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(H)IF applicable: promotion of neurogenesis by induced HIF-2 signalling after ischaemia
HIF-2 represents a tissue-specific isoform of the hypoxia-inducible factors (HIFs) which regulate oxygen homeostasis in the cell. In acute oxygen deficiency, HIF transcription factors ensure the timely restoration of adequate oxygen supply. Particularly in medical conditions such as stroke, which ha...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Springer Berlin Heidelberg
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8302505/ https://www.ncbi.nlm.nih.gov/pubmed/34251509 http://dx.doi.org/10.1007/s00424-021-02600-8 |
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author | Leu, Tristan Fandrey, Joachim Schreiber, Timm |
author_facet | Leu, Tristan Fandrey, Joachim Schreiber, Timm |
author_sort | Leu, Tristan |
collection | PubMed |
description | HIF-2 represents a tissue-specific isoform of the hypoxia-inducible factors (HIFs) which regulate oxygen homeostasis in the cell. In acute oxygen deficiency, HIF transcription factors ensure the timely restoration of adequate oxygen supply. Particularly in medical conditions such as stroke, which have a high mortality risk due to ischaemic brain damage, rapid recovery of oxygen supply is of extraordinary importance. Nevertheless, the endogenous mechanisms are often not sufficient to respond to severe hypoxic stress with restoring oxygenation and fail to protect the tissue. Herein, we analysed murine neurospheres without functioning HIF-2α and found that special importance in the differentiation of neurons can be attributed to HIF-2 in the brain. Other processes, such as cell migration and signal transduction of different signalling pathways, appear to be mediated to some extent via HIF-2 and illustrate the function of HIF-2 in brain remodelling. Without hypoxic stress, HIF-2 in the brain presumably focuses on the fine-tuning of the neural network. However, a therapeutically increase of HIF-2 has the potential to regenerate or replace destroyed brain tissue and help minimize the consequences of an ischaemic stroke. |
format | Online Article Text |
id | pubmed-8302505 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Springer Berlin Heidelberg |
record_format | MEDLINE/PubMed |
spelling | pubmed-83025052021-07-27 (H)IF applicable: promotion of neurogenesis by induced HIF-2 signalling after ischaemia Leu, Tristan Fandrey, Joachim Schreiber, Timm Pflugers Arch Molecular and Cellular Mechanisms of Disease HIF-2 represents a tissue-specific isoform of the hypoxia-inducible factors (HIFs) which regulate oxygen homeostasis in the cell. In acute oxygen deficiency, HIF transcription factors ensure the timely restoration of adequate oxygen supply. Particularly in medical conditions such as stroke, which have a high mortality risk due to ischaemic brain damage, rapid recovery of oxygen supply is of extraordinary importance. Nevertheless, the endogenous mechanisms are often not sufficient to respond to severe hypoxic stress with restoring oxygenation and fail to protect the tissue. Herein, we analysed murine neurospheres without functioning HIF-2α and found that special importance in the differentiation of neurons can be attributed to HIF-2 in the brain. Other processes, such as cell migration and signal transduction of different signalling pathways, appear to be mediated to some extent via HIF-2 and illustrate the function of HIF-2 in brain remodelling. Without hypoxic stress, HIF-2 in the brain presumably focuses on the fine-tuning of the neural network. However, a therapeutically increase of HIF-2 has the potential to regenerate or replace destroyed brain tissue and help minimize the consequences of an ischaemic stroke. Springer Berlin Heidelberg 2021-07-12 2021 /pmc/articles/PMC8302505/ /pubmed/34251509 http://dx.doi.org/10.1007/s00424-021-02600-8 Text en © The Author(s) 2021 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Molecular and Cellular Mechanisms of Disease Leu, Tristan Fandrey, Joachim Schreiber, Timm (H)IF applicable: promotion of neurogenesis by induced HIF-2 signalling after ischaemia |
title | (H)IF applicable: promotion of neurogenesis by induced HIF-2 signalling after ischaemia |
title_full | (H)IF applicable: promotion of neurogenesis by induced HIF-2 signalling after ischaemia |
title_fullStr | (H)IF applicable: promotion of neurogenesis by induced HIF-2 signalling after ischaemia |
title_full_unstemmed | (H)IF applicable: promotion of neurogenesis by induced HIF-2 signalling after ischaemia |
title_short | (H)IF applicable: promotion of neurogenesis by induced HIF-2 signalling after ischaemia |
title_sort | (h)if applicable: promotion of neurogenesis by induced hif-2 signalling after ischaemia |
topic | Molecular and Cellular Mechanisms of Disease |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8302505/ https://www.ncbi.nlm.nih.gov/pubmed/34251509 http://dx.doi.org/10.1007/s00424-021-02600-8 |
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