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HIF-1α is required for development of the sympathetic nervous system
R. Bohuslavova, R. Cerychova, F. Papousek, V. Olejnickova, M. Bartos, A. Görlach, F. Kolar, D. Sedmera, GL. Semenza, G. Pavlinkova,
Jazyk angličtina Země Spojené státy americké
Typ dokumentu časopisecké články, práce podpořená grantem
NLK
Free Medical Journals
od 1915 do Před 6 měsíci
Freely Accessible Science Journals
od 1915 do Před 6 měsíci
PubMed Central
od 1915 do Před 6 měsíci
Europe PubMed Central
od 1915 do Před 6 měsíci
Open Access Digital Library
od 1915-01-01
Open Access Digital Library
od 1915-01-15
PubMed
31196952
DOI
10.1073/pnas.1903510116
Knihovny.cz E-zdroje
- MeSH
- anomálie koronárních cév embryologie MeSH
- chromafinní buňky MeSH
- dřeň nadledvin embryologie inervace MeSH
- faktor 1 indukovatelný hypoxií - podjednotka alfa fyziologie MeSH
- koronární cévy embryologie MeSH
- myši knockoutované MeSH
- myši transgenní MeSH
- myši MeSH
- srdce embryologie inervace MeSH
- sympatická ganglia embryologie růst a vývoj MeSH
- sympatický nervový systém enzymologie růst a vývoj MeSH
- zvířata MeSH
- Check Tag
- mužské pohlaví MeSH
- myši MeSH
- ženské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
The molecular mechanisms regulating sympathetic innervation of the heart during embryogenesis and its importance for cardiac development and function remain to be fully elucidated. We generated mice in which conditional knockout (CKO) of the Hif1a gene encoding the transcription factor hypoxia-inducible factor 1α (HIF-1α) is mediated by an Islet1-Cre transgene expressed in the cardiac outflow tract, right ventricle and atrium, pharyngeal mesoderm, peripheral neurons, and hindlimbs. These Hif1aCKO mice demonstrate significantly decreased perinatal survival and impaired left ventricular function. The absence of HIF-1α impaired the survival and proliferation of preganglionic and postganglionic neurons of the sympathetic system, respectively. These defects resulted in hypoplasia of the sympathetic ganglion chain and decreased sympathetic innervation of the Hif1aCKO heart, which was associated with decreased cardiac contractility. The number of chromaffin cells in the adrenal medulla was also decreased, indicating a broad dependence on HIF-1α for development of the sympathetic nervous system.
Institute for Cell Engineering Johns Hopkins University School of Medicine Baltimore MD 21205
Institute of Physiology Czech Academy of Sciences 142 00 Prague Czechia
Citace poskytuje Crossref.org
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- $a The molecular mechanisms regulating sympathetic innervation of the heart during embryogenesis and its importance for cardiac development and function remain to be fully elucidated. We generated mice in which conditional knockout (CKO) of the Hif1a gene encoding the transcription factor hypoxia-inducible factor 1α (HIF-1α) is mediated by an Islet1-Cre transgene expressed in the cardiac outflow tract, right ventricle and atrium, pharyngeal mesoderm, peripheral neurons, and hindlimbs. These Hif1aCKO mice demonstrate significantly decreased perinatal survival and impaired left ventricular function. The absence of HIF-1α impaired the survival and proliferation of preganglionic and postganglionic neurons of the sympathetic system, respectively. These defects resulted in hypoplasia of the sympathetic ganglion chain and decreased sympathetic innervation of the Hif1aCKO heart, which was associated with decreased cardiac contractility. The number of chromaffin cells in the adrenal medulla was also decreased, indicating a broad dependence on HIF-1α for development of the sympathetic nervous system.
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