| Apoptosis in the developing mouse heart. | |
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MedLine Citation:
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PMID: 16881058 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Apoptosis occurs at high frequency in the myocardium of the developing avian cardiac outflow tract (OFT). Up- or down-regulating apoptosis results in defects resembling human conotruncal heart anomalies. This finding suggested that regulated levels of apoptosis are critical for normal morphogenesis of the four-chambered heart. Recent evidence supports an important role for hypoxia of the OFT myocardium in regulating cell death and vasculogenesis. The purpose of this study was to determine whether apoptosis in the outflow tract myocardium occurs in the mouse heart during developmental stages comparable to the avian heart and to determine whether differential hypoxia is also present at this site in the murine heart. Apoptosis was detected using a fluorescent vital dye, Lysotracker Red (LTR), in the OFT myocardium of the mouse starting at embryonic day (E) 12.5, peaking at E13.5-14.5, and declining thereafter to low or background levels by E18.5. In addition, high levels of apoptosis were detected in other cardiac regions, including the apices of the ventricles and along the interventricular sulcus. Apoptosis in the myocardium was detected by double-labeling with LTR and cardiomyocyte markers. Terminal deoxynucleotidyl transferase-mediated deoxyuridinetriphosphate nick end-labeling (TUNEL) and immunostaining for cleaved Caspase-3 were used to confirm the LTR results. At the peak of OFT apoptosis in the mouse, the OFT myocardium was relatively hypoxic, as indicated by specific and intense EF5 staining and HIF1alpha nuclear localization, and was surrounded by the developing vasculature as in the chicken embryo. These findings suggest that cardiomyocyte apoptosis is an evolutionarily conserved mechanism for normal morphogenesis of the outflow tract myocardium in avian and mammalian species. |
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Authors:
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Laura Barbosky; David K Lawrence; Ganga Karunamuni; Jamie C Wikenheiser; Yong-Qiu Doughman; Richard P Visconti; John B E Burch; Michiko Watanabe |
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Publication Detail:
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Type: Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S. |
Journal Detail:
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Title: Developmental dynamics : an official publication of the American Association of Anatomists Volume: 235 ISSN: 1058-8388 ISO Abbreviation: Dev. Dyn. Publication Date: 2006 Sep |
Date Detail:
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Created Date: 2006-08-30 Completed Date: 2006-11-13 Revised Date: 2007-11-14 |
Medline Journal Info:
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Nlm Unique ID: 9201927 Medline TA: Dev Dyn Country: United States |
Other Details:
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Languages: eng Pagination: 2592-602 Citation Subset: IM |
Copyright Information:
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Copyright 2006 Wiley-Liss, Inc. |
Affiliation:
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Department of Pediatrics, Rainbow Babies and Children's Hospital, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106-6011, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Anoxia / metabolism Apoptosis* Caspase 3 Caspases / metabolism Chick Embryo Female Fetal Heart / cytology*, metabolism Gestational Age Heart / embryology Humans In Situ Nick-End Labeling Male Mice Mice, Inbred C57BL Mice, Transgenic Pregnancy Species Specificity Staining and Labeling |
| Grant Support | |
ID/Acronym/Agency:
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HL-075436/HL/NHLBI NIH HHS; HL-65314/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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EC 3.4.22.-/CASP3 protein, human; EC 3.4.22.-/Casp3 protein, mouse; EC 3.4.22.-/Caspase 3; EC 3.4.22.-/Caspases |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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