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1.
Mol Med Rep ; 20(3): 2597-2608, 2019 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-31524257

RESUMO

Type 2 diabetes mellitus (T2DM) is a metabolic disorder. Numerous proteins have been identified that are associated with the occurrence and development of T2DM. This study aimed to identify potential core genes and pathways involved in T2DM, through exhaustive bioinformatic analyses using GSE20966 microarray profiles of pancreatic ß­cells obtained from healthy controls and patients with T2DM. The original microarray data were downloaded from the Gene Expression Omnibus database. Data were processed by the limma package in R software and the differentially expressed genes (DEGs) were identified. Gene Ontology functional analysis and Kyoto Encyclopedia of Genes and Genomes pathway analysis were carried out to identify potential biological functions and pathways of the DEGs. Key transcription factors were identified using the WEB­based GEne SeT AnaLysis Toolkit (WebGestalt) and Enrichr. The Search Tool for the Retrieval of Interacting Genes (STRING) database was used to establish a protein­protein interaction (PPI) network for the DEGs. In total, 329 DEGs were involved in T2DM, with 208 upregulated genes enriched in pancreatic secretion and the complement and coagulation cascades, and 121 downregulated genes enriched in insulin secretion, carbohydrate digestion and absorption, and the Toll­like receptor pathway. Furthermore, hepatocyte nuclear factor 1­alpha (HNF1A), signal transducer and activator of transcription 3 (STAT3) and glucocorticoid receptor (GR) were key transcription factors in T2DM. Twenty important nodes were detected in the PPI network. Finally, two core genes, serpin family G member 1 (SERPING1) and alanyl aminopeptidase, membrane (ANPEP), were shown to be associated with the development of T2DM. On the whole, the findings of this study enhance our understanding of the potential molecular mechanisms of T2DM and provide potential targets for further research.


Assuntos
Biologia Computacional , Diabetes Mellitus Tipo 2/genética , Diabetes Mellitus Tipo 2/metabolismo , Regulação da Expressão Gênica , Transdução de Sinais , Animais , Biomarcadores , Linhagem Celular , Biologia Computacional/métodos , Bases de Dados Genéticas , Suscetibilidade a Doenças , Ontologia Genética , Redes Reguladoras de Genes , Humanos , Camundongos
2.
Phys Rev Lett ; 119(5): 056601, 2017 Aug 04.
Artigo em Inglês | MEDLINE | ID: mdl-28949739

RESUMO

We present a study of electric, thermal and thermoelectric response in noncollinear antiferromagnet Mn_{3}Sn, which hosts a large anomalous Hall effect (AHE). Berry curvature generates off-diagonal thermal (Righi-Leduc) and thermoelectric (Nernst) signals, which are detectable at room temperature and invertible with a small magnetic field. The thermal and electrical Hall conductivities respect the Wiedemann-Franz law, implying that the transverse currents induced by the Berry curvature are carried by Fermi surface quasiparticles. In contrast to conventional ferromagnets, the anomalous Lorenz number remains close to the Sommerfeld number over the whole temperature range of study, excluding any contribution by inelastic scattering and pointing to the Berry curvature as the unique source of AHE. The anomalous off-diagonal thermo-electric and Hall conductivities are strongly temperature dependent and their ratio is close to k_{B}/e.

3.
Oncol Lett ; 14(1): 111-118, 2017 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-28693142

RESUMO

The results of our previous study revealed that microRNA (miRNA/miR)-4530 was upregulated in the serum of patients with diabetic retinopathy. The TargetScan miRNA database was used to identify potential targets of miR-4530 and vasohibin-1 (VASH1) was predicted as one of the targets. The results of our previous study demonstrated that miR-4530 was able to promote angiogenesis in human umbilical vein endothelial cells. Therefore, suppressing miR-4530 may be a potentially novel approach towards inhibiting tumor angiogenesis. The present study aimed to investigate the function of miR-4530 and determine whether miR-4530 was able to regulate angiogenesis in breast carcinoma cells by targeting VASH1. MDA-MB-231 and MCF-7 cells were transfected with miR-4530 precursor, anti-miR-4530 and empty vector plasmids. The expression levels of miRNA and mRNA were detected using the reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The expression levels of protein were detected using western blotting. Dual-luciferase reporter assays were used to identify the target of miR-4530. Furthermore, cell proliferation, cell cycle, apoptosis and tube formation assays were used to investigate the function of miR-4530 in vitro. Nude mice were used in a subcutaneous tumor model in vivo study. The results of the present study demonstrated that miR-4530 significantly suppressed proliferation and promoted apoptosis of breast carcinoma cells. In addition, miR-4530 expression promoted angiogenesis in vitro. Results from the western blotting and RT-qPCR revealed that VASH1 was significantly downregulated by miR-4530 in breast carcinoma cells. The results of the present study suggest that miR-4530 promotes angiogenesis, inhibits proliferation and induces apoptosis in breast carcinoma cells by suppressing the expression of VASH1.

