| A differential autophagic response to hyperglycemia in the developing murine embryo. | |
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MedLine Citation:
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PMID: 21367963 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Autophagy is critical to the process of development because mouse models have shown that lack of autophagy leads to developmental arrest during the pre-implantation stage of embryogenesis. The process of autophagy is regulated through signaling pathways, which respond to the cellular environment. Therefore, any alteration in the environment may lead to the dysregulation of the autophagic process potentially resulting in cell death. Using both in vitro and in vivo models to study autophagy in the pre-implantation murine embryo, we observed that the cells respond to environmental stressors (i.e. hyperglycemic environment) by increasing activation of autophagy in a differential pattern within the embryo. This upregulation is accompanied by an increase in apoptosis, which appears to plateau at high concentrations of glucose. The activation of the autophagic pathway was further confirmed by an increase in GAPDH activity in both in vivo and in vitro hyperglycemic models, which has been linked to autophagy through the activation of the Atg12 gene. Furthermore, this increase in autophagy in response to a hyperglycemic environment was observed as early as the oocyte stage. In conclusion, in this study, we provided evidence for a differential response of elevated activation of autophagy in embryos and oocytes exposed to a hyperglycemic environment. |
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Authors:
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Katie L Adastra; Maggie M Chi; Joan K Riley; Kelle H Moley |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural Date: 2011-03-02 |
Journal Detail:
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Title: Reproduction (Cambridge, England) Volume: 141 ISSN: 1741-7899 ISO Abbreviation: Reproduction Publication Date: 2011 May |
Date Detail:
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Created Date: 2011-05-09 Completed Date: 2011-08-26 Revised Date: 2012-02-02 |
Medline Journal Info:
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Nlm Unique ID: 100966036 Medline TA: Reproduction Country: England |
Other Details:
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Languages: eng Pagination: 607-15 Citation Subset: IM |
Affiliation:
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Department of Obstetrics and Gynecology, Washington University School of Medicine, 660 South Euclid Avenue, Campus Box 8064, Saint Louis, Missouri 63110, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Autophagy* Blastocyst / metabolism*, pathology Diabetes Mellitus, Experimental / metabolism, pathology Embryo Culture Techniques Embryonic Development Female Glucose / metabolism* Glyceraldehyde-3-Phosphate Dehydrogenases / metabolism Hyperglycemia / embryology, metabolism*, pathology Mice Oocytes / metabolism, ultrastructure Signal Transduction* Stress, Physiological* Up-Regulation |
| Grant Support | |
ID/Acronym/Agency:
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P30 DK056341-11/DK/NIDDK NIH HHS; R01 HD40390/HD/NICHD NIH HHS; T32 GM07067/GM/NIGMS NIH HHS |
| Chemical | |
Reg. No./Substance:
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50-99-7/Glucose; EC 1.2.1.-/Glyceraldehyde-3-Phosphate Dehydrogenases |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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