scholarly journals microRNA-204-5p participates in atherosclerosis via targeting MMP-9

Open Medicine ◽  
2020 ◽  
Vol 15 (1) ◽  
pp. 231-239 ◽  
Author(s):  
Na Wang ◽  
Yuliang Yuan ◽  
Shipeng Sun ◽  
Guijian Liu
Keyword(s):  
Transwell Assay ◽  
Blood Samples ◽  
Thiazolyl Blue Tetrazolium Bromide ◽  
Promising Therapeutic Target ◽  
Matrix Metallopeptidase ◽  
Matrix Metallopeptidase 9 ◽  
And Migration ◽  
Thiazolyl Blue Tetrazolium ◽  
Normal Controls ◽  
Proliferation And Migration

AbstractThe aim of the present study was to investigate the role and mechanism of microRNA-204-5p (miR-204-5p) in atherosclerosis (AS)-related abnormal human vascular smooth muscle cells (hVSMCs) function. Firstly, we analyzed the expression of miR-204-5p and found that the miR-204-5p expression level was clearly downregulated in atherosclerotic plaque tissues and blood samples compared to the normal controls. Then, matrix metallopeptidase-9 (MMP-9) was predicted to be the potential target of miR-204-5p by TargetScan and this prediction was confirmed by luciferase assays. Besides, we observed that miR-204-5p could negatively regulate the expression of MMP-9 in hVSMCs. Subsequently, Thiazolyl Blue Tetrazolium Bromide (MTT) assay, transwell assay and flow cytometry were performed to detect the proliferation, migration and apoptosis of hVSMCs. Down-expression of miR-204-5p led to the promotion of proliferation and migration accompanied with the suppression of apoptosis in hVSMCs, and these effects were reversed by MMP-9-siRNA. In addition, overexpressed miR-204-5p could inhibit hVSMC proliferation and migration and promote the apoptosis of hVSMCs. However, the effects were also abrogated by overexpressed MMP-9. Together, our findings showed that miR-204-5p plays an important role in the growth and migration of hVSMCs by targeting MMP-9, which might be a novel biomarker and promising therapeutic target for AS.

scholarly journals microRNA-491-5p protects against atherosclerosis by targeting matrix metallopeptidase-9

Open Medicine ◽  
2020 ◽  
Vol 15 (1) ◽  
pp. 492-500
Author(s):  
Zhonghan He ◽  
Yayun Wang ◽  
Qin He ◽  
Manhua Chen
Keyword(s):  
Atherosclerotic Plaque ◽  
Bioinformatic Analysis ◽  
Luciferase Reporter ◽  
Plasma Samples ◽  
Matrix Metallopeptidase ◽  
Matrix Metallopeptidase 9 ◽  
And Migration ◽  
New Biomarkers ◽  
Atherosclerosis Treatment ◽  
Proliferation And Migration

AbstractAbnormal proliferation and migration of vascular smooth muscle cells (VSMCs) are critical processes that are involved in atherosclerosis. The aim of this study was to explore the role of microRNA-491-5p (miR-491-5p) in the progression of atherosclerosis by regulating the growth and migration of VSMCs. In this study, we showed that the expression of miR-491-5p was downregulated in the atherosclerotic plaque tissues and plasma samples of the patients with atherosclerosis. The bioinformatic analysis and dual-luciferase reporter assay identified that matrix metallopeptidase-9 (MMP-9) was a target gene of miR-491-5p. The results showed a significant upregulation of MMP-9 in the atherosclerotic plaque tissues and plasma samples. Subsequently, the results also showed that downregulation of miR-491-5p significantly promoted the proliferation and migration of VSMCs and inhibited the apoptosis in VSMCs. Furthermore, we detected the effects of miR-491-5p mimic on the growth and migration of VSMCs, and the results illustrated that miR-491-5p mimic could inhibit the proliferation and migration of VSMCs and promote the apoptosis of VSMCs. Notably, MMP-9 plasmid could reverse all the effects of miR-491-5p mimic on VSMCs. Collectively, our study provides the first evidence that miR-491-5p inhibited the growth and migration of VSMCs by targeting MMP-9, which might provide new biomarkers and potential therapeutic targets for atherosclerosis treatment.

scholarly journals Circular RNA CircITGA7 Promotes Tumorigenesis of Osteosarcoma via miR-370/PIM1 Axis

