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Titolo:
Hyperglycemia-induced apoptotic cell death in the mouse blastocyst is dependent on expression of p53
Autore:
Keim, AL; Chi, MMY; Moley, KH;
Indirizzi:
Washington Univ, Sch Med, Dept Obstet & Gynecol, St Louis, MO 63110 USA Washington Univ St Louis MO USA 63110 t & Gynecol, St Louis, MO 63110 USA Washington Univ, Sch Med, Dept Cell Biol & Physiol, St Louis, MO 63110 USAWashington Univ St Louis MO USA 63110 l & Physiol, St Louis, MO 63110 USA
Titolo Testata:
MOLECULAR REPRODUCTION AND DEVELOPMENT
fascicolo: 2, volume: 60, anno: 2001,
pagine: 214 - 224
SICI:
1040-452X(200110)60:2<214:HACDIT>2.0.ZU;2-P
Fonte:
ISI
Lingua:
ENG
Soggetto:
PREIMPLANTATION EMBRYO DEVELOPMENT; HYPOXIA-INDUCED APOPTOSIS; NERVE GROWTH-FACTOR; SYMPATHETIC NEURONS; GLUCOSE DEPRIVATION; DIABETIC PREGNANCY; CARDIAC MYOCYTES; FAMILY MEMBER; PATHWAY; BAX;
Keywords:
programmed cell death; diabetes mellitus; preimplantation embryo; p53;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
40
Recensione:
Indirizzi per estratti:
Indirizzo: Moley, KH Washington Univ, Sch Med, Dept Obstet & Gynecol, 4911 Barnes Jewish Hosp Plaza,2nd Floor Matern Ho, St Louis, MO 63110 USA Washington Univ 4911 Barnes Jewish Hosp Plaza,2nd Floor Matern Ho St Louis MO USA 63110
Citazione:
A.L. Keim et al., "Hyperglycemia-induced apoptotic cell death in the mouse blastocyst is dependent on expression of p53", MOL REPROD, 60(2), 2001, pp. 214-224

Abstract

Murine preimplantation embryos exposed to hyperglycemia experience decreased glucose transport, and overexpression of the proapoptotic protein BAX, leading to increased apoptosis. These changes may account for the increased rates of miscarriages and malformations seen in women with diabetes mellitus. To test whether p53 expression is necessary for hyperglycemia-induced apoptosis, P53+/+, +/-, -/- embryos were obtained by superovulation. Two-cellembryos were cultured to a blastocyst stage in 52 mM D- or L-glucose. Apoptosis was detected using terminal dUTP nick end labeling (TUNEL) assays. Invivo studies were performed in the same manner using blastocysts recoveredfrom streptozotocin-induced diabetic mothers. Both in vitro and in vivo studies showed that wildtype embryos had a significantly higher percentage ofTUNEL-positive nuclei than p53+/- and -/- embryos. To test whether p53 is upstream of BAX, immunofluorescent confocal microscopy and immunoprecipitation/ immunoblotting were performed on blastocysts cultured in high vs. control glucose conditions. Blastocysts from P53+/+ mice exhibited increased BAX staining vs. p53+/- and -/- embryos. Next, to determine whether a decrease in glucose transport was upstream or downstream of p53, deoxyglucose transport was measured in individual blastocysts from p53+/+ and +/- diabetic vs. nondiabetic mice. Embryos from diabetic p53+/- mice exhibit a 44% decrease in glucose transport, similar to the 38% decrease seen in embryos from diabetic p53+/+ mice. Taken together, these results strongly indicate that p53 plays a role in hyperglycemia-incluced apoptosis, upstream of BAX overexpression and downstream of the decrease in glucose transport experienced bythe mouse preimplantation embryo. Mol. Reprod. Dev. 60: 214-224, 2001. (C)2001 Wiley-Liss, Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 28/03/20 alle ore 23:08:51