Migration of murine intestinal dendritic cell subsets upon intrinsic and extrinsic TLR3 stimulation

Initiation of adaptive immunity to particulate antigens in lymph nodes largely depends on their presentation by migratory dendritic cells (DCs). DC subsets differ in their capacity to induce specific types of immunity, allowing subset-specific DC-targeting to influence vaccination and therapy outcomes. Faithful drug design, however, requires exact understanding of subset-specific versus global activation mechanisms. cDC1, the subset of DCs that excel in supporting immunity toward viruses, intracellular bacteria, and tumors, express uniquely high levels of the pattern recognition receptor TLR3. Using various murine genetic models, we show here that both, the cDC1 and cDC2 subsets of cDCs are activated and migrate equally well in response to TLR3 stimulation in a cell extrinsic and TNF-α dependent manner, but that cDC1 show a unique requirement for type I interferon signaling. Our findings reveal common and differing pathways regulating DC subset migration, offering important insights for the design of DC-based vaccination and therapy approaches.     

The effect of delivering the chemokine SDF-1α in a matrix-bound manner on myogenesis

Several chemokines are important in muscle myogenesis and in the recruitment of muscle precursors during muscle regeneration. Among these, the SDF-1α chemokine (CXCL12) is a potent chemoattractant known to be involved in muscle repair. SDF-1α was loaded in polyelectrolyte multilayer films made of poly(l-lysine) and hyaluronan to be delivered locally to myoblast cells in a matrix-bound manner. The adsorbed amounts of SDF-1α were tuned over a large range from 100 ng/cm² to 5 μg/cm², depending on the initial concentration of SDF-1α in solution, its pH, and on the film crosslinking extent. Matrix-bound SDF-1α induced a striking increase in myoblast spreading, which was revealed when it was delivered from weakly crosslinked films. It also significantly enhanced cell migration in a dose-dependent manner, which again depended on its presentation by the biopolymeric film. The low-crosslinked film was the most efficient in boosting cell migration. Furthermore, matrix-bound SDF-1α also increased the expression of myogenic markers but the fusion index decreased in a dose-dependent manner with the adsorbed amount of SDF-1α. At high adsorbed amounts of SDF-1α, a large number of Troponin T-positive cells had only one nucleus. Overall, this work reveals the importance of the presentation mode of SDF-1α to emphasize its effect on myogenic processes. These films may be further used to provide insight into the role of SDF-1α presented by a biomaterial in physiological or pathological processes.     

High level of reactive oxygen species impaired mesenchymal stem cell migration via overpolymerization of F-actin cytoskeleton in systemic lupus erythematosus

Some lines of evidence have demonstrated abnormalities of bone marrow mesenchymal stem cells (MSCs) in systemic lupus erythematosus (SLE) patients, characterized by defective phenotype of MSCs and slower growth with enhanced apoptosis and senescence. However, whether SLE MSCs demonstrate aberrant migration capacity or abnormalities in cytoskeleton are issues that remain poorly understood. In this study, we found that MSCs from SLE patients did show impairment in migration capacity as well as abnormalities in F-actin cytoskeleton, accompanied by a high level of intracellular reactive oxygen species (ROS). When normal MSCs were treated in vitro with H₂O₂, which increases intracellular ROS level as an oxidant, both reorganization of F-actin cytoskeleton and impairment of migration capability were observed. On the other hand, treatment with N-acetylcysteine (NAC), as an exogenous antioxidant, made F-actin more orderly and increased migration ratio in SLE MSCs. In addition, oral administration of NAC markedly reduced serum autoantibody levels and ameliorated lupus nephritis (LN) in MRL/lpr mice, partially reversing the abnormalities of MSCs. These results indicate that overpolymerization of F-actin cytoskeleton, which may be associated with high levels of ROS, causes impairment in the migration capacity of SLE MSCs and that oral administration of NAC may have potential therapeutic effects on MRL/lpr mice.     

SNHG11调控miR-154影响结直肠癌细胞增殖、凋亡、迁移和侵袭的机制研究

目的 探讨长链非编码RNA SNHG11对结直肠癌细胞增殖、凋亡、迁移和侵袭的影响及作用机制.方法 选取2014年2月至2017年10月于焦作市人民医院行手术治疗的50例结直肠癌患者的癌组织及对应癌旁组织,实时荧光定量PCR检测组织中SNHG11和miR-154的表达水平.转染SNHG11的小干扰RNA(si-SNHG...     

自发性高血压大鼠淋巴微循环功能受损

目的:观察自发性高血压大鼠(SHRs)淋巴微循环功能变化.方法:8周龄雄性SHR大鼠(SHR组)和WKY大鼠(WKY组),每组各10只.应用VasT rack测量两组大鼠微淋巴管自律运动;取胸导管分离原代淋巴管内皮细胞(LECs).应用免疫荧光和Western Blot检测LECs血管内皮生长因子受体3(VEGFR3)...     

