Phosphoproteomics identifies microglial Siglec‐F inflammatory response during neurodegeneration

Abstract Alzheimer’s disease (AD) is characterized by the appearance of amyloid‐β plaques, neurofibrillary tangles, and inflammation in brain regions involved in memory. Using mass spectrometry, we have quantified the phosphoproteome of the CK‐p25, 5XFAD, and Tau P301S mouse models of neurodegenerat...

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Main Authors: Nader Morshed, William T Ralvenius, Alexi Nott, L Ashley Watson, Felicia H Rodriguez, Leyla A Akay, Brian A Joughin, Ping‐Chieh Pao, Jay Penney, Lauren LaRocque, Diego Mastroeni, Li‐Huei Tsai, Forest M White
Format: Article
Language:English
Published: Springer Nature 2020-12-01
Series:Molecular Systems Biology
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Online Access:https://doi.org/10.15252/msb.20209819
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author Nader Morshed
William T Ralvenius
Alexi Nott
L Ashley Watson
Felicia H Rodriguez
Leyla A Akay
Brian A Joughin
Ping‐Chieh Pao
Jay Penney
Lauren LaRocque
Diego Mastroeni
Li‐Huei Tsai
Forest M White
author_facet Nader Morshed
William T Ralvenius
Alexi Nott
L Ashley Watson
Felicia H Rodriguez
Leyla A Akay
Brian A Joughin
Ping‐Chieh Pao
Jay Penney
Lauren LaRocque
Diego Mastroeni
Li‐Huei Tsai
Forest M White
author_sort Nader Morshed
collection DOAJ
description Abstract Alzheimer’s disease (AD) is characterized by the appearance of amyloid‐β plaques, neurofibrillary tangles, and inflammation in brain regions involved in memory. Using mass spectrometry, we have quantified the phosphoproteome of the CK‐p25, 5XFAD, and Tau P301S mouse models of neurodegeneration. We identified a shared response involving Siglec‐F which was upregulated on a subset of reactive microglia. The human paralog Siglec‐8 was also upregulated on microglia in AD. Siglec‐F and Siglec‐8 were upregulated following microglial activation with interferon gamma (IFNγ) in BV‐2 cell line and human stem cell‐derived microglia models. Siglec‐F overexpression activates an endocytic and pyroptotic inflammatory response in BV‐2 cells, dependent on its sialic acid substrates and immunoreceptor tyrosine‐based inhibition motif (ITIM) phosphorylation sites. Related human Siglecs induced a similar response in BV‐2 cells. Collectively, our results point to an important role for mouse Siglec‐F and human Siglec‐8 in regulating microglial activation during neurodegeneration.
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spelling doaj-art-7b9677d83e734c9bb4414abb7d975e622025-08-20T03:06:10ZengSpringer NatureMolecular Systems Biology1744-42922020-12-01161212710.15252/msb.20209819Phosphoproteomics identifies microglial Siglec‐F inflammatory response during neurodegenerationNader Morshed0William T Ralvenius1Alexi Nott2L Ashley Watson3Felicia H Rodriguez4Leyla A Akay5Brian A Joughin6Ping‐Chieh Pao7Jay Penney8Lauren LaRocque9Diego Mastroeni10Li‐Huei Tsai11Forest M White12Department of Biological Engineering, Massachusetts Institute of TechnologyPicower Institute for Learning and Memory, Massachusetts Institute of TechnologyPicower Institute for Learning and Memory, Massachusetts Institute of TechnologyPicower Institute for Learning and Memory, Massachusetts Institute of TechnologyDepartment of Chemical and Materials Engineering, New Mexico State UniversityPicower Institute for Learning and Memory, Massachusetts Institute of TechnologyDepartment of Biological Engineering, Massachusetts Institute of TechnologyPicower Institute for Learning and Memory, Massachusetts Institute of TechnologyPicower Institute for Learning and Memory, Massachusetts Institute of TechnologyDepartment of Biological Engineering, Massachusetts Institute of TechnologyASU‐Banner Neurodegenerative Disease Research CenterPicower Institute for Learning and Memory, Massachusetts Institute of TechnologyDepartment of Biological Engineering, Massachusetts Institute of TechnologyAbstract Alzheimer’s disease (AD) is characterized by the appearance of amyloid‐β plaques, neurofibrillary tangles, and inflammation in brain regions involved in memory. Using mass spectrometry, we have quantified the phosphoproteome of the CK‐p25, 5XFAD, and Tau P301S mouse models of neurodegeneration. We identified a shared response involving Siglec‐F which was upregulated on a subset of reactive microglia. The human paralog Siglec‐8 was also upregulated on microglia in AD. Siglec‐F and Siglec‐8 were upregulated following microglial activation with interferon gamma (IFNγ) in BV‐2 cell line and human stem cell‐derived microglia models. Siglec‐F overexpression activates an endocytic and pyroptotic inflammatory response in BV‐2 cells, dependent on its sialic acid substrates and immunoreceptor tyrosine‐based inhibition motif (ITIM) phosphorylation sites. Related human Siglecs induced a similar response in BV‐2 cells. Collectively, our results point to an important role for mouse Siglec‐F and human Siglec‐8 in regulating microglial activation during neurodegeneration.https://doi.org/10.15252/msb.20209819Alzheimer's diseasemicrogliaphosphoproteomicsSiglec‐8Siglec‐F
spellingShingle Nader Morshed
William T Ralvenius
Alexi Nott
L Ashley Watson
Felicia H Rodriguez
Leyla A Akay
Brian A Joughin
Ping‐Chieh Pao
Jay Penney
Lauren LaRocque
Diego Mastroeni
Li‐Huei Tsai
Forest M White
Phosphoproteomics identifies microglial Siglec‐F inflammatory response during neurodegeneration
Molecular Systems Biology
Alzheimer's disease
microglia
phosphoproteomics
Siglec‐8
Siglec‐F
title Phosphoproteomics identifies microglial Siglec‐F inflammatory response during neurodegeneration
title_full Phosphoproteomics identifies microglial Siglec‐F inflammatory response during neurodegeneration
title_fullStr Phosphoproteomics identifies microglial Siglec‐F inflammatory response during neurodegeneration
title_full_unstemmed Phosphoproteomics identifies microglial Siglec‐F inflammatory response during neurodegeneration
title_short Phosphoproteomics identifies microglial Siglec‐F inflammatory response during neurodegeneration
title_sort phosphoproteomics identifies microglial siglec f inflammatory response during neurodegeneration
topic Alzheimer's disease
microglia
phosphoproteomics
Siglec‐8
Siglec‐F
url https://doi.org/10.15252/msb.20209819
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