Study on the effect of LncRNA AK094457 on OX-LDL induced vascular smooth muscle cells.
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Atherosclerosis as the common disease has aroused many attentions worldwide. Gene target therapy has become the promising filed for atherosclerosis treatment. Herein, LncRNA AK094457 as a new promising therapy target is investigated in OX-LDL induced vascular smooth muscle cells. The Results showed that LncRNA AK094457 downregulated by shRNA-AK094457-1 have inhibiting effects on proliferation, migration, ROS level and inflammation level in OX-LDL induced vascular smooth muscle cells (VSMCs). In addition, the down regulation of lncRNA suppressed expressions of relevant proteins that are involved in TLR4/MyD88 signal pathway and enhanced expressions of relevant proteins in Nrf2/HO-1 pathway. Taken together, Down regulation of lncRNA AK094457 against effects induced by OXL-LDL in atherosclerosis via Nrf2/HO-1 and TLR4/MyD88 signal pathway is a promising avenue for atherosclerosis treatment.Keywords:
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Atherosclerosis as the common disease has aroused many attentions worldwide. Gene target therapy has become the promising filed for atherosclerosis treatment. Herein, LncRNA AK094457 as a new promising therapy target is investigated in OX-LDL induced vascular smooth muscle cells. The Results showed that LncRNA AK094457 downregulated by shRNA-AK094457-1 have inhibiting effects on proliferation, migration, ROS level and inflammation level in OX-LDL induced vascular smooth muscle cells (VSMCs). In addition, the down regulation of lncRNA suppressed expressions of relevant proteins that are involved in TLR4/MyD88 signal pathway and enhanced expressions of relevant proteins in Nrf2/HO-1 pathway. Taken together, Down regulation of lncRNA AK094457 against effects induced by OXL-LDL in atherosclerosis via Nrf2/HO-1 and TLR4/MyD88 signal pathway is a promising avenue for atherosclerosis treatment.
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TLR4/NF-κB is a key inflammatory signaling transduction pathway, closely involved in cell differentiation, proliferation, apoptosis, and pro-inflammatory response. Toll like receptor 4 (TLR4), the first mammalian TLR to be characterized, is the innate immune receptor that plays a key role in inflammatory signal transductions. Nuclear factor kappa B (NF-κB), the TLR4 downstream, is the key to accounting for the expression of multiple genes involved in inflammatory responses, such as pro-inflammatory cytokines. Inflammatory bowel disease (IBD) in humans is a chronic inflammatory disease with high incidence and prevalence worldwide. Targeting the TLR4/NF-κB signaling pathway might be an effective strategy to alleviate intestinal inflammation. Polyphenol phytochemicals have shown noticeable alleviative effects by acting on the TLR4/NF-κB signaling pathway in intestinal inflammation. This review summarizes the pharmacological effects of more than 20 kinds of polyphenols on intestinal inflammation via targeting the TLR4/NF-κB signaling pathway. We expected that polyphenol phytochemicals targeting the TLR4/NF-κB signaling pathway might be an effective approach to treat IBD in future clinical research applications.
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Inflammation of the vascular microenvironment modulates distinct types of vascular cells, and plays important roles in promoting atherosclerosis, stenosis/restenosis, and vascular-related diseases.Nik-related kinase (Nrk), a member of the Ste20-type kinase family, has been reported to be selectively expressed in embryonic skeletal muscle.However, whether Nrk is expressed in adult vascular smooth muscle, and if it influences intimal hyperplasia is unclear.Here, we found that Nrk is abundantly expressed in cultured vascular smooth muscle cells (VSMC) and mouse arterial intima.Treatment of mouse VSMCs with lipopolysaccharide (LPS) or plateletderived growth factor significantly reduced Nrk expression.In addition, expression of Nrk was significantly reduced in regions of neointimal formation caused by guide-wire carotid artery injuries in mice, as well as in human atherosclerotic tissues, when compared to normal vessels.We identified that expression of matrix metalloproteinases (MMP3, MMP8 and MMP12) and inflammatory cytokines/chemokines (CCL6, CCL8, CCL11, CXCL1, CXCL3, CXCL5 and CXCL9) are synergistically induced by Nrk siRNA in LPS-treated mouse VSMCs.Moreover, we found that resveratrol significantly impaired LPS-and Nrk siRNA-induced expression of MMP3, CCL8, CCL11, CXCL3 and CXCL5.These results suggested that Nrk may play important roles in regulating pathological progression of atherosclerosis or neointimal-hyperplasia-related vascular diseases.
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Correction to: Cell Death and Disease (2014) 5, e1574. doi:10.1038/cddis.2014.535; published online 18 December 2014 Since the publication of this paper, it has been noted that the labelling WT and TLR4−/− was missing from the bottom of Figure 7g in the pdf file. The corrected article appears onlinetogether with this erratum.
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Proper intracellular localization of TLRs is essential for their signaling and biological function. Endocytosis constitutes a key step in protein turnover, as well as maintenance of TLR localization in plasma membrane and intracellular compartments, and thus provides important regulating points to their signaling. In this study, we demonstrate that adenylyl cyclase (AC) activation attenuates TLR4 signaling in a murine macrophage cell line (RAW 264.7) and bone marrow-derived macrophages when stimulated with LPS. We further show that the AC6 isoform plays a key role in negative regulation of TLR4 signaling by promoting protein degradation. TLR4 is normally endocytosed through the clathrin-mediated pathway, but concomitant AC6 activation shifts it to lipid raft-mediated endocytosis, which accelerates degradation of TLR4 and suppresses downstream signaling. Our studies unveil a new mechanism of negative regulation of TLR4 signaling through AC6-mediated endocytosis, which might provide a novel therapeutic approach for limiting inflammatory and autoimmune diseases.
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Toll-like receptors is a group of pattern recognition receptors which are found in the recent years. TLR4 is one of hot topics among the 11 TLR members which have been identifited. Activated TLR4 midiates signal transduction pathway via MyD88 and mitogen activated protein, then induces immune response. TLR4 is expressed in a verity of tumors. TLR4 can promote inflammation and the development and progression of tumor via different signal pathway. TLR4 plays an important role in the cancer pain and immune escape. TLR4 may become a new target for cancer biotherapy.
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