{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,10]],"date-time":"2026-03-10T22:38:35Z","timestamp":1773182315218,"version":"3.50.1"},"reference-count":41,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"6","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2016,6,13]]},"abstract":"<jats:sec xml:lang=\"en\">\n            <jats:title>Background<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              Light chain amyloidosis (AL) is associated with high mortality, especially in patients with advanced cardiovascular involvement. It is caused by toxicity of misfolded light chain proteins (\n              <jats:styled-content style=\"fixed-case\">LC<\/jats:styled-content>\n              ) in vascular, cardiac, and other tissues. There is no treatment to reverse\n              <jats:styled-content style=\"fixed-case\">LC<\/jats:styled-content>\n              tissue toxicity. We tested the hypothesis that nanoliposomes composed of monosialoganglioside, phosphatidylcholine, and cholesterol (GM1 ganglioside\u2013containing nanoliposomes [\n              <jats:styled-content style=\"fixed-case\">NLGM<\/jats:styled-content>\n              1]) can protect against\n              <jats:styled-content style=\"fixed-case\">LC<\/jats:styled-content>\n              \u2010induced human microvascular dysfunction and assess mechanisms behind the protective effect.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Methods and Results<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              The dilator responses of ex\u00a0vivo abdominal adipose arterioles from human participants without AL to acetylcholine and papaverine were measured before and after exposure to\n              <jats:styled-content style=\"fixed-case\">LC<\/jats:styled-content>\n              (20\u00a0\u03bcg\/mL) with or without\n              <jats:styled-content style=\"fixed-case\">NLGM<\/jats:styled-content>\n              1 (1:10 ratio for\n              <jats:styled-content style=\"fixed-case\">LC<\/jats:styled-content>\n              :\n              <jats:styled-content style=\"fixed-case\">NLGM<\/jats:styled-content>\n              1 mass). Human umbilical vein endothelial cells were exposed for 18 to 20\u00a0hours to vehicle, LC with or without\n              <jats:styled-content style=\"fixed-case\">NLGM<\/jats:styled-content>\n              1, or\n              <jats:styled-content style=\"fixed-case\">NLGM<\/jats:styled-content>\n              1 and compared for oxidative and nitrative stress response and cellular viability. LC impaired arteriole dilator response to acetylcholine, which was restored by co\u2010treatment with\n              <jats:styled-content style=\"fixed-case\">NLGM<\/jats:styled-content>\n              1.\n              <jats:styled-content style=\"fixed-case\">LC<\/jats:styled-content>\n              decreased endothelial cell nitric oxide production and cell viability while increasing superoxide and peroxynitrite; these adverse effects were reversed by\n              <jats:styled-content style=\"fixed-case\">NLGM<\/jats:styled-content>\n              1.\n              <jats:styled-content style=\"fixed-case\">NLGM<\/jats:styled-content>\n              1 increased endothelial cell protein expression of antioxidant enzymes heme oxygenase 1 and\n              <jats:styled-content style=\"fixed-case\">NAD<\/jats:styled-content>\n              (P)H quinone dehydrogenase 1 and increased nuclear factor, erythroid 2 like 2 (Nrf\u20102) protein. Nrf\u20102 gene knockdown reduced antioxidant stress response and reversed the protective effects of\n              <jats:styled-content style=\"fixed-case\">NLGM<\/jats:styled-content>\n              1.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Conclusions<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              NLGM1 protects against\n              <jats:styled-content style=\"fixed-case\">LC<\/jats:styled-content>\n              \u2010induced human microvascular endothelial dysfunction through increased nitric oxide bioavailability and reduced oxidative and nitrative stress mediated by Nrf\u20102\u2013dependent antioxidant stress response. These findings point to a potential novel therapeutic approach for light chain amyloidosis.