The main aim of our study was to investigate the roles and molecular basis of long noncoding RNA myocardial infarction associated transcript (MIAT) in the development of thoracic aortic aneurysm. RT‐qPCR assay was performed to measure the expressions of MIAT, microRNA‐145 (miR‐145), along with Bcl‐2 and Bcl‐xl messenger RNAs. Western blot assay was conducted to determine protein levels of Bcl‐2, Bcl‐xl, phosphorylated‐Akt (p‐Akt), and total Akt (t‐Akt). Cell viability was detected by the (3‐(4,5‐dimethyl‐2‐thiazolyl)‐2,5‐diphenyl‐2‐H‐tetrazolium bromide (MTT) assay. The relationship of MIAT and miR‐145 was examined by bioinformatics analysis and luciferase reporter assay. MIAT expression was significantly increased, and miR‐145 expression was markedly reduced in thoracic aortic aneurysms compared with normal thoracic aortic tissues. MIAT overexpression or miR‐145 depletion improved cell viability and inhibited cell apoptosis in human aortic vascular smooth muscle cells (h‐VSMCs). Further exploration revealed that MIAT could inhibit miR‐145 expression by direct interaction. And miR‐145 upregulation abrogated MIAT‐induced viability increase and apoptosis inhibition in h‐VSMCs. Moreover, MIAT inhibited the activation of Akt signaling, while this effect was abated by miR‐145 overexpression in h‐VSMCs. The inhibition of the Akt pathway by MK‐22062HCl resulted in the reduction of cell viability and the increase of cell apoptotic activity in h‐VSMCs. Akt activation by HY‐18749 improved cell viability and suppressed cell apoptosis in h‐VSMCs. And the introduction of HY‐18749 raised cell viability and curbed cell apoptosis in h‐VSMCs cotransfected with MIAT overexpression plasmid and miR‐145 mimic. lncRNA‐MIAT could target miR‐145 to affect the viability and apoptosis of h‐VSMCs, which was implicated in the regulation of the PI3K/Akt signaling pathway.

As an atherosclerotic disease, the process of peripheral arterial disease (PAD) is complicated and includes the abnormal proliferation of vascular smooth muscle. The current study aimed to determine the role of microRNA-15b (miR-15b) in the development of PAD and its associated mechanisms. Human vascular smooth muscle cells (hVSMCs) were used in the current study. To assess the effects of miR-15b on hVSMCs, miR-15b was up- or downregulated in hVSMCs using miR-15b mimics or miR-15b inhibitors respectively. Cell viability, migration and apoptosis were then determined via MTT, transwell and flow cytometry assays, respectively. TargetScan bioinformatics software was utilized to predict the targets of miR-15b, and the binding sites between insulin growth factor 1 receptor (IGF1R) and miR-15b were confirmed by dual-luciferase reporter assay. The results reveled that the miR-15b mimic significantly reduced hVSMC cell viability and migration, and promoted cell apoptosis. However, the opposite effect was observed following miR-15b inhibitor transfection. It was also determined that miR-15b directly targeted IGF1R and negatively regulated its expression in hVSMCs. Additionally, the results demonstrated that the miR-15b mimic inhibited the PI3K/AKT signaling pathway in hVSMCs, whereas the miR-15b inhibitor promoted it. Furthermore, the results indicated that the effect of the miR-15b mimic on hVSMCs was reversed by IGF1R overexpression. In conclusion, the data indicated that miR-15b participated in the occurrence and development of PAD by modulating hVSMC proliferation, apoptosis and migration via the regulation of IGF1R expression.

