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Functional hypoxia drives neuroplasticity and neurogenesis via brain erythropoietin

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Functional hypoxia drives neuroplasticity and neurogenesis via brain erythropoietin. / Wakhloo, Debia; Scharkowski, Franziska; Curto, Yasmina; Javed Butt, Umer; Bansal, Vikas; Steixner-Kumar, Agnes A; Wüstefeld, Liane; Rajput, Ashish; Arinrad, Sahab; Zillmann, Matthias R; Seelbach, Anna; Hassouna, Imam; Schneider, Katharina; Qadir Ibrahim, Abdul; Werner, Hauke B; Martens, Henrik; Miskowiak, Kamilla; Wojcik, Sonja M; Bonn, Stefan; Nacher, Juan; Nave, Klaus-Armin; Ehrenreich, Hannelore.

in: NAT COMMUN, Jahrgang 11, Nr. 1, 09.03.2020, S. 1313.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Wakhloo, D, Scharkowski, F, Curto, Y, Javed Butt, U, Bansal, V, Steixner-Kumar, AA, Wüstefeld, L, Rajput, A, Arinrad, S, Zillmann, MR, Seelbach, A, Hassouna, I, Schneider, K, Qadir Ibrahim, A, Werner, HB, Martens, H, Miskowiak, K, Wojcik, SM, Bonn, S, Nacher, J, Nave, K-A & Ehrenreich, H 2020, 'Functional hypoxia drives neuroplasticity and neurogenesis via brain erythropoietin', NAT COMMUN, Jg. 11, Nr. 1, S. 1313. https://doi.org/10.1038/s41467-020-15041-1

APA

Wakhloo, D., Scharkowski, F., Curto, Y., Javed Butt, U., Bansal, V., Steixner-Kumar, A. A., Wüstefeld, L., Rajput, A., Arinrad, S., Zillmann, M. R., Seelbach, A., Hassouna, I., Schneider, K., Qadir Ibrahim, A., Werner, H. B., Martens, H., Miskowiak, K., Wojcik, S. M., Bonn, S., ... Ehrenreich, H. (2020). Functional hypoxia drives neuroplasticity and neurogenesis via brain erythropoietin. NAT COMMUN, 11(1), 1313. https://doi.org/10.1038/s41467-020-15041-1

Vancouver

Wakhloo D, Scharkowski F, Curto Y, Javed Butt U, Bansal V, Steixner-Kumar AA et al. Functional hypoxia drives neuroplasticity and neurogenesis via brain erythropoietin. NAT COMMUN. 2020 Mär 9;11(1):1313. https://doi.org/10.1038/s41467-020-15041-1

Bibtex

@article{f0aeb217cebd4bbfb4e561481a3cdea9,
title = "Functional hypoxia drives neuroplasticity and neurogenesis via brain erythropoietin",
abstract = "Erythropoietin (EPO), named after its role in hematopoiesis, is also expressed in mammalian brain. In clinical settings, recombinant EPO treatment has revealed a remarkable improvement of cognition, but underlying mechanisms have remained obscure. Here, we show with a novel line of reporter mice that cognitive challenge induces local/endogenous hypoxia in hippocampal pyramidal neurons, hence enhancing expression of EPO and EPO receptor (EPOR). High-dose EPO administration, amplifying auto/paracrine EPO/EPOR signaling, prompts the emergence of new CA1 neurons and enhanced dendritic spine densities. Single-cell sequencing reveals rapid increase in newly differentiating neurons. Importantly, improved performance on complex running wheels after EPO is imitated by exposure to mild exogenous/inspiratory hypoxia. All these effects depend on neuronal expression of the Epor gene. This suggests a model of neuroplasticity in form of a fundamental regulatory circle, in which neuronal networks-challenged by cognitive tasks-drift into transient hypoxia, thereby triggering neuronal EPO/EPOR expression.",
keywords = "Animals, Brain/metabolism, Cell Differentiation/drug effects, Cognition/drug effects, Dendritic Spines/drug effects, Erythropoietin/metabolism, Female, Gene Deletion, Humans, Hypoxia/metabolism, Male, Mice, Inbred C57BL, Models, Neurological, Motor Activity/drug effects, Neurogenesis/drug effects, Neuronal Plasticity/drug effects, Physical Conditioning, Animal, Physical Endurance/drug effects, Proto-Oncogene Proteins c-fos/metabolism, Pyramidal Cells/drug effects, Receptors, Erythropoietin/metabolism, Transcriptome/drug effects",
author = "Debia Wakhloo and Franziska Scharkowski and Yasmina Curto and {Javed Butt}, Umer and Vikas Bansal and Steixner-Kumar, {Agnes A} and Liane W{\"u}stefeld and Ashish Rajput and Sahab Arinrad and Zillmann, {Matthias R} and Anna Seelbach and Imam Hassouna and Katharina Schneider and {Qadir Ibrahim}, Abdul and Werner, {Hauke B} and Henrik Martens and Kamilla Miskowiak and Wojcik, {Sonja M} and Stefan Bonn and Juan Nacher and Klaus-Armin Nave and Hannelore Ehrenreich",
year = "2020",
month = mar,
day = "9",
doi = "10.1038/s41467-020-15041-1",
language = "English",
volume = "11",
pages = "1313",
journal = "NAT COMMUN",
issn = "2041-1723",
publisher = "NATURE PUBLISHING GROUP",
number = "1",

