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1.
Eur Rev Med Pharmacol Sci ; 17(23): 3169-77, 2013 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-24338458

RESUMO

BACKGROUND AND AIM: To investigate the effects of systemic inflammatory response syndrome (SIRS) and multiple organ dysfunction syndromes (MODS) on human peripheral blood endothelial progenitor cells. PATIENTS AND METHODS: Twenty patients admitted to Changhai Hospital, Second Military Medical University, from February, 2011 to November, 2011 were recruited consecutively. The serum samples were collected from the twenty patients who were divided into four groups as following: normal group, post-traumatic group without SIRS, post-traumatic group with SIRS, and post-traumatic group with MODS. Endothelial progenitor cells (EPCs) were isolated from peripheral blood of healthy subjects by using density gradient centrifugation and the effect of the serum on EPCs was detected after stimulating by the serum samples for 0, 6, 12, 24, and 36 h. RESULTS: Compared with the normal group, the proliferation of EPCs was significantly increased in a time-independent manner in the other three groups, especially in the SIRS serum treated group. The expression of pro-inflammation cytokines was increased in the other three groups compared with the normal group, but the expression of IL-10 in the normal group was higher than the other groups. CONCLUSIONS: Oxidative stress balance was also broken as the disease progressed. Serum from patients with sepsis could influence proliferation and the inflammation and oxidative stress states of EPCs.


Assuntos
Células Endoteliais/metabolismo , Insuficiência de Múltiplos Órgãos/sangue , Células-Tronco/metabolismo , Síndrome de Resposta Inflamatória Sistêmica/sangue , Movimento Celular , Proliferação de Células , Forma Celular , Células Cultivadas , Microambiente Celular , China , Citocinas/metabolismo , Células Endoteliais/patologia , Heme Oxigenase-1/genética , Heme Oxigenase-1/metabolismo , Humanos , Mediadores da Inflamação/metabolismo , NADPH Oxidases/genética , NADPH Oxidases/metabolismo , Neovascularização Fisiológica , Estresse Oxidativo , RNA Mensageiro/metabolismo , Células-Tronco/patologia , Fatores de Tempo
2.
Eur Rev Med Pharmacol Sci ; 24(17): 8812-8821, 2020 09.
Artigo em Inglês | MEDLINE | ID: mdl-32964969

RESUMO

OBJECTIVE: Colorectal cancer (CRC) has a very high morbidity and mortality worldwide. Related studies have shown that microRNA-543 (miR-543) is involved in the development of many cancers, including CRC. The purpose of this study was to explore the potential molecular mechanism of miR-543's involvement in the development of CRC. PATIENTS AND METHODS: QRT-PCR and Western blot were used to detect the expression of proliferation and migration-related proteins, signal transduction and transcriptional activator 3 and protein inhibitor of activated signal transducer and activators of transcription 3 (PIAS3). Cell proliferation and metastasis were measured by MTT, transwell and Western blot. The binding sites of miR-543 and PIAS3 were predicted by TargetScan database and verified by double-luciferase report experiment. RESULTS: The expression of miR-543 was high in CRC tissues and cell lines, while the mRNA and protein levels of PIAS3 were decreased. Meanwhile, a negative correlation between miR-543 and PIAS3 was also observed in CRC tissues. Moreover, the downregulation of miR-543 led to the inhibition of viability and the expression of proliferation and migration related proteins. Subsequently, miR-543 depletion also blocked cell migration and invasion. MiR-543 inhibits the expression of PISA3. Furthermore, downregulation of PIAS3 undermined the miR-543 depletion-mediated suppression effect on SW480 and LOVO cells. Notably, loss of miR-543 downregulated STAT3 activity, which was rescued by PIAS3 ablation. CONCLUSIONS: MiR-543 participated in cell proliferation and metastasis by targeting PIAS3 in CRC.


Assuntos
Neoplasias Colorretais , MicroRNAs , Chaperonas Moleculares , Proteínas Inibidoras de STAT Ativados , Linhagem Celular , Movimento Celular/genética , Proliferação de Células/genética , Neoplasias Colorretais/genética , Neoplasias Colorretais/metabolismo , Neoplasias Colorretais/patologia , Células Epiteliais/metabolismo , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Chaperonas Moleculares/genética , Chaperonas Moleculares/metabolismo , Proteínas Inibidoras de STAT Ativados/genética , Proteínas Inibidoras de STAT Ativados/metabolismo
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