Data/hora: 16/05/2024 18:00:46

Provedor de dados: 	42	
País: 	Brazil	
Título: 	6-Bromoindirubin-3’-oxime promotes osteogenic differentiation of canine BMSCs through inhibition of GSK3β activity and activation of the Wnt/β-catenin signaling pathway	
Autores: 	ZHAO,XIAO-E; YANG,ZHENSHAN; GAO,ZHEN; GE,JUNBANG; WEI,QIANG; MA,BAOHUA.	
Data: 	2019-01-01	
Ano: 	2019	
Palavras-chave: 	Bone mesenchymal stem cells; Bromoindirubin oxime; Osteogenetic differentiation; Canine.	
Resumo: 	﻿﻿This﻿﻿ study aimed to investigate how 6-bromoindirubin-3’-oxime (BIO) increases the osteogenic differentiation of canine bone mesenchymal stem cells (BMSCs) and the role of the Wnt/β-catenin signaling pathway in this process. We mimicked the effect of Wnt by adding BIO to the culture medium of BMSCs and examined whether canonical Wnt signaling positively affects the differentiation of these cells into osteoblasts. Canine BMSCs were cultured with 0.5 and 1.0 μM BIO under osteogenic conditions and then differentiation markers were investigated. It was found that BIO significantly increased the activity of alkaline phosphatase (ALP), the number of ALP-positive cells, the mineralization level and calcium deposits. Moreover, cells cultured with 0.5 and 1.0 μM BIO exhibited detectable β-catenin expression in their nuclei, and showed upregulated β-catenin and glycogen synthase kinase 3 beta(GSK3β) phosphorylation compared to untreated cells. In addition, BIO enhanced the mRNA expression of osteoblast differentiation markers such as ALP, runt-related transcription factor 2, collagen I, osteocalcin, and osteonectin. In conclusion, BIO upregulated GSK3β phosphorylation and inhibited its activity, thereby activating the Wnt/β-catenin signaling pathway and promoting the osteogenic differentiation of canine BMSCs. The effect of 1.0 μM BIO on BMSCs differentiation was stronger than that of 0.5 μM BIO.	
Tipo: 	Info:eu-repo/semantics/article	
Idioma: 	Inglês	
Identificador: 	http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0001-37652019000100610	
Editor: 	Academia Brasileira de Ciências	
Relação: 	10.1590/0001-3765201920180459	
Formato: 	text/html	
Fonte: 	Anais da Academia Brasileira de Ciências  v.91 n.1 2019	
Fonte: 	info:eu-repo/semantics/openAccess