}

RIS

TY - JOUR

T1 - Functional hypoxia drives neuroplasticity and neurogenesis via brain erythropoietin

AU - Wakhloo, Debia

AU - Scharkowski, Franziska

AU - Curto, Yasmina

AU - Javed Butt, Umer

AU - Bansal, Vikas

AU - Steixner-Kumar, Agnes A

AU - Wüstefeld, Liane

AU - Rajput, Ashish

AU - Arinrad, Sahab

AU - Zillmann, Matthias R

AU - Seelbach, Anna

AU - Hassouna, Imam

AU - Schneider, Katharina

AU - Qadir Ibrahim, Abdul

AU - Werner, Hauke B

AU - Martens, Henrik

AU - Miskowiak, Kamilla

AU - Wojcik, Sonja M

AU - Bonn, Stefan

AU - Nacher, Juan

AU - Nave, Klaus-Armin

AU - Ehrenreich, Hannelore

PY - 2020/3/9

Y1 - 2020/3/9

N2 - Erythropoietin (EPO), named after its role in hematopoiesis, is also expressed in mammalian brain. In clinical settings, recombinant EPO treatment has revealed a remarkable improvement of cognition, but underlying mechanisms have remained obscure. Here, we show with a novel line of reporter mice that cognitive challenge induces local/endogenous hypoxia in hippocampal pyramidal neurons, hence enhancing expression of EPO and EPO receptor (EPOR). High-dose EPO administration, amplifying auto/paracrine EPO/EPOR signaling, prompts the emergence of new CA1 neurons and enhanced dendritic spine densities. Single-cell sequencing reveals rapid increase in newly differentiating neurons. Importantly, improved performance on complex running wheels after EPO is imitated by exposure to mild exogenous/inspiratory hypoxia. All these effects depend on neuronal expression of the Epor gene. This suggests a model of neuroplasticity in form of a fundamental regulatory circle, in which neuronal networks-challenged by cognitive tasks-drift into transient hypoxia, thereby triggering neuronal EPO/EPOR expression.

AB - Erythropoietin (EPO), named after its role in hematopoiesis, is also expressed in mammalian brain. In clinical settings, recombinant EPO treatment has revealed a remarkable improvement of cognition, but underlying mechanisms have remained obscure. Here, we show with a novel line of reporter mice that cognitive challenge induces local/endogenous hypoxia in hippocampal pyramidal neurons, hence enhancing expression of EPO and EPO receptor (EPOR). High-dose EPO administration, amplifying auto/paracrine EPO/EPOR signaling, prompts the emergence of new CA1 neurons and enhanced dendritic spine densities. Single-cell sequencing reveals rapid increase in newly differentiating neurons. Importantly, improved performance on complex running wheels after EPO is imitated by exposure to mild exogenous/inspiratory hypoxia. All these effects depend on neuronal expression of the Epor gene. This suggests a model of neuroplasticity in form of a fundamental regulatory circle, in which neuronal networks-challenged by cognitive tasks-drift into transient hypoxia, thereby triggering neuronal EPO/EPOR expression.

KW - Animals

KW - Brain/metabolism

KW - Cell Differentiation/drug effects

KW - Cognition/drug effects

KW - Dendritic Spines/drug effects

KW - Erythropoietin/metabolism

KW - Female

KW - Gene Deletion

KW - Humans

KW - Hypoxia/metabolism

KW - Male

KW - Mice, Inbred C57BL

KW - Models, Neurological

KW - Motor Activity/drug effects

KW - Neurogenesis/drug effects

KW - Neuronal Plasticity/drug effects

KW - Physical Conditioning, Animal

KW - Physical Endurance/drug effects

KW - Proto-Oncogene Proteins c-fos/metabolism

KW - Pyramidal Cells/drug effects

KW - Receptors, Erythropoietin/metabolism

KW - Transcriptome/drug effects

U2 - 10.1038/s41467-020-15041-1

DO - 10.1038/s41467-020-15041-1

M3 - SCORING: Journal article

C2 - 32152318

VL - 11

SP - 1313

JO - NAT COMMUN

JF - NAT COMMUN

SN - 2041-1723

IS - 1

ER -