14-3-3epsilon controls multiple developmental processes in the mouse heart
| العنوان: | 14-3-3epsilon controls multiple developmental processes in the mouse heart |
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| المؤلفون: | Gittenberger-de Groot, A.C., Hoppenbrouwers, T., Miquerol, L., Kosaka, Y., Poelmann, R.E., Wisse, L.J., Yost, H.J., Jongbloed, M.R.M., Deruiter, M.C., Brunelli, L. |
| المساهمون: | Institut de Biologie du Développement de Marseille (IBDM), Aix Marseille Université (AMU)-Collège de France (CdF (institution))-Centre National de la Recherche Scientifique (CNRS) |
| المصدر: | Developmental Dynamics Developmental Dynamics, 2016, 245 (11), pp.1107-1123. ⟨10.1002/dvdy.24440.Epub2016Sep18⟩ Developmental Dynamics, Wiley, 2016, 245 (11), pp.1107-1123. ⟨10.1002/dvdy.24440.Epub2016Sep18⟩ Developmental Dynamics, 245(11), 1107-1123 |
| بيانات النشر: | HAL CCSD, 2016. |
| سنة النشر: | 2016 |
| مصطلحات موضوعية: | ventricular septal defect, coronary artery hypoplasia, endocardial cushion, cardiovascular system, cardiovascular diseases, heart development, [SDV.BC]Life Sciences [q-bio]/Cellular Biology, myocardial hypoplasia, 14-3-3, mouse, cardiac outflow tract |
| الوصف: | International audience; BACKGROUND:14-3-3ε plays an important role in the maturation of the compact ventricular myocardium by modulating the cardiomyocyte cell cycle via p27kip1 . However, additional cardiac defects are possible given the ubiquitous expression pattern of this protein.RESULTS:Germ line deletion of 14-3-3ε led to malalignment of both the outflow tract (OFT) and atrioventricular (AV) cushions, with resulting tricuspid stenosis and atresia, mitral valve abnormalities, and perimembranous ventricular septal defects (VSDs). We confirmed myocardial non-compaction and detected a spongy septum with muscular VSDs and blebbing of the epicardium. These defects were associated with abnormal patterning of p27kip1 expression in the subendocardial and possibly the epicardial cell populations. In addition to abnormal pharyngeal arch artery patterning, we found deep endocardial recesses and paucity of intramyocardial coronary vasculature as a result of defective coronary plexus remodeling.CONCLUSIONS:The malalignment of both endocardial cushions provides a new explanation for tricuspid and mitral valve defects, while myocardial non-compaction provides the basis for the abnormal coronary vasculature patterning. These abnormalities might arise from p27kip1 dysregulation and a resulting defect in epithelial-to-mesenchymal transformation. These data suggest that 14-3-3ε, in addition to left ventricular non-compaction (LVNC), might be linked to different forms of congenital heart disease (CHD). Developmental Dynamics 245:1107-1123, 2016. © 2016 Wiley Periodicals, Inc. |
| اللغة: | English |
| تدمد: | 1058-8388 1097-0177 |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=dedup_wf_001::7d4f7b49d182620369a66d381e9e2c05Test https://hal.science/hal-01444427Test |
| حقوق: | CLOSED |
| رقم الانضمام: | edsair.dedup.wf.001..7d4f7b49d182620369a66d381e9e2c05 |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 10588388 10970177 |
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