2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Chuanwu Fang ◽  
Xiaohong Wang ◽  
Dongliang Guo ◽  
Run Fang ◽  
Ting Zhu
Keyword(s):  
Circular Rna ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Functional Assay ◽  
Transwell Assay ◽  
Qrt Pcr ◽  
Proliferation And Metastasis ◽  
And Migration ◽  
Dual Luciferase Reporter Assay ◽  
Proliferation And Migration

Many studies have shown that there are many circular RNA (circRNA) expression abnormalities in osteosarcoma (OS), and this abnormality is related to the development of osteosarcoma. But at present, it is unclear as to what circITGA7 has in the OS and what it does. In this study, qRT-PCR was used to detect the expression of circITGA7, miR-370, and PIM1 mRNA in OS tissues and cells. The CCK-8 assay was used to detect the effect of circITGA7 on cell proliferation. Later, the transwell assay was used to detect cell migration and invasion. The dual-luciferase reporter assay confirmed the existence of the targeting relationship between circITGA7 and miR-370, and miR-370 and PIM1. We found that circITGA7 was upregulated in OS tissues and cell lines. Knockdown of circITGA7 weakened the cell’s ability to proliferate and metastasize. Furthermore, we observed that miR-370 was negatively regulated by circITGA7, while PIM1 was positively regulated by it. A functional assay validated that circITGA7 promoted OS progression via suppressing miR-370 and miR-370 affected OS proliferation and migration via PIM6 in OS. In summary, this study shows that circITGA7 promotes OS proliferation and metastasis via miR-370/PIM1.

scholarly journals Post-Translational Modification of Adiponectin Affects Lipid Accumulation, Proliferation and Migration of Vascular Smooth Muscle Cells

2017 ◽  
Vol 43 (1) ◽  
pp. 172-181 ◽  
Author(s):  
Xinzhong Chen ◽  
Yanhong Yuan ◽  
Qin Wang ◽  
Fei Xie ◽  
Dongsheng Xia ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Lipid Accumulation ◽  
Oxidized Ldl ◽  
Muscle Cells ◽  
Blood Samples ◽  
And Migration ◽  
Proliferation And Migration

Background/Aims: Adiponectin (Apn) is a multifunctional adipokine that circulates as several oligomeric complexes in the blood stream. Previous reports showed that several conserved lysine residues within the N-terminal collagenous domain of Apn are modified by hydroxylation and glycosylation. Here, we investigated the potential roles of post-translational modifications of Apn on the function of human vascular smooth muscle cells (VSMCs). Methods: Blood samples of 92 coronary artery disease (CAD) patients and 20 healthy volunteers were collected and total and high molecular weight (HMW) Apn concentration and glycosylation were analyzed. Results: The results revealed that total and HMW Apn derived from blood samples of CAD patients with severe stenosis significantly increased, however the glycosylation of HMW Apn significantly decreased. Functional studies of human VSMCs revealed that glycosylated Apn significantly inhibited the oxidized LDL-induced lipid accumulation, proliferation and migration of VSMCs, whereas non-glycosylated Apn had no inhibitory effects. Conclusion: Taken together, these data suggest that glycosylation of Apn is critically involved in regulating function against atherosclerosis by inhibiting lipid accumulation and proliferation and migration of VSMCs.

scholarly journals MICAL2 Promotes Proliferation and Migration of Glioblastoma Cells Through TGF-β/p-Smad2/EMT-Like Signaling Pathway

2021 ◽  
Vol 11 ◽  
Author(s):  
Bei Pu ◽  
Xu Zhang ◽  
Tengfeng Yan ◽  
Yuntao Li ◽  
Baohui Liu ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Signaling Pathway ◽  
Type I ◽  
Glioblastoma Cells ◽  
Cycle Arrest ◽  
Tumor Growth Factor ◽  
Promising Therapeutic Target ◽  
Human Gbm ◽  
And Migration ◽  
Proliferation And Migration

Recent studies showed that molecule interacting with CasL2 (MICAL2) could be a novel tumor growth factor, and it is closely associated with tumor growth and invasion. However, the role it plays in glioblastoma (GBM) and its potential mechanisms are currently unknown. Our study is designed to identify the effect of MICAL2 on GBM cells and the potential mechanisms behind it. Here, we found that MICAL2 interacts with TGF receptor-type I (TGFRI) and promotes the proliferation and migration of glioblastoma through the TGF-β/p-Smad2/EMT-like signaling pathway. MICAL2-knockdown inhibited the proliferation of glioblastoma cells, which was related to cell cycle arrest and downregulation of DNA replication. The invasion abilities of U87 and U251 cells were reduced after the knockdown of MICAL2. MICAL2 promoted the growth of GBM in nude mice. High MICAL2 predicts poor outcome of GBM patients. MICAL2 could be identified as a novel promising therapeutic target for human GBM.

