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1.
Cell Tissue Res ; 394(3): 471-485, 2023 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-37851113

RESUMO

The aggravating role of long noncoding RNA (lncRNA) HOTAIR has been indicated in liver injury caused by hepatic ischemia/reperfusion. However, under the condition of alcoholic hepatitis (AH), its effects remain unclear. The present study aimed to examine the effect of lncRNA HOTAIR on hepatic stellate cell viability and apoptosis during liver injury caused by AH. In the liver tissues of AH rats, HOTAIR and S1PR1 were overexpressed, and microRNA (miR)-148a-3p was poorly expressed. Loss-of-function assays revealed that silencing of HOTAIR alleviated liver injury in AH by inhibiting the activated phenotype of hepatic stellate cells, inflammation, and fibrosis. Using the bioinformatics databases, dual-luciferase, RIP, and FISH assays, we observed that HOTAIR was mainly localized in the cytoplasm of hepatic stellate cells, and HOTAIR could bind specifically to miR-148a-3p. In addition, miR-148a-3p could target S1PR1 expression. Rescue experiments showed that silencing of miR-148a-3p or overexpression of S1PR1 reversed the alleviating effects of HOTAIR silencing on liver injury. Taken together, our findings revealed that HOTAIR regulates hepatic stellate cell proliferation via the miR-148a-3p/S1PR1 axis in liver injury, which may serve as the basis for developing novel therapeutic strategies to treat AH.


Assuntos
Hepatite Alcoólica , MicroRNAs , RNA Longo não Codificante , Ratos , Animais , MicroRNAs/genética , MicroRNAs/metabolismo , RNA Longo não Codificante/genética , RNA Longo não Codificante/metabolismo , Hepatite Alcoólica/genética , Receptores de Esfingosina-1-Fosfato , Proliferação de Células/genética
2.
Sci Total Environ ; 806(Pt 2): 150562, 2022 Feb 01.
Artigo em Inglês | MEDLINE | ID: mdl-34852432

RESUMO

The aim of this review is to identify the worldwide trend of waterborne protozoan outbreaks and how it varies between geographic regions during the period from 2017 to 2020. Data about waterborne protozoan outbreaks were gathered and stratified by continent, country, water source, and protozoan species associated with the outbreak. The highest prevalence of waterborne protozoan outbreaks was reported in developed countries. Out of 251 outbreaks reported worldwide during the studied period, 141, 51 and 24 outbreaks were recorded in the USA, UK, and New Zealand, respectively. These outbreaks were mainly associated with Cryptosporidium (192 outbreaks) and Giardia (48 outbreaks). Cyclospora cayetanensis, Dientamoebafragilis and Toxoplasma gondii were associated with 7 outbreaks. One outbreak was associated with each of Blastocystis hominis, Entamoeba histolytica, Microsporidia or Naegleria fowleri. This data suggests large discrepancies in the number of outbreaks reported between geographic regions, with most outbreaks recorded in developed countries. Differences in the prevalence of outbreaks between countries are likely attributed to the availability of diagnostic capabilities and surveillance programs to monitor water contamination with pathogenic protozoa. More attention and concerted efforts are required to improve water safety and to alleviate the impact of waterborne protozoan infections. Appropriate surveillance of water contamination with protozoa can enable public health officials to identify source of contamination and implement the necessary measures to limit transmission and prevent outbreaks.


Assuntos
Criptosporidiose , Cryptosporidium , Giardíase , Criptosporidiose/epidemiologia , Surtos de Doenças , Giardíase/epidemiologia , Humanos , Prevalência
3.
J Biochem ; 170(5): 663-673, 2021 Dec 28.
Artigo em Inglês | MEDLINE | ID: mdl-34347084

RESUMO

ETS variant 4 (ETV4) has been implicated in the development of various cancers. However, the molecular events mediated by ETV4 in liver cancer are poorly understood, especially in hepatitis B virus (HBV)-associated liver hepatocellular carcinoma (LIHC). Here, we aimed to identify the target involved in ETV4-driven hepatocarcinogenesis. Bioinformatics analysis revealed that ETV4 was highly expressed in patients with HBV-associated LIHC, and HBV infection promoted the expression of ETV4 in LIHC cells. Inhibition of ETV4 repressed the proliferation, migration, invasion of LIHC cells and suppressed the secretion of HBV and the replication of HBV DNA. ANXA2 expression in LIHC patients was positively correlated with ETV4 expression. Chromatin immunoprecipitation and dual-luciferase reporter assays revealed that ETV4 elevated the ANXA2 expression at the transcriptional level by binding to the ANXA2 promoter. Overexpression of ANXA2 reversed the inhibitory effect of sh-ETV4 on the malignant biological behaviours of HBV-infected LIHC cells by activating the Wnt/ß-catenin pathway. In conclusion, ETV4 mediates the activation of Wnt/ß-catenin pathway through transcriptional activation of ANXA2 expression to promote HBV-associated LIHC progression.


Assuntos
Anexina A2/genética , Carcinoma Hepatocelular/metabolismo , Vírus da Hepatite B/metabolismo , Hepatite B Crônica/metabolismo , Neoplasias Hepáticas/metabolismo , Proteínas Proto-Oncogênicas c-ets/metabolismo , Via de Sinalização Wnt , Anexina A2/metabolismo , Carcinoma Hepatocelular/genética , Carcinoma Hepatocelular/patologia , Carcinoma Hepatocelular/virologia , Linhagem Celular , Movimento Celular , Biologia Computacional/métodos , Bases de Dados Genéticas , Progressão da Doença , Feminino , Vírus da Hepatite B/isolamento & purificação , Hepatite B Crônica/patologia , Hepatite B Crônica/virologia , Humanos , Neoplasias Hepáticas/genética , Neoplasias Hepáticas/patologia , Neoplasias Hepáticas/virologia , Masculino , Pessoa de Meia-Idade , Proteínas Proto-Oncogênicas c-ets/genética , Via de Sinalização Wnt/fisiologia , beta Catenina/genética , beta Catenina/metabolismo
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