\n            <\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/jaha.116.003318","type":"journal-article","created":{"date-parts":[[2016,6,14]],"date-time":"2016-06-14T03:00:59Z","timestamp":1465873259000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":13,"title":["Monosialoganglioside\u2010Containing Nanoliposomes Restore Endothelial Function Impaired by AL Amyloidosis Light Chain Proteins"],"prefix":"10.1161","volume":"5","author":[{"given":"Daniel A.","family":"Franco","sequence":"first","affiliation":[{"name":"Phoenix Veterans Affairs Health Care System, Phoenix, AZ"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Seth","family":"Truran","sequence":"additional","affiliation":[{"name":"Phoenix Veterans Affairs Health Care System, Phoenix, AZ"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Volkmar","family":"Weissig","sequence":"additional","affiliation":[{"name":"Midwestern University, Glendale, AZ"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Diana","family":"Guzman\u2010Villanueva","sequence":"additional","affiliation":[{"name":"Midwestern University, Glendale, AZ"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Nina","family":"Karamanova","sequence":"additional","affiliation":[{"name":"Phoenix Veterans Affairs Health Care System, Phoenix, AZ"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Subhadip","family":"Senapati","sequence":"additional","affiliation":[{"name":"Arizona State University, Tempe, AZ"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Camelia","family":"Burciu","sequence":"additional","affiliation":[{"name":"Phoenix Veterans Affairs Health Care System, Phoenix, AZ"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Marina","family":"Ramirez\u2010Alvarado","sequence":"additional","affiliation":[{"name":"Mayo Clinic, Rochester, MN"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Luis M.","family":"Blancas\u2010Mejia","sequence":"additional","affiliation":[{"name":"Mayo Clinic, Rochester, MN"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Stuart","family":"Lindsay","sequence":"additional","affiliation":[{"name":"Arizona State University, Tempe, AZ"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Parameswaran","family":"Hari","sequence":"additional","affiliation":[{"name":"Medical College of Wisconsin, Milwaukee, WI"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Raymond Q.","family":"Migrino","sequence":"additional","affiliation":[{"name":"Phoenix Veterans Affairs Health Care System, Phoenix, AZ"},{"name":"University of Arizona College of Medicine, Phoenix, AZ"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"276","reference":[{"key":"e_1_3_4_2_2","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCULATIONAHA.104.489187"},{"key":"e_1_3_4_3_2","doi-asserted-by":"publisher","DOI":"10.7326\/0003-4819-125-6-199609150-00009"},{"key":"e_1_3_4_4_2","doi-asserted-by":"publisher","DOI":"10.1001\/archinte.1982.00340210037009"},{"key":"e_1_3_4_5_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.atherosclerosis.2012.08.028"},{"key":"e_1_3_4_6_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.ijcard.2009.04.044"},{"key":"e_1_3_4_7_2","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00503.2011"},{"key":"e_1_3_4_8_2","doi-asserted-by":"publisher","DOI":"10.3109\/08982104.2013.838258"},{"key":"e_1_3_4_9_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.biomaterials.2010.04.044"},{"key":"e_1_3_4_10_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.jbiotec.2011.06.037"},{"key":"e_1_3_4_11_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.jmb.2008.06.062"},{"key":"e_1_3_4_12_2","doi-asserted-by":"publisher","DOI":"10.1186\/1743-8977-7-3"},{"key":"e_1_3_4_13_2","doi-asserted-by":"publisher","DOI":"10.1177\/0271678X15610134"},{"key":"e_1_3_4_14_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.nbd.2006.01.002"},{"key":"e_1_3_4_15_2","doi-asserted-by":"publisher","DOI":"10.1097\/00005344-199307000-00013"},{"key":"e_1_3_4_16_2","doi-asserted-by":"publisher","DOI":"10.1016\/0197-0186(92)90055-V"},{"key":"e_1_3_4_17_2","doi-asserted-by":"publisher","DOI":"10.1038\/srep01278"},{"key":"e_1_3_4_18_2","doi-asserted-by":"publisher","DOI":"10.1182\/blood-2005-11-4385"},{"key":"e_1_3_4_19_2","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.16-04-01324.1996"},{"key":"e_1_3_4_20_2","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M110.110080"},{"key":"e_1_3_4_21_2","doi-asserted-by":"publisher","DOI":"10.1128\/CDLI.8.6.1131-1135.2001"},{"key":"e_1_3_4_22_2","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.0000126569.75419.74"},{"key":"e_1_3_4_23_2","unstructured":"Liao R. 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