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Bulk RNA-seq of pericytes isolated from mouse brain and heart

ABSTRACT: Bulk RNA-seq of pericytes isolated from mouse brain and heart

PROVIDER: PRJNA1191030 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31520773_1.fastq.gz	Fastqsanger.gz
	SRR31520773_2.fastq.gz	Fastqsanger.gz
	SRR31520774_1.fastq.gz	Fastqsanger.gz
	SRR31520774_2.fastq.gz	Fastqsanger.gz
	SRR31520775_1.fastq.gz	Fastqsanger.gz

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Bulk RNA-seq of pericytes isolated from mouse brain and heart

Project description:The goal of the experiment was to characterize the transcriptome of Pericytes from mouse brain and heart. Data were analyzed to examine the ion channels, exchangers and pumps that are enriched in pericytes

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Project description:Background. Ageing is one of the main risk factors of cardiovascular disease. Pericytes are capillary-associated mural cells involved in the maintenance and stability of the vascular network. In the heart, the consequences of ageing on cardiac pericytes are unknown. Methods. In this study, we have combined single nucleus RNA sequencing and histological analysis to determine the effects of ageing on cardiac pericytes. Furthermore, we have conducted in vivo and in vitro analysis of RGS5 loss of function and finally have perfomed pericytes-fibroblasts co-culture studies to understand the effect of RGS5 loss of function in pericytes on the neighbouring fibroblasts. Results. We showed that ageing reduces the pericyte area and coverage. Single nucleus RNA sequencing analysis further revealed that the expression of the Regulator of G protein signalling 5 (Rgs5) is reduced in old cardiac pericytes. In vivo and in vitro studies showed that the deletion of RGS5 induces morphological changes and a pro-fibrotic gene expression signature characterized by the expression of different extracellular matrix components and growth factors like TGFB2 and PDGFB in pericytes. Indeed, the culture of fibroblasts with the supernatant of RGS5 deficient pericytes induced their activation characterized by the increased expression of α smooth muscle actin in a TFGβ2 dependent mechanism. Conclusions. Our results identify RGS5 as a crucial regulator of pericyte function during cardiac ageing. The deletion of RGS5 causes cardiac dysfunction and induces myocardial fibrosis, one of the hallmarks of cardiac ageing.

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Project description:Ischemic injury leads to irreversible loss of neurons and cardiomyocytes in the brain and heart, respectively which ultimately results in fibrotic scar formation. Despite recent advances in tissue fibrosis, cellular mediators of scar formation in the heart and brain remain elusive. Pericytes are a heterogeneous population of mural cells that surround microvessels in various organs including the brain and heart. Their function beyond vascular integrity and contractility is poorly understood, although recent studies have suggested they may be a major contributor to tissue fibrosis. In both the heart and brain, differences in injury models, lack of proper transgenic mouse models for lineage tracing and absence of pericyte-specific markers have contributed to discrepancies in the literature regarding their direct contributions to fibrosis. Here, by performing a set of complementary experiments using a common pericyte transgenic model and clinically-relevant ischemic injury models of stroke and myocardial infarction, we demonstrated the parallel pro-fibrotic response of pericyte after vascular injury.

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