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.
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.
Authors: Stephan Fichtlscherer; Salvatore De Rosa; Henrik Fox; Thomas Schwietz; Ariane Fischer; Christoph Liebetrau; Michael Weber; Christian W Hamm; Tino Röxe; Marga Müller-Ardogan; Angelika Bonauer; Andreas M Zeiher; Stefanie Dimmeler Journal: Circ Res Date: 2010-07-01 Impact factor: 17.367
Authors: David M Leistner; Jes-Niels Boeckel; Sophia M Reis; Claudia E Thome; Roberta De Rosa; Till Keller; Lars Palapies; Stephan Fichtlscherer; Stefanie Dimmeler; Andreas M Zeiher Journal: Eur Heart J Date: 2016-02-24 Impact factor: 29.983
Authors: Ryan M O'Connell; Konstantin D Taganov; Mark P Boldin; Genhong Cheng; David Baltimore Journal: Proc Natl Acad Sci U S A Date: 2007-01-22 Impact factor: 11.205