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Transcriptional profiling of human microglia reveals grey-white matter heterogeneity and multiple sclerosis-associated changes. / van der Poel, Marlijn; Ulas, T.; Mizee, Mark R; Hsiao, C.C.; Miedema, Suzanne S M; Adelia; Schuurman, Karianne; Helder, B.; Tas, S.W.; Schultze, J.L.; Hamann, Jörg; Huitinga, I.

In: Nature Communications, Vol. 10, 1139, 13.03.2019.

Research output: Contribution to journal/periodicalArticleScientificpeer-review

Harvard

van der Poel, M, Ulas, T, Mizee, MR, Hsiao, CC, Miedema, SSM, Adelia, Schuurman, K, Helder, B, Tas, SW, Schultze, JL, Hamann, J & Huitinga, I 2019, 'Transcriptional profiling of human microglia reveals grey-white matter heterogeneity and multiple sclerosis-associated changes.' Nature Communications, vol. 10, 1139. DOI: 10.1038/s41467-019-08976-7

APA

van der Poel, M., Ulas, T., Mizee, M. R., Hsiao, C. C., Miedema, S. S. M., Adelia, ... Huitinga, I. (2019). Transcriptional profiling of human microglia reveals grey-white matter heterogeneity and multiple sclerosis-associated changes. Nature Communications, 10, [1139]. DOI: 10.1038/s41467-019-08976-7

Vancouver

van der Poel M, Ulas T, Mizee MR, Hsiao CC, Miedema SSM, Adelia et al. Transcriptional profiling of human microglia reveals grey-white matter heterogeneity and multiple sclerosis-associated changes. Nature Communications. 2019 Mar 13;10. 1139. Available from, DOI: 10.1038/s41467-019-08976-7

Author

van der Poel, Marlijn ; Ulas, T. ; Mizee, Mark R ; Hsiao, C.C. ; Miedema, Suzanne S M ; Adelia ; Schuurman, Karianne ; Helder, B. ; Tas, S.W. ; Schultze, J.L. ; Hamann, Jörg ; Huitinga, I./ Transcriptional profiling of human microglia reveals grey-white matter heterogeneity and multiple sclerosis-associated changes.In: Nature Communications. 2019 ; Vol. 10.

BibTeX

@article{f4b4c9005353410788a1c4b25760c310,
title = "Transcriptional profiling of human microglia reveals grey-white matter heterogeneity and multiple sclerosis-associated changes.",
abstract = "Here we report the transcriptional profile of human microglia, isolated from normal-appearing grey matter (GM) and white matter (WM) of multiple sclerosis (MS) and non-neurological control donors, to find possible early changes related to MS pathology. Microglia show a clear region-specific profile, indicated by higher expression of type-I interferon genes in GM and higher expression of NF-κB pathway genes in WM. Transcriptional changes in MS microglia also differ between GM and WM. MS WM microglia show increased lipid metabolism gene expression, which relates to MS pathology since active MS lesionderivedmicroglial nuclei show similar altered gene expression. Microglia from MS GM show increased expression of genes associated with glycolysis and iron homeostasis, possibly reflecting microglia reacting to iron depositions. Except for ADGRG1/GPR56, expression of homeostatic genes, such as P2RY12 and TMEM119, is unaltered in normal-appearing MS tissue, demonstrating overall preservation of microglia homeostatic functions in the initiation phase of MS.",
author = "{van der Poel}, Marlijn and T. Ulas and Mizee, {Mark R} and C.C. Hsiao and Miedema, {Suzanne S M} and Adelia and Karianne Schuurman and B. Helder and S.W. Tas and J.L. Schultze and J{\"o}rg Hamann and I. Huitinga",
year = "2019",
month = "3",
day = "13",
doi = "10.1038/s41467-019-08976-7",
language = "English",
volume = "10",
journal = "Nature Communications",
issn = "2041-1723",

}

RIS

TY - JOUR

T1 - Transcriptional profiling of human microglia reveals grey-white matter heterogeneity and multiple sclerosis-associated changes.

AU - van der Poel,Marlijn

AU - Ulas,T.

AU - Mizee,Mark R

AU - Hsiao,C.C.

AU - Miedema,Suzanne S M

AU - Adelia,

AU - Schuurman,Karianne

AU - Helder,B.

AU - Tas,S.W.

AU - Schultze,J.L.

AU - Hamann,Jörg

AU - Huitinga,I.

PY - 2019/3/13

Y1 - 2019/3/13

N2 - Here we report the transcriptional profile of human microglia, isolated from normal-appearing grey matter (GM) and white matter (WM) of multiple sclerosis (MS) and non-neurological control donors, to find possible early changes related to MS pathology. Microglia show a clear region-specific profile, indicated by higher expression of type-I interferon genes in GM and higher expression of NF-κB pathway genes in WM. Transcriptional changes in MS microglia also differ between GM and WM. MS WM microglia show increased lipid metabolism gene expression, which relates to MS pathology since active MS lesionderivedmicroglial nuclei show similar altered gene expression. Microglia from MS GM show increased expression of genes associated with glycolysis and iron homeostasis, possibly reflecting microglia reacting to iron depositions. Except for ADGRG1/GPR56, expression of homeostatic genes, such as P2RY12 and TMEM119, is unaltered in normal-appearing MS tissue, demonstrating overall preservation of microglia homeostatic functions in the initiation phase of MS.

AB - Here we report the transcriptional profile of human microglia, isolated from normal-appearing grey matter (GM) and white matter (WM) of multiple sclerosis (MS) and non-neurological control donors, to find possible early changes related to MS pathology. Microglia show a clear region-specific profile, indicated by higher expression of type-I interferon genes in GM and higher expression of NF-κB pathway genes in WM. Transcriptional changes in MS microglia also differ between GM and WM. MS WM microglia show increased lipid metabolism gene expression, which relates to MS pathology since active MS lesionderivedmicroglial nuclei show similar altered gene expression. Microglia from MS GM show increased expression of genes associated with glycolysis and iron homeostasis, possibly reflecting microglia reacting to iron depositions. Except for ADGRG1/GPR56, expression of homeostatic genes, such as P2RY12 and TMEM119, is unaltered in normal-appearing MS tissue, demonstrating overall preservation of microglia homeostatic functions in the initiation phase of MS.

U2 - 10.1038/s41467-019-08976-7

DO - 10.1038/s41467-019-08976-7

M3 - Article

VL - 10

JO - Nature Communications

T2 - Nature Communications

JF - Nature Communications

SN - 2041-1723

M1 - 1139

ER -

ID: 9721498