MedElevator
Войти в исследования Journal of clinical laboratory analysis · 2017
Role of TLR4 and miR-155 in peripheral blood mononuclear cell-mediated inflammatory reaction in coronary slow flow and coronary arteriosclerosis patients.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Huang Jiangyan, Yang Qin, He Longmiao, Huang Jun
Аннотация
BACKGROUND: To study the role of toll-like receptor 4 (TLR4) and MicroRNA-155 (miR-155) in the peripheral blood mononuclear cell (PBMC)-mediated inflammation in coronary slow flow (CSF) and coronary arteriosclerosis.
METHODS: Patients were divided into acute coronary syndrome (ACS), stable angina pectoris (SAP), CSF, and healthy control (HC) groups. The isolated PBMCs were treated with lipopolysaccharide (LPS)/and antagomiR-155. TLR4, miR-155, and the concentrations of tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-1, and IL-10 were measured.
RESULTS: Before LPS intervention, the TLR4, TNF-α, IL-1, and IL-6 levels were higher and the level of miR-155, IL-10 was lower in the ACS group compared with the SAP, CSF, and HC groups. After exposure to LPS, the levels of TLR4, miR-155, TNF-α, IL-1, and IL-6 were increased and the level of IL-10 was decreased in the SAP and CSF groups compared with the HC group. But when over-expressing antagomiR-155 into PBMCs from SAP and CSF groups, the miR-155 expression, and TNF-α, IL-6, and IL-1 secretion increase induced by LPS were restrained.
CONCLUSIONS: TLR4, miR-155, and inflammatory cytokines may be closely related to ACS. LPS can induce TLR4, miR-155 expression and inflammatory response in SAP and CSF patients. AntagomiR-155 can inhibit this inflammatory response.
METHODS: Patients were divided into acute coronary syndrome (ACS), stable angina pectoris (SAP), CSF, and healthy control (HC) groups. The isolated PBMCs were treated with lipopolysaccharide (LPS)/and antagomiR-155. TLR4, miR-155, and the concentrations of tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-1, and IL-10 were measured.
RESULTS: Before LPS intervention, the TLR4, TNF-α, IL-1, and IL-6 levels were higher and the level of miR-155, IL-10 was lower in the ACS group compared with the SAP, CSF, and HC groups. After exposure to LPS, the levels of TLR4, miR-155, TNF-α, IL-1, and IL-6 were increased and the level of IL-10 was decreased in the SAP and CSF groups compared with the HC group. But when over-expressing antagomiR-155 into PBMCs from SAP and CSF groups, the miR-155 expression, and TNF-α, IL-6, and IL-1 secretion increase induced by LPS were restrained.
CONCLUSIONS: TLR4, miR-155, and inflammatory cytokines may be closely related to ACS. LPS can induce TLR4, miR-155 expression and inflammatory response in SAP and CSF patients. AntagomiR-155 can inhibit this inflammatory response.