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RNA sequencing of secondary heart field- and cardiac neural crest-derived cells from murine aortas

ABSTRACT: To better understand the role of lineage in smooth muscle cell heterogenity along the length of the aorta, we performed bulk RNA-sequencing transcriptomic analysis on secondary heart field (SHF)-derived and cardiac neural crest derived (CNC)-derived sorted cells from murine aortas.

ORGANISM(S): Mus musculus

PROVIDER: GSE189544 | GEO | 2022/03/14

REPOSITORIES: GEO

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Expression profile in Plk1(+/-) aortas

Project description:Transcriptional profiling of mouse aortas comparing control wild-type animals with aortas from three different Plk1(+/-) mice. Goal was to determine the effects of Plk1 haploinsufficiency in aorta expression profiles.

2017-07-01 | GSE85199 | GEO

RNA sequencing of secondary heart field- and cardiac neural crest-derived cells from murine aortas

Project description:RNA sequencing of secondary heart field- and cardiac neural crest-derived cells from murine aortas

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Gene expression profiling in thoracic aortas of 8 week and 16 week ApoE knockout mice on a western type diet

Project description:Identification of novel pathways in the development of atherosclerosis. Here, we are looking at changes in gene expression that occur in the aorta with the development of atherosclerosis Analysis used RNA from thoracic aortas from chow fed ApoE knockout mice as control samples for comparison to the experimental samples from 8 week and 16 week ApoE knockout mice fed a western-type diet

2015-02-03 | E-GEOD-65494 | biostudies-arrayexpress

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Project description:Seq data of aortas

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ECM characterization of aortas from Adamts5+/+ and Adamts5∆cat AngII-treated mice by LC-MS/MS

Project description:Objective - Thoracic aortic aneurysm (TAA), a degenerative disease of the aortic wall, is accompanied by changes in the structure and composition of the aortic extracellular matrix (ECM). The ADAMTS (a disintegrin and metalloproteinase with thrombospondin motifs) family has recently been implicated in TAA formation. This study aimed to investigate the contribution of ADAMTS-5 to TAA development. Approach and Results - A model of aortic dilatation by angiotensin II (AngII) infusion was adopted in mice lacking the catalytic domain of ADAMTS-5 (Adamts5Δcat). Adamts5Δcat mice showed an attenuated rise in blood pressure whilst displaying increased dilatation of the ascending aorta. Interestingly, a comparison of the aortic ECM from AngII-treated wildtype and Adamts5Δcat mice revealed versican as the most up-regulated ECM protein in Adamts5Δcat mice. This was accompanied by a marked reduction of ADAMTS-specific versican cleavage products (versikine) and a decrease of low-density lipoprotein-related protein 1 (LRP1). Silencing LRP1 expression in human aortic smooth muscle cells reduced the expression of ADAMTS5, attenuated the generation of versikine but increased soluble ADAMTS-1. A similar increase in ADAMTS-1 was observed in aortas of AngII-treated Adamts5Δcat mice, but was not sufficient to maintain versican processing and prevent aortic dilatation. Conclusions - Our results support the emerging role of ADAMTS proteases in TAA. ADAMTS-5 rather than ADAMTS-1 is the key protease for versican regulation in murine aortas. Further studies are needed to define the ECM substrates of the different ADAMTS proteases and their contribution to TAA formation.

2018-05-08 | PXD009410 | Pride

Dlx5 signaling cascade controls cranial neural crest and myoblast interaction during oropharyngeal patterning and development

Project description:Craniofacial development depends on cell-cell interactions, coordinated cellular movement and differentiation under the control of regulatory gene networks, which include the distal-less (Dlx) gene family. However, the functional significance of Dlx5 in patterning the oropharyngeal region has remained unknown. Here we show that loss of Dlx5 leads to a shortened soft palate and an absence of the levator veli palatini, palatopharyngeus, and palatoglossus muscles that are derived from the 4th pharyngeal arch (PA), but the tensor veli palatini, derived from the 1st PA, is unaffected. Dlx5-positive cranial neural crest (CNC) cells are in direct contact with myoblasts derived from the pharyngeal mesoderm, and Dlx5 disruption leads to altered proliferation and apoptosis of CNC and muscle progenitor cells. Moreover, the FGF10 pathway is downregulated in Dlx5-/- mice, and activation of FGF10 signaling rescues CNC cell proliferation and myogenic differentiation in these mutant mice. Collectively, our results indicate that Dlx5 plays critical roles in patterning of the oropharyngeal region and development of muscles derived from the 4th PA mesoderm in the soft palate, likely via interactions between CNC-derived and myogenic progenitor cells.

