Detailed Information on Publication Record
2017
Neural Differentiation Is Inhibited through HIF1 alpha/ beta-Catenin Signaling in Embryoid Bodies
VEČEŘA, Josef, Jana KUDOVÁ, Jan KUČERA, Lukáš KUBALA, Jiří PACHERNÍK et. al.Basic information
Original name
Neural Differentiation Is Inhibited through HIF1 alpha/ beta-Catenin Signaling in Embryoid Bodies
Authors
VEČEŘA, Josef (203 Czech Republic, guarantor, belonging to the institution), Jana KUDOVÁ (203 Czech Republic), Jan KUČERA (203 Czech Republic, belonging to the institution), Lukáš KUBALA (203 Czech Republic, belonging to the institution) and Jiří PACHERNÍK (203 Czech Republic, belonging to the institution)
Edition
Stem Cells International, London, HINDAWI LTD, 2017, 1687-966X
Other information
Language
English
Type of outcome
Článek v odborném periodiku
Field of Study
10605 Developmental biology
Country of publisher
United Kingdom of Great Britain and Northern Ireland
Confidentiality degree
není předmětem státního či obchodního tajemství
References:
Impact factor
Impact factor: 3.989
RIV identification code
RIV/00216224:14310/17:00095557
Organization unit
Faculty of Science
UT WoS
000419057500001
Keywords in English
STEM-CELL FATE; HYPOXIA; OXYGEN; HIF; CATENIN
Změněno: 9/4/2018 15:50, Ing. Nicole Zrilić
Abstract
V originále
Extensive research in the field of stem cells and developmental biology has revealed evidence of the role of hypoxia as an important factor regulating self-renewal and differentiation. However, comprehensive information about the exact hypoxia-mediated regulatory mechanism of stem cell fate during early embryonic development is still missing. Using a model of embryoid bodies (EBs) derived from murine embryonic stem cells (ESC), we here tried to encrypt the role of hypoxia-inducible factor 1 alpha (HIF1 alpha) in neural fate during spontaneous differentiation. EBs derived from ESC with the ablated gene for HIF1a had abnormally increased neuronal characteristics during differentiation. An increased neural phenotype in Hif1 alpha(-/-) EBs was accompanied by the disruption of beta-catenin signaling together with the increased cytoplasmic degradation of beta-catenin. The knock-in of Hif1 alpha, as well as beta-catenin ectopic overexpression in Hif1 alpha(-/-) EBs, induced a reduction in neural markers to the levels observed in wild-type EBs. Interestingly, direct interaction between HIF1 alpha and beta-catenin was demonstrated by immunoprecipitation analysis of the nuclear fraction of wild-type EBs. Together, these results emphasize the regulatory role of HIF1 alpha in beta-catenin stabilization during spontaneous differentiation, which seems to be a crucial mechanism for the natural inhibition of premature neural differentiation.
Links
| GJ15-13443Y, research and development project |
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