4.
Biosci Biotechnol Biochem ; 80(3): 461-5, 2016.
Artigo em Inglês | MEDLINE | ID: mdl-26554942

RESUMO

The identification of disease-specific alterations in miRNA expression and the ability to detect miRNAs in serum furnish the basis for identified potential research value. This study was aimed to characterize the expression of miRNAs in the serum samples from people with type 2 diabetes mellitus (T2DM) and healthy individuals in order to detect the differential expression of miRNAs in T2DM. In total, 582 participants were recruited. Microarray-based miRNA expression profiles were screened in pooled serum samples from two groups (T2DM and healthy control). The candidates' miRNAs were validated by reverse transcription quantitative real-time polymerase chain reaction (RT-qPCR). Five significantly different serum miRNAs were identified in T2DM patients (hsa-miR-320d, hsa-miR-4534, hsa-miR-3960, hsa-miR-451a, and hsa-miR-572) compared to those in the serum of healthy controls. This study provided evidence that serum miRNAs had differential expressions between healthy controls and T2DM patients. These five differential expression miRNAs might be of help for subsequent study in T2DM.


Assuntos
Diabetes Mellitus Tipo 2/genética , MicroRNAs/sangue , Diabetes Mellitus Tipo 2/sangue , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Análise de Sequência com Séries de Oligonucleotídeos , Reação em Cadeia da Polimerase em Tempo Real , Reação em Cadeia da Polimerase Via Transcriptase Reversa
5.
J Pharmacol Sci ; 124(4): 445-56, 2014.
Artigo em Inglês | MEDLINE | ID: mdl-24671054

RESUMO

Aristolochic acid (AA) is known as a potent mutagen that induces significant cytotoxic and mutagenic effects on renal tubular epithelial cells. Clinically, the persistent injury of AA results in the infiltration of inflammatory cells, epithelial-to-mesenchymal transition (EMT), and renal tubulointerstitial fibrosis. There are no truly effective pharmaceuticals. In this study, we investigated the potential role of the extract of Sedum sarmentosum Bunge (SSB), a traditional Chinese herbal medicine, on rat tubuloepithelial (NRK-52E) cells after AA injury in vitro. Evidence revealed that AA induced mitochondrial-pathway-mediated cellular apoptosis, accompanied by cell proliferation in a feedback mechanism. Treatment with SSB also induced cells to enter early apoptosis, but inhibited cell proliferation. In cultured NRK-52E cells, AA induced the imbalance of MMP-2/TIMP-2 and promoted EMT and ECM accumulation. SSB treatment significantly alleviated AA-induced NRK-52E cells fibrosis-like appearance, inhibited the induction of EMT, and deposition of ECM. SSB also decreased the activity of the NF-κB signaling pathway, resulting in down-regulated expression of NF-κB-controlled chemokines and pro-inflammatory cytokines, including MCP-1, MIF, and M-CSF, which may regulate the macrophage-mediated inflammatory reaction during renal fibrosis in vivo. Therefore, these findings suggest that SSB exerts protective effects against AA-induced tubular epithelial cells injury through suppressing the synthesis of inflammatory factors, EMT, and ECM production.


Assuntos
Ácidos Aristolóquicos/toxicidade , Medicamentos de Ervas Chinesas/farmacologia , Células Epiteliais/efeitos dos fármacos , Túbulos Renais/citologia , Mutagênicos/toxicidade , Extratos Vegetais/farmacologia , Sedum , Animais , Apoptose/efeitos dos fármacos , Proliferação de Células/efeitos dos fármacos , Células Cultivadas , Células Epiteliais/metabolismo , Células Epiteliais/patologia , Transição Epitelial-Mesenquimal , Matriz Extracelular/metabolismo , Fibrose , Inflamação , Metaloproteinase 2 da Matriz/metabolismo , Ratos , Inibidor Tecidual de Metaloproteinase-2/metabolismo
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