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Nt5e deficiency does not affect post-stroke inflammation and lesion size in a murine ischemia/reperfusion stroke model

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Nt5e deficiency does not affect post-stroke inflammation and lesion size in a murine ischemia/reperfusion stroke model. / Schädlich, Ines Sophie; Schnapauff, Oliver; Pöls, Lennart; Schrader, Jürgen; Tolosa, Eva; Rissiek, Björn; Magnus, Tim.

In: ISCIENCE, Vol. 25, No. 6, 104470, 17.06.2022.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Schädlich, IS, Schnapauff, O, Pöls, L, Schrader, J, Tolosa, E, Rissiek, B & Magnus, T 2022, 'Nt5e deficiency does not affect post-stroke inflammation and lesion size in a murine ischemia/reperfusion stroke model', ISCIENCE, vol. 25, no. 6, 104470. https://doi.org/10.1016/j.isci.2022.104470

APA

Schädlich, I. S., Schnapauff, O., Pöls, L., Schrader, J., Tolosa, E., Rissiek, B., & Magnus, T. (2022). Nt5e deficiency does not affect post-stroke inflammation and lesion size in a murine ischemia/reperfusion stroke model. ISCIENCE, 25(6), [104470]. https://doi.org/10.1016/j.isci.2022.104470

Vancouver

Schädlich IS, Schnapauff O, Pöls L, Schrader J, Tolosa E, Rissiek B et al. Nt5e deficiency does not affect post-stroke inflammation and lesion size in a murine ischemia/reperfusion stroke model. ISCIENCE. 2022 Jun 17;25(6). 104470. https://doi.org/10.1016/j.isci.2022.104470

Bibtex

@article{36cb670cca234d59a0e0b8782c9019f3,
title = "Nt5e deficiency does not affect post-stroke inflammation and lesion size in a murine ischemia/reperfusion stroke model",
abstract = "Extracellular ATP released to the ischemic brain parenchyma is quickly metabolized by ectonucleotidases. Among them, the ecto-5'-nucleotidase CD73 encoded by Nt5e generates immunosuppressive adenosine. Genetic deletion of Nt5e led to increased infarct size in the murine photothrombotic stroke model. We aimed at validating this result using the transient middle cerebral artery occlusion (tMCAO) stroke model that represents pathophysiological aspects of penumbra and reperfusion. Three days after tMACO, we did not detect a difference in stroke size between CD73-deficient (CD73-/-) and control mice. Consistent with this finding, CD73-/- and control mice showed comparable numbers and composition of brain-infiltrating leukocytes measured by flow cytometry. Using NanoString technology, we further demonstrated that CD73-/- and control mice do not differ regarding glia cell gene expression profiles. Our findings highlight the potential impact of stroke models on study outcome and the need for cross-validation of originally promising immunomodulatory candidates.",
author = "Sch{\"a}dlich, {Ines Sophie} and Oliver Schnapauff and Lennart P{\"o}ls and J{\"u}rgen Schrader and Eva Tolosa and Bj{\"o}rn Rissiek and Tim Magnus",
note = "{\textcopyright} 2022 The Author(s).",
year = "2022",
month = jun,
day = "17",
doi = "10.1016/j.isci.2022.104470",
language = "English",
volume = "25",
journal = "ISCIENCE",
issn = "2589-0042",
publisher = "Elsevier Inc.",
number = "6",

}

RIS

TY - JOUR

T1 - Nt5e deficiency does not affect post-stroke inflammation and lesion size in a murine ischemia/reperfusion stroke model

AU - Schädlich, Ines Sophie

AU - Schnapauff, Oliver

AU - Pöls, Lennart

AU - Schrader, Jürgen

AU - Tolosa, Eva

AU - Rissiek, Björn

AU - Magnus, Tim

N1 - © 2022 The Author(s).

PY - 2022/6/17

Y1 - 2022/6/17

N2 - Extracellular ATP released to the ischemic brain parenchyma is quickly metabolized by ectonucleotidases. Among them, the ecto-5'-nucleotidase CD73 encoded by Nt5e generates immunosuppressive adenosine. Genetic deletion of Nt5e led to increased infarct size in the murine photothrombotic stroke model. We aimed at validating this result using the transient middle cerebral artery occlusion (tMCAO) stroke model that represents pathophysiological aspects of penumbra and reperfusion. Three days after tMACO, we did not detect a difference in stroke size between CD73-deficient (CD73-/-) and control mice. Consistent with this finding, CD73-/- and control mice showed comparable numbers and composition of brain-infiltrating leukocytes measured by flow cytometry. Using NanoString technology, we further demonstrated that CD73-/- and control mice do not differ regarding glia cell gene expression profiles. Our findings highlight the potential impact of stroke models on study outcome and the need for cross-validation of originally promising immunomodulatory candidates.

AB - Extracellular ATP released to the ischemic brain parenchyma is quickly metabolized by ectonucleotidases. Among them, the ecto-5'-nucleotidase CD73 encoded by Nt5e generates immunosuppressive adenosine. Genetic deletion of Nt5e led to increased infarct size in the murine photothrombotic stroke model. We aimed at validating this result using the transient middle cerebral artery occlusion (tMCAO) stroke model that represents pathophysiological aspects of penumbra and reperfusion. Three days after tMACO, we did not detect a difference in stroke size between CD73-deficient (CD73-/-) and control mice. Consistent with this finding, CD73-/- and control mice showed comparable numbers and composition of brain-infiltrating leukocytes measured by flow cytometry. Using NanoString technology, we further demonstrated that CD73-/- and control mice do not differ regarding glia cell gene expression profiles. Our findings highlight the potential impact of stroke models on study outcome and the need for cross-validation of originally promising immunomodulatory candidates.

U2 - 10.1016/j.isci.2022.104470

DO - 10.1016/j.isci.2022.104470

M3 - SCORING: Journal article

C2 - 35692634

VL - 25

JO - ISCIENCE

JF - ISCIENCE

SN - 2589-0042

IS - 6

M1 - 104470

ER -