1008","volume":"126","year":"1981","unstructured":"Curtiss LK, Edgington TS. Immunoregulatory plasma low density lipoprotein: the biologic activity and receptor binding specificity is independent of neutral lipids. J Immunol. 1981; 126: 1008\u20131012.","journal-title":"J Immunol"},{"key":"e_1_3_3_25_2","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.136.10.3716"},{"key":"e_1_3_3_26_2","doi-asserted-by":"publisher","DOI":"10.1084\/jem.170.5.1595"},{"key":"e_1_3_3_27_2","doi-asserted-by":"publisher","DOI":"10.1161\/circ.102.24.2919"},{"key":"e_1_3_3_28_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9149(00)01094-8"},{"key":"e_1_3_3_29_2","doi-asserted-by":"publisher","DOI":"10.1159\/000416895"},{"key":"e_1_3_3_30_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.84.24.9265"},{"key":"e_1_3_3_31_2","doi-asserted-by":"publisher","DOI":"10.1038\/327524a0"},{"key":"e_1_3_3_32_2","doi-asserted-by":"publisher","DOI":"10.1161\/res.82.1.21"},{"key":"e_1_3_3_33_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0021-9150(96)05976-X"},{"key":"e_1_3_3_34_2","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1997.7408"},{"key":"e_1_3_3_35_2","doi-asserted-by":"publisher","DOI":"10.1161\/res.71.5.1394884"}],"container-title":["Arteriosclerosis, Thrombosis, and Vascular Biology"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/www.ahajournals.org\/doi\/full\/10.1161\/hq0302.105377","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2024,5,14]],"date-time":"2024-05-14T02:12:47Z","timestamp":1715652767000},"score":1,"resource":{"primary":{"URL":"https:\/\/www.ahajournals.org\/doi\/10.1161\/hq0302.105377"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2002,3]]},"references-count":35,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2002,3]]}},"alternative-id":["10.1161\/hq0302.105377"],"URL":"https:\/\/doi.org\/10.1161\/hq0302.105377","relation":{},"ISSN":["1079-5642","1524-4636"],"issn-type":[{"value":"1079-5642","type":"print"},{"value":"1524-4636","type":"electronic"}],"subject":[],"published":{"date-parts":[[2002,3]]},"assertion":[{"value":"2002-03-01","order":2,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]}}