Autophagy-related gene Beclin-1 expression in neuron-like differentiation of human bone marrow mesenchymal stem cells / 中国组织工程研究
Chinese Journal of Tissue Engineering Research
;
(53): 841-846, 2014.
Artículo
en Chino
| WPRIM
| ID: wpr-443891
ABSTRACT
BACKGROUND:
Bone marrow mesenchymal stem cells have potential to self-renewal and multi-lineage differentiation. But after a long period of culture in vitro, the proliferation and differentiation capacities of bone marrow mesenchymal stem cells gradual y loss, the mechanism underlying which is not clear now.OBJECTIVE:
To observe the expression of autophagy-related gene Beclin-1 in differentiation from human bone marrow mesenchymal stem cells into neuron-like cells in vitro.METHODS:
The changes of morphological characteristics of neuron-like cells differentiated from human bone marrow mesenchymal stem cells induced by epidermal growth factor were observed. The expression of neuron-specific enolase and glial fibril ary acidic protein in treated and untreated human bone marrow mesenchymal stem cells were detected using immunocytochemistry. The Beclin-1 protein expressions were detected by western blot before and after induction. RESULTS ANDCONCLUSION:
After being induced, human bone marrow mesenchymal stem cells presented classical neuron-like morphology;the expressions of neuron-specific enolase and glial fibril ary acidic protein were 78.7%and 8.1%, respectively. The expression of Beclin-1 protein was changed correspondingly during the induction, which increased after 30 minutes of induction and decreased gradual y after 1 hour of induction. Human bone marrow mesenchymal stem cells could be induced into neuron-like cells in vitro by epidermal growth factor. Autophagy-related gene was highly expressed in the induction of early differentiation and the expression gradual y reduced until it remained at a low level during the differentiation.
Texto completo:
Disponible
Índice:
WPRIM (Pacífico Occidental)
Idioma:
Chino
Revista:
Chinese Journal of Tissue Engineering Research
Año:
2014
Tipo del documento:
Artículo
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