{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,22]],"date-time":"2026-10-22T01:16:08Z","timestamp":1792631768191,"version":"4.5.0"},"reference-count":89,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"1","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation Research"],"published-print":{"date-parts":[[2024,1,5]]},"abstract":"\n BACKGROUND:<\/jats:title>\n \n Increasing evidence suggests that long noncoding RNAs play significant roles in vascular biology and disease development. One such long noncoding RNA,\n PSMB8-AS1<\/jats:italic>\n , has been implicated in the development of tumors. Nevertheless, the precise role of\n PSMB8-AS1<\/jats:italic>\n in cardiovascular diseases, particularly atherosclerosis, has not been thoroughly elucidated. Thus, the primary aim of this investigation is to assess the influence of\n PSMB8-AS1<\/jats:italic>\n on vascular inflammation and the initiation of atherosclerosis.\n <\/jats:p>\n <\/jats:sec>\n \n METHODS:<\/jats:title>\n \n We generated\n PSMB8-AS1<\/jats:italic>\n knockin and\n Apoe<\/jats:italic>\n (Apolipoprotein E) knockout mice (\n \n Apoe\n \u2212\/\u2212<\/jats:sup>\n PSMB8-AS1\n KI<\/jats:sup>\n <\/jats:italic>\n ) and global\n Apoe<\/jats:italic>\n and proteasome subunit-\u03b2 type-9 (\n Psmb9<\/jats:italic>\n ) double knockout mice (\n \n Apoe\n \u2212\/\u2212<\/jats:sup>\n Psmb9\n \u2212\/\u2212<\/jats:sup>\n <\/jats:italic>\n ). To explore the roles of\n PSMB8-AS1<\/jats:italic>\n and\n Psmb9<\/jats:italic>\n in atherosclerosis, we fed the mice with a Western diet for 12 weeks.\n <\/jats:p>\n <\/jats:sec>\n \n RESULTS:<\/jats:title>\n \n Long noncoding RNA\n PSMB8-AS1<\/jats:italic>\n is significantly elevated in human atherosclerotic plaques. Strikingly,\n \n Apoe\n \u2212\/\u2212<\/jats:sup>\n PSMB8-AS1\n KI<\/jats:sup>\n <\/jats:italic>\n mice exhibited increased atherosclerosis development, plaque vulnerability, and vascular inflammation compared with\n \n Apoe\n \u2212\/\u2212<\/jats:sup>\n <\/jats:italic>\n mice. Moreover, the levels of VCAM1 (vascular adhesion molecule 1) and ICAM1 (intracellular adhesion molecule 1) were significantly upregulated in atherosclerotic lesions and serum of\n \n Apoe\n \u2212\/\u2212<\/jats:sup>\n PSMB8-AS1\n KI<\/jats:sup>\n <\/jats:italic>\n mice. Consistently, in vitro gain- and loss-of-function studies demonstrated that\n PSMB8-AS1<\/jats:italic>\n induced monocyte\/macrophage adhesion to endothelial cells and increased VCAM1 and ICAM1 levels in a PSMB9-dependent manner. Mechanistic studies revealed that\n PSMB8-AS1<\/jats:italic>\n induced\n PSMB9<\/jats:italic>\n transcription by recruiting the transcription factor NONO (non-POU domain-containing octamer-binding protein) and binding to the\n PSMB9<\/jats:italic>\n promoter. PSMB9 (proteasome subunit-\u03b2 type-9) elevated VCAM1 and ICAM1 expression via the upregulation of ZEB1 (zinc finger E-box-binding homeobox 1).\n Psmb9<\/jats:italic>\n deficiency decreased atherosclerotic lesion size, plaque vulnerability, and vascular inflammation in\n \n Apoe\n \u2212\/\u2212<\/jats:sup>\n <\/jats:italic>\n mice in vivo. Importantly, endothelial overexpression of\n PSMB8-AS1<\/jats:italic>\n -increased atherosclerosis and vascular inflammation were attenuated by\n Psmb9<\/jats:italic>\n knockout.\n <\/jats:p>\n <\/jats:sec>\n \n CONCLUSIONS:<\/jats:title>\n \n PSMB8-AS1<\/jats:italic>\n promotes vascular inflammation and atherosclerosis via the NONO\n \/<\/jats:italic>\n PSMB9\/ZEB1 axis. Our findings support the development of new long noncoding RNA\u2013based strategies to counteract atherosclerotic cardiovascular disease.\n <\/jats:p>\n <\/jats:sec>","DOI":"10.1161\/circresaha.122.322360","type":"journal-article","created":{"date-parts":[[2023,12,12]],"date-time":"2023-12-12T05:06:37Z","timestamp":1702357597000},"page":"60-80","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":74,"title":["LncRNA\n PSMB8-AS1<\/i>\n Instigates Vascular Inflammation to Aggravate Atherosclerosis"],"prefix":"10.1161","volume":"134","author":[{"given":"Shu","family":"Li","sequence":"first","affiliation":[{"name":"Department of Clinical Laboratory, Guangzhou Women & Children Medical Center, Guangzhou Medical University, Guangdong, China (S.L., R.-C.H., Y.S., K.-L.Z., M.-L.T., T.Z., M.J., X.-H.D., J.W., Y.-W.H.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4338-7562","authenticated-orcid":true,"given":"Run-Chao","family":"He","sequence":"additional","affiliation":[{"name":"Department of Clinical Laboratory, Guangzhou Women & Children Medical Center, Guangzhou Medical University, Guangdong, China (S.L., R.-C.H., Y.S., K.-L.Z., M.-L.T., T.Z., M.J., X.-H.D., J.W., Y.-W.H.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8587-3334","authenticated-orcid":true,"given":"Shao-Guo","family":"Wu","sequence":"additional","affiliation":[{"name":"Department of Clinical Laboratory, Guangzhou Twelfth People\u2019s Hospital, Guangdong, China (S.-G.W.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0712-0139","authenticated-orcid":true,"given":"Yu","family":"Song","sequence":"additional","affiliation":[{"name":"Department of Clinical Laboratory, 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