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PI3K-AKT activation resculpts integrin signaling to drive filamentous tau-induced proinflammatory astrogliosis [Tau vs OPN]

ABSTRACT: PI3K-AKT activation resculpts integrin signaling to drive filamentous tau-induced proinflammatory astrogliosis [Tau vs OPN]

PROVIDER: PRJNA988450 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25050573.fastq.gz	Fastqsanger.gz
	SRR25050574.fastq.gz	Fastqsanger.gz
	SRR25050575.fastq.gz	Fastqsanger.gz
	SRR25050576.fastq.gz	Fastqsanger.gz
	SRR25050577.fastq.gz	Fastqsanger.gz

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PI3K-AKT activation resculpts integrin signaling to drive filamentous tau-induced proinflammatory astrogliosis [Tau vs OPN]

Project description:Microtubule-binding protein tau is a misfolding-prone protein associated with tauopathies. As tau undergoes cell-to-cell transmission, extracellular tau aggregates convert astrocytes into a pro- inflammatory state via integrin activation, causing them to release unknown neurotoxic factors. Here we combine transcriptomics with isotope labeling-based quantitative mass spectrometry analysis of mouse primary astrocyte secretome to establish PI3K-AKT as a critical differentiator between pathogenic and physiological integrin activation; simultaneous activation of PI3K-AKT and focal adhesion kinase (FAK) in tau fibril-treated astrocytes changes the output of integrin signaling, causing pro-inflammatory gene upregulation, trans-Golgi network restructuring, and altered secretory flow. Furthermore, NCAM1, as a proximal signaling component in tau-stimulated integrin and PI3K-AKT activation, facilitates the secretion of complement C3 as a main neurotoxic factor. Significantly, tau fibrils-associated astrogliosis and C3 secretion can be mitigated by FAK or PI3K inhibitors. These findings reveal an unexpected function for PI3K-AKT in tauopathy-associated astrogliosis and a target for anti-inflammation-based Alzheimer’s therapy.

2023-10-04 | GSE236024 | GEO

PI3K-AKT activation resculpts integrin signaling to drive filamentous tau-induced proinflammatory astrogliosis [Tau with inhibitors]

2023-10-04 | GSE236866 | GEO

PI3K-AKT activation resculpts integrin signaling to drive filamentous tau-induced proinflammatory astrogliosis

Project description:PI3K-AKT activation resculpts integrin signaling to drive filamentous tau-induced proinflammatory astrogliosis

| PRJNA992540 | ENA

PI3K-AKT activation resculpts integrin signaling to drive filamentous tau-induced proinflammatory astrogliosis [Tau with inhibitors]

Project description:PI3K-AKT activation resculpts integrin signaling to drive filamentous tau-induced proinflammatory astrogliosis [Tau with inhibitors]

| PRJNA992547 | ENA

PI3K-AKT activation resculpts integrin signaling to drive filamentous tau-induced proinflammatory astrogliosis.

Project description:BackgroundMicrotubule-binding protein tau is a misfolding-prone protein associated with tauopathies. As tau undergoes cell-to-cell transmission, extracellular tau aggregates convert astrocytes into a pro-inflammatory state via integrin activation, causing them to release unknown neurotoxic factors.ResultsHere, we combine transcriptomics with isotope labeling-based quantitative mass spectrometry analysis of mouse primary astrocyte secretome to establish PI3K-AKT as a critical differentiator between pathogenic and physiological integrin activation; simultaneous activation of PI3K-AKT and focal adhesion kinase (FAK) in tau fibril-treated astrocytes changes the output of integrin signaling, causing pro-inflammatory gene upregulation, trans-Golgi network restructuring, and altered secretory flow. Furthermore, NCAM1, as a proximal signaling component in tau-stimulated integrin and PI3K-AKT activation, facilitates the secretion of complement C3 as a main neurotoxic factor. Significantly, tau fibrils-associated astrogliosis and C3 secretion can be mitigated by FAK or PI3K inhibitors.ConclusionsThese findings reveal an unexpected function for PI3K-AKT in tauopathy-associated reactive astrogliosis, which may be a promising target for anti-inflammation-based Alzheimer's therapy.

| S-EPMC10536728 | biostudies-literature

PI3K-AKT activation resculpts integrin signaling to drive filamentous tau-induced proinflammatory astrogliosis.

Project description:Background Microtubule-binding protein tau is a misfolding-prone protein associated with tauopathies. As tau undergoes cell-to-cell transmission, extracellular tau aggregates convert astrocytes into a pro-inflammatory state via integrin activation, causing them to release unknown neurotoxic factors. Results Here, we combine transcriptomics with isotope labeling-based quantitative mass spectrometry analysis of mouse primary astrocyte secretome to establish PI3K-AKT as a critical differentiator between pathogenic and physiological integrin activation; simultaneous activation of PI3K-AKT and focal adhesion kinase (FAK) in tau fibril-treated astrocytes changes the output of integrin signaling, causing pro-inflammatory gene upregulation, trans-Golgi network restructuring, and altered secretory flow. Furthermore, NCAM1, as a proximal signaling component in tau-stimulated integrin and PI3K-AKT activation, facilitates the secretion of complement C3 as a main neurotoxic factor. Significantly, tau fibrils-associated astrogliosis and C3 secretion can be mitigated by FAK or PI3K inhibitors. Conclusions These findings reveal an unexpected function for PI3K-AKT in tauopathy-associated reactive astrogliosis, which may be a promising target for anti-inflammation-based Alzheimer's therapy.

| S-EPMC10479431 | biostudies-literature

PI3K-AKT activation resculpts integrin signaling to drive filamentous tau-induced proinflammatory astrogliosis

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-10-04 | GSE236868 | GEO

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Gene expression profile of B cells from OPN-competent and deficient Faslpr autoimmune mice

Project description:We performed gene expression profile on splenic CD19+ cells from autoimmune Faslpr/lpr and OPN-/-Faslpr/lpr mice to investigate the dynamics at the basis of the more incident transformation characterizing OPN-deficient animals. GEP on splenic CD19+ from BALB/c and OPN-/- mice was performed as control.

2022-12-21 | GSE193790 | GEO

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