scholarly journals AMPK-SIRT1 Pathway Modulates The Apoptosis, Proliferation and Migration of AR42J Cells By Regulating p53 and NF-κB

2021 ◽  
Author(s):  
Wei-Li Yu ◽  
Xiao-Die Wang ◽  
Fu-Gui Wang ◽  
Zhong-Hua Lu ◽  
Yun Sun
Keyword(s):  
Flow Cytometry ◽  
Cell Apoptosis ◽  
Transwell Assay ◽  
Qrt Pcr ◽  
Ar42j Cells ◽  
Compound C ◽  
Protein Expressions ◽  
And Migration ◽  
Inflammation Reaction ◽  
Proliferation And Migration

Abstract Background: Acute pancreatitis (AP) is an acute abdomen caused by abnormal activation of trypsin. AMPK-SIRT1 pathway has been reported to be related to various diseases, but the function in AP remains unclear. This study is designed to investigate the mechanism and effect of AMPK-SIRT1 pathway in AP.Methods: An experimental AP model of AR42J cells was stimulated with caerulein after pretreated with compound C or metformin. The mRNA and protein expressions of genes were analyzed by qRT-PCR and western blot. Cell apoptosis, proliferation and migration were measured using flow cytometry, MTT and transwell assay. Results: After pretreated with metformin, expressions of p-AMPKα, SIRT1 were elevated, ace-p53, ace-NF-κB were attenuated, cell apoptosis, proliferation, and migration were decreased. After pretreated with compound C, the reverse effects occurred. p-AMPKα and SIRT1 expressions were decreased, ace-p53 and ace-NF-κB were rasied, and cell apoptosis, proliferation, and migration were enhanced after caerulein induced in each group. Conclusion: When AP happened, expressions of p-AMPKα and SIRT1 were reduced, resulting in up-regulation of acetylation levels of p53 and NF-κB, acceleration of cell apoptosis, proliferation and migration. It hinted that AMPK-SIRT1 pathway could modulate the apoptosis, proliferation, migration and inflammation reaction of AR42J cells by regulating p53 and NF-κB.

TIGAR reduces smooth muscle cell autophagy to prevent pulmonary hypertension

2020 ◽  
Vol 319 (5) ◽  
pp. H1087-H1096
Author(s):  
Ryoetsu Yamanaka ◽  
Atsushi Hoshino ◽  
Kuniyoshi Fukai ◽  
Ryota Urata ◽  
Yoshito Minami ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Refractory Disease ◽  
Oxygen Species ◽  
Downstream Target ◽  
Promising Therapeutic Target ◽  
Pulmonary Arterial ◽  
Pulmonary Artery Smooth Muscle ◽  
Human Pulmonary Artery ◽  
And Migration ◽  
Proliferation And Migration

Pulmonary arterial hypertension is a refractory disease. TP53-induced glycolysis and apoptosis regulator (TIGAR) is a downstream target of p53 and exhibits functions inhibiting autophagy and reactive oxygen species (ROS). By using TIGAR-deficient knockout mice and human pulmonary artery smooth muscle cells, we found that TIGAR suppressed the proliferation and migration of PASMCs via inhibiting autophagy and ROS and, therefore, improved hypoxia-induced PH. TIGAR will be a promising therapeutic target for PAH.

scholarly journals miR-129-5p inhibits oxidized low-density lipoprotein-induced A7r5 cells  proliferation and migration through targeting HMGB1 involving a PI3K/Akt signal pathway

2020 ◽  
Author(s):  
Hongfei Jiang ◽  
Ren Gong ◽  
Yanqing Wu
Keyword(s):  
Cell Viability ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Signal Pathway ◽  
Luciferase Assay ◽  
Transwell Assay ◽  
A7r5 Cells ◽  
And Migration ◽  
Proliferation And Migration