2017-10-15 | GSE104163 | GEO

Pbx4 limits vertebrate heart size and promotes pharyngeal arch artery development through partitioning progenitor fates within the second heart field and restricting proliferation

Project description:Development of the vertebrate heart requires the appropriate integration of temporally-distinct differentiating progenitor populations. While factors that promote accrual of later-differentiating second heart field (SHF)-derived cells to the outflow tract (OFT) have been intensively investigated, few signals are understood that specifically restrict the size of the vertebrate OFT. Here, we show that improper specification and proliferation of SHF progenitors in zebrafish lazarus (lzr) mutants, which lack the transcription factor Pbx4, produces enlarged hearts with a specific increase in ventricular cardiomyocytes and smooth muscle cells within the OFT. Specifically, optogenetic lineage-tracing demonstrates Pbx4 initially promotes the proper partitioning of the SHF into anterior progenitors, which contribute to the OFT, and adjacent endothelial cell progenitors, which contribute to posterior pharyngeal arch arteries. Subsequently, Pbx4 also limits the size of the SHF through repressing SHF progenitor proliferation. Single-cell RNA sequencing of nkx2.5+ cells revealed that the enlarged SHF progenitor population within Pbx4-deficient embryos assimilates characteristics of normally distinct proliferative and more anterior, differentiated cardiomyocyte populations. Therefore, the generation of proper OFT size and great arteries in vertebrates requires Pbx-dependent stratification of unique progenitor differentiation states to facilitate homeotic-like transformations and limit progenitor production within the SHF.

2020-02-19 | GSE126647 | GEO

Gene expression changes in aortas of db/db versus control db/+ mice

Project description:To determine effects of hyperglycemia and insulin resistance on arterial wall biology, aortic gene expression profiles were generated using aortas from Lepr^db/db and their respective nondiabetic Lepr^db/+ controls. Keywords: Chip Experiment was done in triplicate with three independent pool of test Lepr^db/db and control Lepr^db/+ pooled samples. For RNA isolation aortas were striped of adventitia and periaortic fat. RNA from six aortas was pooled for the synthesis of probe for affymetrix array analysis.

2011-12-23 | E-GEOD-6733 | biostudies-arrayexpress

HDAC1-mediated repression of the retinoic acid-responsive gene ripply3 promotes second heart field development

Project description:Coordinated transcriptional and epigenetic mechanisms that direct development of the later differentiating second heart field (SHF) progenitors remain largely unknown. Here, we show that a novel zebrafish histone deacetylase 1 (hdac1) mutant allele cardiac really gone (crg) has a deficit of ventricular CMs and smooth muscle within the outflow tract (OFT) due to both cell and non-cell autonomous loss in SHF progenitor proliferation. Cyp26-deficient embryos, which have increased retinoic acid (RA) levels, have similar defects in SHF-derived OFT development. We found that nkx2.5+ progenitors from hdac1 and cyp26-deficient embryos have ectopic expression of ripply3, a transcriptional co-repressor of T-box transcription factors that is normally restricted to the posterior pharyngeal endoderm. Furthermore, the ripply3 expression domain is expanded anteriorly into the posterior nkx2.5+ progenitor domain in crg mutants. Importantly, excess ripply3 is sufficient to repress VC development, while genetic depletion of Ripply3 and Tbx1 in crg mutants can partially restore VC number. We find that in crg mutants the epigenetic signature at RA response elements (RAREs) that can associate with Hdac1 and RA receptors (RARs) becomes indicative of transcriptional activation. Our study highlights that transcriptional repression via the epigenetic regulator Hdac1 facilitates OFT development through directly preventing expression of the RA-responsive gene ripply3 within SHF progenitors.

2019-05-11 | GSE126747 | GEO

MicroRNA-29 in Aortic Dilation: Implications for Aneurysm Formation

Project description:We compared the aorta of 6-weeks-old mice (young) with 18-months-old mice (old). Using the publicly available tools Sylamer and DIANA-mirExTra, we identified an enrichment for miR-29 binding sites in the 3'UTR of genes downregulated in the aged aortas. We subsequently showed that inhibition of miR-29 in aged mice prevented dilation of the aorta. aortas of 6 week old and 18 month old mice

2011-10-13 | E-GEOD-32937 | biostudies-arrayexpress

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