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Heart failure impairs the mechanotransduction properties of human cardiac pericytes

ABSTRACT: Heart failure impairs the mechanotransduction properties of human cardiac pericytes

PROVIDER: PRJNA660440 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12554868.fastq.gz	Fastqsanger.gz
	SRR12554869.fastq.gz	Fastqsanger.gz
	SRR12554870.fastq.gz	Fastqsanger.gz
	SRR12554871.fastq.gz	Fastqsanger.gz
	SRR12554872.fastq.gz	Fastqsanger.gz

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Heart failure impairs the mechanotransduction properties of human cardiac pericytes

Project description:Aim of this work is to verify if pericytes (Pc) residing in ischemic failing human hearts display altered mechano-transduction properties and to assess which alterations of the mechano-sensing machinery are associated with the observed impaired response to mechanical cues. Results: microvascular rarefaction and defects of YAP/TAZ activation characterize failing human hearts. Although both donor (D-) and explanted (E-) heart derived cardiac pericytes (CPc) support angiogenesis, D-CPc exert this effect significantly better than E-CPc. The latter are characterized by reduced focal adhesion density, decreased activation of the focal adhesion kinase (FAK)/ Crk-associated substrate(CAS) pathway, low expression of caveolin-1, and defective transduction of extracellular stiffness into cytoskeletal stiffening, together with an impaired response to both fibronectin and lysophosphatidic acid. Importantly, Mitogen-activated protein kinase kinase inhibition restores YAP/TAZ nuclear translocation.

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Reconstruction of the Human Blood-Brain Barrier in vitro reveals a Pathogenic Mechanism of APOE4 in Pericytes

Project description:The majority of Alzheimer’s disease patients and 20–40% of non-demented elderly experience amyloid deposits along their cerebral vasculature, a condition known as cerebral amyloid angiopathy (CAA). CAA impairs the function of the blood-brain barrier (BBB) leading to ischemia, hemorrhages, and accelerated cognitive dysfunction. The APOE4 allele is the strongest known genetic risk factor for CAA and sporadic AD, however the pathogenic mechanisms underlying this predisposition are unknown. Here, we recreate the human BBB in vitro by co-culturing the three cellular components of the BBB, endothelial cells, pericytes, and astrocytes in 3D scaffolding to construct a tractable model that recapitulates key anatomical and physiological properties of the BBB. Similar to the in vivo BBB, we find amyloid accumulates on our in vitro BBB (iBBB) and both APOE4 homozygous and heterozygous iBBBs exhibit significantly more amyloid accumulation than APOE3/3 iBBBs. Combinatorial experiments revealed that pericytes have a causal role in the development of CAA. We found that APOE expression is markedly up-regulated in APOE4 pericytes, but not in astrocytes or endothelial cells. Transcriptional profiling revealed that calcineurin/NFAT signaling is dysregulated in APOE4 pericytes. Pharmacologically inhibiting calcineurin led to downregulation of APOE and subsequently reduced amyloid deposition on the iBBB. These results demonstrate an unexpected role of pericytes in cerebral amyloid deposition and advocate for inhibiting calcineurin/NFAT-signaling as a therapeutic strategy to mitigate APOE4 predisposition to CAA and potentially AD.

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