LncRNA MIAT靶向miR-206促进食管鳞状细胞癌细胞的增殖、凋亡、迁移和侵袭的作用研究

目的 探讨长链非编码RNA(LncRNA)MIAT靶向微小RNA(miR)-206促进食管鳞状细胞癌细胞的增殖、凋亡、迁移和侵袭的作用。方法 将食管鳞状细胞癌(ESCC)细胞分为ctrl组(正常培养的ESCC细胞)、si-NC组、si-MIAT组、si-MIAT+miR-NC组和si-MIAT+miR-206 inhibitor组。实时qRT-PCR检测各组细胞MIAT、miR-206表达;CCK-8法检测细胞增殖情况;划痕实验检测细胞迁移能力;流式细胞术分析细胞凋亡情况;蛋白质印迹技术检测PCNA、MMP-9蛋白表达;双荧光素酶报告基因实验验证MIAT和miR-206的关系。结果 与ctrl组、si-NC组比较,si-MIAT组ESCC细胞中miR-206表达、细胞凋亡率升高,MIAT、OD₄₅₀值(24、48、72 h)、划痕愈合率、PCNA和MMP9蛋白表达降低(P<0.05);干扰LncRNA MIAT表达能降低ESCC细胞增殖、迁移、侵袭能力,提高细胞凋亡能力,MIAT靶向调控miR-206表达。结论 干扰LncRNA MIAT表达能够阻滞ESCC...     

罗哌卡因通过circ_0044516/微小RNA-198通路调控肺癌A549细胞增殖、迁移和侵袭的实验研究

目的:探讨罗哌卡因对肺癌A549细胞增殖、迁移和侵袭的影响及其机制。方法:2019年1月至2020年4月,将体外培养A549细胞(购自中国科学院上海细胞库)分为对照组、不同剂量[25、50、100 mg/L,罗哌卡因组(Rop组)]、乱序无意义阴性序列组(si-NC组)、si-circ_0044516组、Rop＋pcD...     

Junctional adhesion molecule-like protein as a novel target for kaempferol to ameliorate lung adenocarcinoma

Objective: Although there have been improvements in targeted therapy and immunotherapy, the majority of lung adenocarcinoma(LUAD) patients still lack effective therapies. Consequently, it is urgent to screen for new diagnosis biomarkers and pharmacological targets. Junctional adhesion molecule-like protein(JAML) was considered to be an oncogenic protein and may be a novel therapeutic target in LUAD.Kaempferol is a natural flavonoid that exhibits antitumor activities in LUAD. However, the effect ...     

Endovascular management of spontaneous delayed migration of the flow-diverter stent

Background and purposeSpontaneous delayed migration of the flow-diverter stent (FD) is an unusual complication that can be fatal. The purpose of this study is to report our experience and review the literature for the management of delayed FD migration.Materials and methodsBetween November 2013 and June 2017, 122 patients treated by FD at our institution were enrolled. We also performed a comprehensive review of the literature.ResultsSix patients (4.9%) were found to have spontaneous delayed migration of their FD. The device migrated proximally in 4 patients and distally in 2 patients. One patient had temporal lobe infarction due to stent migration, and another had subarachnoid haemorrhage (SAH). Three patients were treated with a 2nd or 3rd FD, while 2 were treated with stent-assisted coiling, and one was treated with sacrifice of the parent internal carotid artery. According to our results and the literature, the prevalence rate of delayed FD migration ranges from 2.2% to 4.9%, and the mortality and morbidity rate of delayed FD migration is 40%.ConclusionsNeuro-interventionalists should be aware of this complication and be familiar with risk factors, preventive methods and treatment options. If there is any concern regarding the size or position of the FD, early imaging follow-up and endovascular treatment should be indicated.     

MicroRNA-107抑制喉癌细胞的迁移及侵袭能力的临床分析

目的通过观察microRNA 107（miR 107）在喉癌及癌旁组织中的表达,并且在喉癌细胞系选择性上调及敲减miR 107,检测其对喉癌细胞迁移及侵袭能力的影响。方法收集40例喉癌及其邻近癌旁组织标本,运用RT qPCR检测miR 107的表达,并分析其在喉癌中的临床意义。在人喉癌细胞TU212及TU686中过表达或敲减miR 107,通过Transwell法检测其对喉癌细胞迁移及侵袭能力的影响。结果MiR 107在喉癌组织中的表达显著低于癌旁组织,差异具有统计学意义（P<0.05）,miR 107的表达水平与肿瘤细胞分化程度、淋巴结转移及原发部位相关（P<0.05）。细胞实验显示,过表达miR 107后喉癌细胞迁移及侵袭能力明显下降（P<0.05）,而敲减miR 107后细胞迁移及侵袭能力明显增强（P<0.05）。结论MiR 107在喉癌中表达显著下调,它能够抑制喉癌细胞的迁移和侵袭能力。