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Phosphoproteomics identifies microglial Siglec-F inflammatory response during neurodegeneration

ABSTRACT: Phosphoproteomics identifies microglial Siglec-F inflammatory response during neurodegeneration

PROVIDER: PRJNA627466 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11590500.fastq.gz	Fastqsanger.gz
	SRR11590501.fastq.gz	Fastqsanger.gz
	SRR11590502.fastq.gz	Fastqsanger.gz
	SRR11590503.fastq.gz	Fastqsanger.gz
	SRR11590504.fastq.gz	Fastqsanger.gz

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Phosphoproteomics identifies microglial Siglec-F inflammatory response during neurodegeneration

Project description:This study sought to explore phosphoproteome signaling dysregulation in different models of neurodegeneration. We collected phosphotyrosine, MAPK/CDK substrates, global phosphoproteome, and protein expression data from hippocampus and/or cortex tissue from each model. Tryptic peptides were multiplexd with TMT, enriched for phosphopeptides, and then identified and quantified by LC-MS/MS. We additionally quantified phosphotyrosine peptides from BV-2 cells expressing various Siglec receptor constructs.

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Phosphoproteomics identifies microglial Siglec-F inflammatory response during neurodegeneration

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Phosphoproteomics identifies microglial Siglec-F inflammatory response during neurodegeneration.

Project description: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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