Expression of metabotropic glutamate receptor 4 in cardiomyocytes differentiated from mouse embryonic stem cells in vitro / 浙江大学学报·医学版
Journal of Zhejiang University. Medical sciences
;
(6): 366-372, 2012.
Artigo
em Chinês
| WPRIM
| ID: wpr-336782
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the expression of metabotropic glutamate receptor 4 (mGluR4) in cardiomyocytes differentiated from mouse embryonic stem cells (ES cells).</p><p><b>METHODS</b>ES cells were differentiated into cardiomyocytes with hanging-drop cultures. Retinoic acid (RA) and dimethyl sulfoxide (DMSO) were used as positive and negative controls, respectively. The co-expression of cardiac sarcomeric protein (α-actinin or troponin-T) and mGluR4 were verified by immunocytochemistry and flow cytometry analysis. The mRNA and protein expressions of mGluR4 were verified by RT-PCR and Western blot analysis, respectively. Meanwhile, the expression of mGluR4 in prenatal mouse heart was also examined.</p><p><b>RESULTS</b>mGluR4 was expressed in both mouse ES cells and ES cell-derived cardiomyocytes. The level of mGluR4 protein expression decreased during the maturation of the cardiomyocytes. The co-expression rate of mGluR4 and Troponin T in the beating embryoid bodies (EBs) was only (3.00 ±1.00)%. On the other hand, mGluR4 gene and protein expressions showed remarkable down-regulation in the development of mouse fetal heart, which was not detected in mouse adult heart.</p><p><b>CONCLUSION</b>The expression of mGluR4 is down-regulated in the cardiomyocyte differentiation of ES cells. The trend of expression is consistent with that in the prenatal mouse heart development.</p>
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Fisiologia
/
RNA Mensageiro
/
Diferenciação Celular
/
Linhagem Celular
/
Receptores de Glutamato Metabotrópico
/
Biologia Celular
/
Miócitos Cardíacos
/
Células-Tronco Embrionárias
/
Genética
/
Metabolismo
Limite:
Animais
Idioma:
Chinês
Revista:
Journal of Zhejiang University. Medical sciences
Ano de publicação:
2012
Tipo de documento:
Artigo
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