Abstract Background Currently, gene therapy for cardiovascular diseases has been widely concerned, but its mechanism is still unclear. Objective Recently miRNAs have been recognized as a key regulator in vascular smooth muscle cells (VSMCs) which involved in the formation of atherosclerosis. The aim of the study was to explore the role of miR-129-5p in regulation of HMGB1 involving a PI3K/Akt signal pathway as well as the proliferation and migration in A7r5 cells induced by ox-LDL. Methods Cell viability, proliferation and migration were conducted by CCK-8, colony formation, wound healing assay and transwell assay. The expressions of miR-129-5p and HMGB1 were detected by real-time quantitative-qPCR (RT-qPCR) and western blot. Luciferase assay was used to confirm that miR-129-5p directly targeted HMGB1. Results The expression of miR-129-5p in A7r5 cells induced by ox-LDL was significantly decreased in comparison with the control cells. Cell viability, proliferation and migration of A7r5 cells induced by ox-LDL were increased. MiR-129-5p could down-regulate the expression of HMGB1 in A7r5 cells. More studies showed that miR-129-5p could inhibit cell viability, proliferation on and migration of A7r5 cells induced by ox-LDL and target HMGB1 to regulate PI3K/Akt signal pathway. Conclusion miR-129-5p could inhibit PI3K/Akt signal pathway by target HMGB1 and further restrain the cell viability, proliferation and migration of A7r5 cells induced by ox-LDL.

scholarly journals Rab1A promotes cell proliferation and migration by upregulating Gli1 in colorectal cancer

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Chaozhong Peng ◽  
Xiao Li ◽  
Zhixue Ye ◽  
Wenqing Wu
Keyword(s):  
Colorectal Cancer ◽  
Cell Proliferation ◽  
Molecular Mechanisms ◽  
Node Metastasis ◽  
Cell Proliferation And Migration ◽  
Promising Therapeutic Target ◽  
Promotive Effect ◽  
Guanosine Triphosphatase ◽  
And Migration ◽  
Proliferation And Migration

AbstractRab1A, as a highly conserved small guanosine triphosphatase (GTPase), plays contentious roles in different types of cancers. The role of Rab1A in colorectal cancer (CRC) has been described in previous studies, but the molecular mechanisms of Rab1A in CRC remain far from being addressed. In the present study, we found that Rab1A expression was significantly upregulated in CRC tissues and increased Rab1A expression correlated with tumor size, lymph node metastasis (LNM) and tumor-node-metastasis (TNM) stage of CRC patients. We also found that Rab1A exerts its promotive effect on CRC cell proliferation, migration and EMT progress. Further mechanistic experiments showed that glioma-associated oncogene-1 (Gli1), as a key transcriptional factor of the Hedgehog pathway, was implicated in Rab1A-mediated regulation of CRC cell proliferation and migration. In addition, Rab1A upregulated Gli1 expression through Smoothened homolog (SMO)-independent pathway. Finally, Rab1A activated mechanistic target of rapamycin (mTOR) signaling in CRC cells. Collectively, our results define Rab1A as a novel regulator of Gli1 to promote CRC cell proliferation and migration, and suggest that the Rab1A/mTOR/Gli1 axis may serve as a promising therapeutic target for the treatment of CRC.

scholarly journals NPC2 as a Prognostic Biomarker for Glioblastoma Based on Integrated Bioinformatics Analysis and Cytological Experiments

2021 ◽  
Vol 12 ◽  
Author(s):  
De Wei ◽  
Shanghang Shen ◽  
Kun Lin ◽  
Feng Lu ◽  
Pengfeng Zheng ◽  
...  
Keyword(s):  
Bioinformatics Analysis ◽  
Prognostic Biomarker ◽  
Prognostic Significance ◽  
Lipoprotein Metabolism ◽  
Innate Immune ◽  
Transwell Assay ◽  
Cell Proliferation And Migration ◽  
Tumor Purity ◽  
And Migration ◽  
Proliferation And Migration

Glioblastoma (GBM) is one of the most common and fatal malignancies worldwide, while its prognostic biomarkers are still being explored. This study aims to identify potential genes with clinical and prognostic significance by integrating bioinformatics analysis and investigating their function in HNSCC. Based on the Single-cell RNA sequencing (scRNA-seq) results of H3K27M-glioma cells, computational bioinformatics methods were employed for selecting prognostic biomarker for GBM. The protein NPC2 (NPC Intracellular Cholesterol Transporter 2), which has been shown to be related to lipoprotein metabolism and innate immune system, was identified to be upregulated in GBM. NPC2 showed a relatively higher expression in GBM samples, and a negative correlation with tumor purity and tumor infiltrating immune cells. Additionally, NPC2 was knocked down in U87-MG and U251 cells line, and cell proliferation and migration capability were evaluated with CCK-8, scratch and transwell assay, respectively. Cytological experiments has shown that NPC2 overexpression inhibited GBM cells proliferation and migration, indicating its important role in GBM progression. This is the first investigation into the prognostic value of NPC2 interact with GBM. The potential molecular factor NPC2 have been identified as a prognostic biomarker for GBM.

Sign in / Sign up

Export Citation Format

Share Document