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Anti-microRNA-21 therapy on top of ACE-inhibition delays renal failure in Alport syndrome mouse models

ABSTRACT: Anti-microRNA-21 therapy on top of ACE-inhibition delays renal failure in Alport syndrome mouse models

PROVIDER: PRJNA745946 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15102716_1.fastq.gz	Fastqsanger.gz
	SRR15102716_2.fastq.gz	Fastqsanger.gz
	SRR15102717_1.fastq.gz	Fastqsanger.gz
	SRR15102717_2.fastq.gz	Fastqsanger.gz
	SRR15102718_1.fastq.gz	Fastqsanger.gz

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Anti-microRNA-21 therapy on top of ACE-inhibition delays renal failure in Alport syndrome mouse models

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Project description:Transient angiotensin converting enzyme (ACE) inhibition in spontaneously hypertensive rats (SHR) protects against future injury-induced cardiac inflammation, fibrosis, and dysfunction. Here, we used single cell RNA sequencing (scRNA-Seq) to test the hypothesis that transient ACE inhibitor treatment would induce a persistent shift in hypertensive cardiac fibroblast subpopulations. Adult male SHRs (11 weeks old) were treated for 2 weeks with an ACE inhibitor, enalapril (30mg/kg/day, p.o.), or water (control) followed by a 2-week washout period (n=7/group). Cardiac fibroblasts were isolated from the left ventricle and subjected to scRNA-Seq. Nine clusters of fibroblasts (numbered 0-8) were identified with 98% of cells clustering into subsets 0-6. Transient treatment produced significant changes within and across clusters. Cluster 1 depicted the highly fibrogenic gene profile, with cluster 6 serving as a gateway to cluster 1. Transient ACE inhibition depleted the gateway and expanded cluster 0, which was the least fibrogenic profile. Moreover, within cluster 1 fibroblasts, ACE inhibition reduced expression of individual fibrosis genes (e.g. COL1A1, COL3A1, and FN1; all p<0.05). Clusters 2-5 reflected proliferative, moderately fibrogenic, translationally active, and lowly inflammatory subsets of fibroblasts, all of which exhibit attenuated fibrogenic gene expression after transient ACE inhibition. In conclusion, transient ACE inhibition shifts cardiac fibroblast subpopulations and degree of activation resulting in an overall reduced fibrogenic phenotype.

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