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Retinoic acid influences the embryoid body formation in mouse embryonic stem cells by induction of caspase and p38 MAPK/JNK-mediated apoptosis.
Huang, Fu-Jen; Lan, Kuo-Chung; Kang, Hong-Yo; Lin, Pin-Yao; Chan, Wen-Hsiung; Hsu, Yu-Cheng; Liu, Yen-Chih; Huang, Ko-En.
Afiliación
  • Huang FJ; Department of Obstetrics and Gynecology, Kaohsiung Chang Gung Memorial Hospital, Taiwan. huangfj@seed.net.tw
Environ Toxicol ; 28(4): 190-200, 2013 Apr.
Article en En | MEDLINE | ID: mdl-21626648
Although all-trans retinoic acid (RA), the oxidative metabolite of vitamin A, is essential for normal development, high levels are teratogenic in many species. RA results in immediate effects on the preimplantation embryo and on blastocyst development in vitro and in vivo. To further elucidate the cellular mechanisms of early postimplantation embryo development induced by RA, we present an embryonic cell line, B5, as a candidate system for the investigation of these processes. We used undifferentiated ES cells as the model, which is from the undifferentiated status to differentiated status [embryoid body (EB) formation] mimicking postimplantation embryo development (egg-cylinder stage of embryo formation) to clarify the cellular mechanism of action of RA in the implanted blastocysts and cell apoptosis following the series of exposures to differing RA concentrations. Using an in vitro model, we identified the impact of RA on undifferentiated embryonic stem (ES) cells, including inhibition of cell proliferation and induction of cell apoptosis. JNK, P-38 and caspase activation were shown in the nature of RA-triggered apoptotic signaling in ES cells. The carry-on influences of RA on the ES cell were shown in the formation of EB from the pretreated ES cells. RA resulted in apparent impact on undifferentiated ES cells in vitro, with increased numbers of apoptotic cells initially and inhibited cell proliferation, which led to decreased size of EB. The process of EB formation (mimicking the early postimplantation embryo development) is regulated by RA-induced apoptosis through the activation of caspase and P38 MAPK/JNK pathway.
Asunto(s)

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Tretinoina / Apoptosis / Caspasas / Sistema de Señalización de MAP Quinasas / Proteínas Quinasas p38 Activadas por Mitógenos / Células Madre Embrionarias / Cuerpos Embrioides Límite: Animals / Pregnancy Idioma: En Revista: Environ Toxicol Asunto de la revista: SAUDE AMBIENTAL / TOXICOLOGIA Año: 2013 Tipo del documento: Article País de afiliación: Taiwán Pais de publicación: Estados Unidos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Tretinoina / Apoptosis / Caspasas / Sistema de Señalización de MAP Quinasas / Proteínas Quinasas p38 Activadas por Mitógenos / Células Madre Embrionarias / Cuerpos Embrioides Límite: Animals / Pregnancy Idioma: En Revista: Environ Toxicol Asunto de la revista: SAUDE AMBIENTAL / TOXICOLOGIA Año: 2013 Tipo del documento: Article País de afiliación: Taiwán Pais de publicación: Estados Unidos