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MicroRNA microarray of aortae from 4-week male Fbn1mgR/mgR and wild-type mice [4-week_miRNA]

ABSTRACT: Thoracic aortic aneurysms (TAA) in Marfan syndrome, caused by fibrillin-1 mutations, are characterized by elevated cytokines and fragmentated elastic laminae in the aortic wall. This study explored whether and how specific fibrillin-1-regulated miRNAs mediate inflammatory cytokine expression and elastic laminae degradation in TAA. miRNA expression profiling at early and late TAA stages using a severe Marfan mouse model (Fbn1mgR/mgR) revealed a spectrum of differentially regulated miRNAs. Bioinformatic analyses predicted the involvement of these miRNAs in inflammatory and extracellular matrix related pathways. Complementing mRNA microarray demonstrated the upregulation of multiple pro-inflammatory cytokines and matrix metalloproteases. Correlation analyses between the altered miRNAs and mRNAs present miR-122, the most downregulated miRNAs in the TAA tissue of Fbn1mgR/mgR, to be a core regulatory miRNA to pro-inflammatory cytokines, Ccl2 and Il1b, which were upregulated in the TAA tissues. 3 miRNAs were downregulated and 14 upregulated more than 2-fold

ORGANISM(S): synthetic construct Mus musculus

PROVIDER: GSE199282 | GEO | 2022/05/21

REPOSITORIES: GEO

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microRNA microarray of aortae from 10-week male Fbn1mgR/mgR and wild-type mice [10-week_miRNA]

Project description:Thoracic aortic aneurysms (TAA) in Marfan syndrome, caused by fibrillin-1 mutations, are characterized by elevated cytokines and fragmentated elastic laminae in the aortic wall. This study explored whether and how specific fibrillin-1-regulated miRNAs mediate inflammatory cytokine expression and elastic laminae degradation in TAA. miRNA expression profiling at early and late TAA stages using a severe Marfan mouse model (Fbn1mgR/mgR) revealed a spectrum of differentially regulated miRNAs. Bioinformatic analyses predicted the involvement of these miRNAs in inflammatory and extracellular matrix related pathways. Complementing mRNA microarray demonstrated the upregulation of multiple pro-inflammatory cytokines and matrix metalloproteases. Correlation analyses between the altered miRNAs and mRNAs present miR-122, the most downregulated miRNAs in the TAA tissue of Fbn1mgR/mgR, to be a core regulatory miRNA to pro-inflammatory cytokines, Ccl2 and Il1b, which were upregulated in the TAA tissues. At 10 weeks, the number of differentially regulated miRNAs (>2-fold) increased to 129 with 5 down- and 124 upregulated miRNAs

2022-05-21 | GSE199283 | GEO

mRNA microarray of aortae from 10-week male Fbn1mgR/mgR and wild-type mice [10-week_mRNA]

Project description:Thoracic aortic aneurysms (TAA) in Marfan syndrome, caused by fibrillin-1 mutations, are characterized by elevated cytokines and fragmentated elastic laminae in the aortic wall. This study explored whether and how specific fibrillin-1-regulated miRNAs mediate inflammatory cytokine expression and elastic laminae degradation in TAA. miRNA expression profiling at early and late TAA stages using a severe Marfan mouse model (Fbn1mgR/mgR) revealed a spectrum of differentially regulated miRNAs. Bioinformatic analyses predicted the involvement of these miRNAs in inflammatory and extracellular matrix related pathways. Complementing mRNA microarray demonstrated the upregulation of multiple pro-inflammatory cytokines and matrix metalloproteases. Correlation analyses between the altered miRNAs and mRNAs present miR-122, the most downregulated miRNAs in the TAA tissue of Fbn1mgR/mgR, to be a core regulatory miRNA to pro-inflammatory cytokines, Ccl2 and Il1b, which were upregulated in the TAA tissues. A total of 471 mRNAs were up-regulated (green) and 253 downregulated (red) more than 2-fold (p<0.05) in the aneurysmal versus the wild-type tissues.

2022-05-21 | GSE199284 | GEO

Ang II type 1a receptor in Marfan syndrome

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Dissecting aortic aneurysm in Marfan syndrome is associated with losartan-sensitive transcriptomic modulation of aortic cells

Project description:To improve our limited understanding of the pathogenesis of thoracic aortic aneurysm (TAA) leading to acute aortic dissection, we used single-cell RNA sequencing to profile disease-relevant transcriptomic changes of aortic cell populations in a well-characterized mouse model of the most commonly diagnosed form of Marfan syndrome (MFS). As result,MFSmod were identified only in the aorta of Fbn1mgR/mgR mice. In situ hybridizations of diagnostic transcripts located MFSmod cells to the intima of Fbn1mgR/mgR aortas. Consistent with angiotensin II type I receptor (At1r) contribution to TAA development, MFSmod cells were absent in the aorta of Fbn1mgR/mgR mice treated with the At1r antagonist losartan. Altogether, our findings indicate that a discrete dynamic alteration of aortic cell identity is associated with dissecting TAA in MFS mice and increased risk of aortic dissection in MFS patients.

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Marfan syndrome in mice

Project description:Comparison of whole genome expression profiles to characterize gene expression during development of thoracic aortic aneurysm in fibrillin-1 hypomorphic mice (Fbn1mgR/mgR).

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The RGD sequence in fibrillin-1 regulates mRNA expression

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2018-12-10 | GSE82079 | GEO

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Project description:Thoracic aortic aneurysms have a higher prevalence in male patients compared to female patients. Marfan syndrome causes a hereditary form of TAA with dilation of the aortic root. Male patients with Marfan syndrome are more likely than women to have aortic dilation and dissection and mouse models of Marfan syndrome demonstrate larger aortic roots in males compared to females even after adjustment for body size. Similar sex disparities are present in patients and models of abdominal aortic aneurysms where estrogen has been demonstrated to attenuate aneurysm formation perhaps through anti-inflammatory mechanisms. In this study we demonstrate the effects of estrogen on aortic dilation and rupture in a Marfan mouse model and we investigate if these effects operate through suppression of complement components of the immune system.

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