AbstractBackgroundAbnormal proliferation and migration of vascular smooth muscle cells (VSMCs) accelerated vascular diseases progression, like atherosclerosis and restenosis. MicroRNAs were reported to participate in modulating diverse cellular processes. Here, we focused on exploring the role of miR-638 in VSMCs glycolysis and underlying mechanism.MethodsCell Counting Kit-8 (CCK-8) assay was used to measure cell viability. Western blot assay was conducted to determine the expression of cell proliferation markers proliferating cell nuclear antigen (PCNA) and Ki-67, as well as Lactate dehydrogenase A (LDHA). VSMCs migration and invasion were evaluated by Transwell assay. Luciferase reporter gene assay and RNA immunoprecipitation were performed to validate the target relationship between miR-638 and LDHA. LDHA and miR-638 expression were also determined. Glycolysis of VSMCs was tested by corresponding Kits.ResultsPlatelet-derived growth factor-bb (PDGF-bb) promoted the VSMCs viability and down-regulated miR-638. Overexpression of miR-638 inhibited cell proliferation, migration and invasion of VSMCs. LDHA was identified as a target of miR-638, and counter-regulated by miR-638. Loss of miR-638 attenuated the suppressor effects on the proliferation, migration and invasion of VSMCs induced by LDHA down-regulation. MiR-638 inhibited the glycolysis of VSMCs by targeting LDHA.ConclusionMiR-638 is down-regulated by PDGF-bb treatment and suppressed the glycolysis of VSMCs via targeting LDHA.

BackgroundInferior vena cava (IVC) filters have proven valuable for the prevention of pulmonary embolism. However, retrieval of IVC filters can be challenging and complicated techniques are needed. The aim of this study was to retrospectively review the outcomes after retrieval of retrievable IVC filters which required complicated retrieval techniques.Material/MethodsThis study was a single-center retrospective observational study. All patients who underwent complicated IVC filter retrieval from September 2012 to May 2016 were included. Patient demographics and filter retrieval procedure were documented. Clinical outcomes and procedure-related complications were evaluated. Villalta score and VEINES-QOL/Sym were recorded to assess post-thrombotic syndrome.ResultsA total of 79 consecutive patients, 37 males and 42 were female, with a mean age of 46.5 years (age range: 22–65 years) were included in this study. IVC filters, with mean indwell time of 108 days (range: 74–157 days), were refractory to standard treatment and underwent complicated IVC filter retrieval. There were 6 serious procedure-related complications: 4 popliteal puncture area hematoma complications and 2 hematuria complications. With a mean follow-up of 20.5 months (range: 18–24 months), no pulmonary embolisms occurred, and 2 patients experienced recurrent deep venous thrombosis. Twenty-seven patients developed post-thrombotic syndrome within the first 2 years after IVC retrieval.ConclusionsComplicated methods can be used to safely remove IVC filters, alleviate filter-related morbidity, and reduce risk for post-thrombotic syndrome. The application of these techniques was safe and effective for patients with refractory IVC filters.

Excessive proliferation and migration of vascular smooth muscle cells (VSMCs) is the main cause of arteriosclerosis obliterans (ASO). The present study aimed to investigate the role of microRNA (miR)-125b on the proliferation and migration of VSMCs. Platelet-derived growth factor-BB (PDGF-BB; 20 ng/ml) was used to treat VSMCs to establish an in vitro model of ASO. VSMCs were transfected with miR-125b mimic to overexpress miR-125. Cell Counting kit-8 (CCK-8) and BrdU assays were performed to assess the proliferative ability of VSMCs, while Transwell and wound healing assays were performed to assess the migratory ability of VSMCs. Western blot and immunofluorescence analyses were performed to detect the expression levels of angio-associated migratory cell protein (AAMP) and serum response factor (SRF) in VSMCs following transfection with miR-125b mimic or inhibitor. The results demonstrated that miR-125b expression decreased following treatment with PDGF-BB, the effects of which were reversed following transfection with miR-125b mimic. According to the CCK-8 assay, the cell proliferative ability decreased by ~50% compared with the negative control (NC) group, and ~40% at day 4 based on the BrdU assay. The results of the Transwell and wound healing assays indicated that the migratory ability of VSMCs significantly decreased in the miR-125b mimic group compared with the NC group. Furthermore, western blot and immunofluorescence analyses demonstrated that AAMP and SRF expression levels decreased following transfection with miR-125b mimic compared with the NC group, the effects of which were reversed following transfection with miR-125 inhibitor. Taken together, the results of the present study suggested that miR-125b inhibits the proliferative and migratory abilities of VSMCs by regulating the expression levels of AAMP and SRF.