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High-throughput sequencing analysis of miRNAs expression profiles in the thoracic ascending aortic aneurysm (TAA) tissues and plasma samples.

ABSTRACT: High-throughput sequencing analysis of miRNAs expression profiles in the thoracic ascending aortic aneurysm (TAA) tissues and plasma samples.

PROVIDER: PRJNA504426 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8170860.fastq.gz	Fastqsanger.gz
	SRR8170870.fastq.gz	Fastqsanger.gz
	SRR8170861.fastq.gz	Fastqsanger.gz
	SRR8170871.fastq.gz	Fastqsanger.gz
	SRR8170862.fastq.gz	Fastqsanger.gz

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High-throughput sequencing analysis of miRNAs expression profiles in the thoracic ascending aortic aneurysm (TAA) tissues and plasma samples.

Project description:In the present study, we evaluated miRNA expression profiles of 32 patient aortic aneurysm tissue and plasma samples using Illumina next-generation sequencing platform. A total of 20 miRNA were differentially expressed in tissues, 17 miRNAs - in plasma samples. Differentially expressed miRNAs determined in the present study could be applied for thoracic ascending aneurysm diagnosis.

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Inhibition of Intimal CX3CR1+ Macrophages Mitigates Thoracic Aortic Aneurysm Progression in Marfan Syndrome

Project description:Current understanding on the pathogenesis of thoracic aortic aneurysms (TAAs) in Marfan Syndrome (MFS) mainly focuses on vascular smooth muscle cell (VSMC) pathologies. Whether immune cell-mediated inflammation drives the progression of TAAs is still elusive. Using single-cell RNA sequencing, a subset of macrophages highly expressing CX3CR1 and mainly locating in the aortic intima was identified in aortic root and ascending aortas from Fbn1C1041G/+ mice, and further validated in MFS patients. Specific elimination of CX3CR1+ macrophages by diphtheria toxin in Cx3cr1-CreERT2iDTRF/+Fbn1C1041G/+ mice efficiently ameliorated TAA progression, suggesting their pathogenic action. Using monoclonal antibodies Adalimumab and Teprotumumab to respectively neutralize the proinflammatory cytokines TNFalpha and IGF1 produced by CX3CR1+ macrophages from MFS patients substantially suppressed CX3CR1+ macrophage-mediated inflammation in MFS patient-specific induced pluripotent stem cell (iPSC)-derived VSMCs. Furthermore, bone marrow transplantation and parabiosis using Cx3cr1GFP/+ mice revealed the intimal CX3CR1+ macrophages derived from circulating monocytes. Administration of CCR2 antagonist RS504393 to inhibit monocyte infiltration significantly reduced intimal CX3CR1+ macrophages and subsequently alleviated TAA development in Fbn1C1041G/+ mice. In conclusion, intimal CX3CR1+ macrophages mediated TAA formation through paracrinally causing VSMC inflammation. Targeting intimal CX3CR1+ macrophages would be a promising anti-inflammatory strategy in TAA therapy for MFS.

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