{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,21]],"date-time":"2026-10-21T22:44:20Z","timestamp":1792622660728,"version":"4.5.0"},"reference-count":28,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2017,4,13]],"date-time":"2017-04-13T00:00:00Z","timestamp":1492041600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Clinical Laboratory Analysis"],"published-print":{"date-parts":[[2018,2]]},"abstract":"Background<\/jats:title>To study the role of toll\u2010like receptor 4 (TLR<\/jats:styled-content>4) and MicroRNA<\/jats:styled-content>\u2010155 (miR\u2010155) in the peripheral blood mononuclear cell (PBMC<\/jats:styled-content>)\u2010mediated inflammation in coronary slow flow (CSF<\/jats:styled-content>) and coronary arteriosclerosis.<\/jats:p><\/jats:sec>Methods<\/jats:title>Patients were divided into acute coronary syndrome (ACS<\/jats:styled-content>), stable angina pectoris (SAP<\/jats:styled-content>), CSF<\/jats:styled-content>, and healthy control (HC<\/jats:styled-content>) groups. The isolated PBMC<\/jats:styled-content>s were treated with lipopolysaccharide (LPS<\/jats:styled-content>)\/and antagomiR\u2010155. TLR<\/jats:styled-content>4, miR\u2010155, and the concentrations of tumor necrosis factor (TNF<\/jats:styled-content>)\u2010\u03b1, interleukin (IL<\/jats:styled-content>)\u20106, IL<\/jats:styled-content>\u20101, and IL<\/jats:styled-content>\u201010 were measured.<\/jats:p><\/jats:sec>Results<\/jats:title>Before LPS<\/jats:styled-content> intervention, the TLR<\/jats:styled-content>4, TNF<\/jats:styled-content>\u2010\u03b1, IL<\/jats:styled-content>\u20101, and IL<\/jats:styled-content>\u20106 levels were higher and the level of miR\u2010155, IL<\/jats:styled-content>\u201010 was lower in the ACS<\/jats:styled-content> group compared with the SAP<\/jats:styled-content>, CSF<\/jats:styled-content>, and HC<\/jats:styled-content> groups. After exposure to LPS<\/jats:styled-content>, the levels of TLR<\/jats:styled-content>4, miR\u2010155, TNF<\/jats:styled-content>\u2010\u03b1, IL<\/jats:styled-content>\u20101, and IL<\/jats:styled-content>\u20106 were increased and the level of IL<\/jats:styled-content>\u201010 was decreased in the SAP<\/jats:styled-content> and CSF<\/jats:styled-content> groups compared with the HC<\/jats:styled-content> group. But when over\u2010expressing antagomiR\u2010155 into PBMC<\/jats:styled-content>s from SAP<\/jats:styled-content> and CSF<\/jats:styled-content> groups, the miR\u2010155 expression, and TNF<\/jats:styled-content>\u2010\u03b1, IL<\/jats:styled-content>\u20106, and IL<\/jats:styled-content>\u20101 secretion increase induced by LPS<\/jats:styled-content> were restrained.<\/jats:p><\/jats:sec>Conclusions<\/jats:title>TLR<\/jats:styled-content>4, miR\u2010155, and inflammatory cytokines may be closely related to ACS<\/jats:styled-content>. LPS<\/jats:styled-content> can induce TLR<\/jats:styled-content>4, miR\u2010155 expression and inflammatory response in SAP<\/jats:styled-content> and CSF<\/jats:styled-content> patients. AntagomiR\u2010155 can inhibit this inflammatory response.