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P16-expressing microglia and endothelial cells promote tauopathy and neurovascular abnormalities in PS19 mice

ABSTRACT: p16-expressing microglia and endothelial cells promote tauopathy and neurovascular abnormalities in PS19 mice

PROVIDER: PRJNA1251640 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR33168619_1.fastq.gz	Fastqsanger.gz
	SRR33168619_2.fastq.gz	Fastqsanger.gz
	SRR33168620_1.fastq.gz	Fastqsanger.gz
	SRR33168620_2.fastq.gz	Fastqsanger.gz
	SRR33168621_1.fastq.gz	Fastqsanger.gz

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p16-expressing microglia and endothelial cells promote tauopathy and neurovascular abnormalities in PS19 mice

Project description:Cellular senescence is characterized by irreversible cell cycle exit, acquisition of a pro-inflammatory secretory phenotype, macromolecular damage, and deregulated metabolism. Senescent cells have been implicated in many age-related diseases, including neurodegenerative disease. We have previously demonstrated that selective elimination of senescent cells, both pharmacologically and genetically, prevents neurodegenerative disease phenotypes in tau (MAPTP301S;PS19) mutant mice. Here, we show that genetically knocking out the senescence mediator p16Ink4a, a cyclin-dependent kinase inhibitor, is sufficient to attenuate senescence signatures in PS19 mice. Neurodegenerative disease phenotypes dependent on senescent cell accumulation, including neuroinflammation, phosphorylated tau burden, neurodegeneration, and cognitive impairment were blunted in the absence of p16Ink4a. Additionally, we found that PS19 mice display altered neurovascular features—including vessel dilation, increased vessel density, deregulated endothelial cell extracellular matrix, and astrocytic endfoot depolarization—which were also attenuated when p16Ink4a was knocked out. Finally, we utilized a cell-type specific knockout of p16Ink4a to show that p16Ink4a deletion in endothelial cells and microglia alone attenuates many of the same tau-dependent phenotypes as whole-body knockout of p16Ink4a. Taken together, these results indicate that onset and progression of neurodegenerative disease in PS19 mice is driven, at least in part, by p16Ink4a expressing endothelial cells and microglia.

2025-04-30 | GSE294816 | GEO

LncRNA/mRNA sequencing analysis on cerebral cortex of P301S mutant Tau transgenic mice (PS19).

Project description:Aggregation of the microtubule-associated protein, tau, can lead to neurofibrillary tangle formation in neurons and glia, the hallmark of tauopathy. The cellular damages induced by the tau overexpression and aggregation may lead to multiple pathologic features of tauopathy. However, the effect of aging on tauopathy has not been elucidated yet. Here, we conducted lncRNA/mRNA sequencing analysis on P301S mutant Tau transgenic mouse model (PS19) with different ages to track the genetic changes occurred by the aging and progression of tau overexpression.

2019-06-23 | GSE118473 | GEO

PS19 and PS19/C3aR KO RNAseq data

Project description:Hippocampal tissue from 9 month old WT, C3aR KO, PS19 and PS19/C3aR KO mice was processed

2018-11-08 | GSE114910 | GEO

Soluble epoxide hydrolase inhibition confers neuroprotective and anti-inflammatory effect in a tauopathy mouse model

Project description:Inhibition of soluble epoxide hydrolase (sEH) has been shown to suppress neuroinflammation through stabilizing epoxy fatty acids. Here we examined the role of sEH inhibitor TPPU in PS19 tauopathy mouse model by treating the 6-month-old wild-type and PS19 mice with vehicle or TPPU via drinking water continuously for 12 weeks, followed by performing single nucleus RNA-sequencing of the hippocampal tissues of the treated mice.

2025-04-30 | GSE272373 | GEO

RNA sequencing of total RNA from spinal cord total lysates of the PS19 tauopathy mouse model.

Project description:RNA seqeuncing was perfomed to compare transcriptomic profiles of PS19 and control mice at four and nine months.

2021-10-23 | GSE186228 | GEO

Seed-competent tau monomer initiates pathology in PS19 tauopathy mice

Project description:Tau Monomer from age controlled healthy and Alzheimer's Disease LUM2_C10053 LUM2_C10054 LUM2_C10055 LUM2_C10056 LUM2_C10057 LUM2_C10058 Tau fibril from Alzheimer's Disease LUM2_630897 Tau monomer from brain of PS19 mouse at age week 1, 2, 3, 4, 5, 6 LUM1_C11496 to LUM1_C11501 Tau monomer from brain of PS19 mouse at age 1 year LUM1_705666

2022-01-06 | MSV000088651 | MassIVE

TFEB-vacuolar ATPase signaling regulates lysosomal activity and immune response in tauopathy

Project description:Transcription factor EB (TFEB) mediates gene expression through binding to the Coordinated Lysosome Expression And Regulation (CLEAR) sequence. We created a knock-in mouse line in which the CLEAR sequence of ATP6V1H was mutated. Crossing the CLEAR mutant with PS19 mice led to higher tau pathology but dampened glial cell activation. snRNA-seq revealed that the CLEAR mutant failed to be activated in tauopathy conditions.

2023-06-02 | GSE218728 | GEO

Gene Expression of PS19 Tau transgenic mice

Project description:Expression of PS19 Tau Transgenic mice from hippocampus at different ages 3, 6, 9, and 12 months We used Affy arrays to understand the global expression profile of PS19 Tau transgenic mice

2018-08-28 | GSE89979 | GEO

RNA sequencing of total RNA from spinal cord total lysates of the PS19 tauopathy mouse model.

Project description:RNA sequencing of total RNA from spinal cord total lysates of the PS19 tauopathy mouse model.

| PRJNA773047 | ENA

Expression data from RCAS PDGFB/Nestin tv-A glioma cells within Ptprd+/+p16-/- (n=2), Ptprd+/-p16-/- (n=2), and Ptrpd-/-p16-/- (n=3) mice.

Project description:PTPRD is a tumor suppressor of glioma that is frequently co-deleted with CDKN2A/p16. We show that Ptprd and p16 cooperate to promote gliomagenesis in the RCAS PDGFB / Nestin tv-A glioma mouse model. We found unique gene expression changes within tumor cells of Ptprd+/-p16-/- vs. Ptprd+/+p16-/- and Ptprd-/-p16-/- tumor cells. Neonatal mice were injected with RCAS PDGFB GFP. At symptoms, or at 12 weeks post injection, GFP+DAPI- tumor cells were sorted for RNA extraction and hybridization on Affymetrix microarrays. The mouse strain used was a mixed background of C57/BL6 and FVB/N. Ptprd mice were from Uetani et al. 2000 and p16/Nestin-tvA mice were from Tchouganouva et al. 2007.

2014-06-02 | E-GEOD-55061 | biostudies-arrayexpress

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