<\/jats:p><\/jats:sec>","DOI":"10.1002\/jcla.22232","type":"journal-article","created":{"date-parts":[[2017,4,13]],"date-time":"2017-04-13T18:25:49Z","timestamp":1492107949000},"source":"Crossref","is-referenced-by-count":11,"title":["Role of TLR4 and miR\u2010155 in peripheral blood mononuclear cell\u2010mediated inflammatory reaction in coronary slow flow and coronary arteriosclerosis patients"],"prefix":"10.1002","volume":"32","author":[{"given":"Jiangyan","family":"Huang","sequence":"first","affiliation":[{"name":"Department of Cardiology First Affiliated Hospital Nanchang University Nanchang China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qin","family":"Yang","sequence":"additional","affiliation":[{"name":"Department of Cardiology First Affiliated Hospital Nanchang University Nanchang China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Longmiao","family":"He","sequence":"additional","affiliation":[{"name":"Department of Cardiology First Affiliated Hospital Nanchang University Nanchang China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9318-4368","authenticated-orcid":false,"given":"Jun","family":"Huang","sequence":"additional","affiliation":[{"name":"Department of Cardiology First Affiliated Hospital Nanchang University Nanchang China"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2017,4,13]]},"reference":[{"key":"e_1_2_5_2_1","doi-asserted-by":"publisher","DOI":"10.3390\/ijms140714008"},{"key":"e_1_2_5_3_1","first-page":"89","article-title":"Expression of toll\u2010like receptor 4, tumor necrosis factor\u2010 alpha, matrix metalloproteinase\u20109 and effects of benazepril in patients with acute coronary syndromes","volume":"4","author":"Xie P","year":"2010","journal-title":"Clin Med Insights Cardiol"},{"key":"e_1_2_5_4_1","doi-asserted-by":"publisher","DOI":"10.1159\/000430303"},{"key":"e_1_2_5_5_1","first-page":"1817","article-title":"Inflammation: an important mechanism for different clinical entities of coronary artery diseases","volume":"118","author":"Li JJ","year":"2005","journal-title":"Chin Med J"},{"key":"e_1_2_5_6_1","doi-asserted-by":"publisher","DOI":"10.1161\/ATVBAHA.108.179705"},{"key":"e_1_2_5_7_1","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.immunol.021908.132620"},{"key":"e_1_2_5_8_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.cyto.2008.05.009"},{"key":"e_1_2_5_9_1","doi-asserted-by":"publisher","DOI":"10.1007\/s00109-006-0084-y"},{"key":"e_1_2_5_10_1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0403249101"},{"key":"e_1_2_5_11_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.humimm.2010.05.005"},{"key":"e_1_2_5_12_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2567.2008.02827.x"},{"key":"e_1_2_5_13_1","doi-asserted-by":"publisher","DOI":"10.1161\/ATVBAHA.113.302701"},{"key":"e_1_2_5_14_1","doi-asserted-by":"publisher","DOI":"10.1186\/1476-511X-9-117"},{"key":"e_1_2_5_15_1","doi-asserted-by":"publisher","DOI":"10.1007\/s10753-012-9472-3"},{"key":"e_1_2_5_16_1","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCRESAHA.109.215566"},{"key":"e_1_2_5_17_1","doi-asserted-by":"publisher","DOI":"10.1038\/cmi.2011.22"},{"key":"e_1_2_5_18_1","doi-asserted-by":"publisher","DOI":"10.1152\/ajplung.00001.2016"},{"key":"e_1_2_5_19_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0008-6363(02)00537-0"},{"key":"e_1_2_5_20_1","first-page":"484","article-title":"Role of inflammatory mediators in the pathogenesis of plaque rupture","volume":"26","author":"Gopalakrishnan M","year":"2014","journal-title":"J\u00a0Invasive Cardiol"},{"key":"e_1_2_5_21_1","doi-asserted-by":"publisher","DOI":"10.1007\/s00380-014-0565-9"},{"key":"e_1_2_5_22_1","doi-asserted-by":"publisher","DOI":"10.1253\/circj.CJ-08-1146"},{"key":"e_1_2_5_23_1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0610731104"},{"key":"e_1_2_5_24_1","first-page":"14050","article-title":"MicroRNA\u2010155 induces differentiation of RAW264.7 cells into dendritic\u2010like cells. 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