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Specialized post-arterial capillaries facilitate adult bone remodeling

ABSTRACT: Specialized post-arterial capillaries facilitate adult bone remodeling

PROVIDER: PRJNA1000440 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25473566_1.fastq.gz	Fastqsanger.gz
	SRR25473566_2.fastq.gz	Fastqsanger.gz
	SRR25473567_1.fastq.gz	Fastqsanger.gz
	SRR25473567_2.fastq.gz	Fastqsanger.gz
	SRR25473568_1.fastq.gz	Fastqsanger.gz

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Specialized post-arterial capillaries for adult bone remodeling [BoneEC]

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Specialized post-arterial capillaries facilitate adult bone remodeling

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Specialized post-arterial capillaries for adult bone remodeling [Dach1OE]

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Genetic ablation of TonEBP/NFAT5 in smooth muscle cells inhibits arterial remodeling

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Caveolin1 Deficiency: A Type I Endothelial Interferonopathy Associated with Pulmonary Arterial Hypertension

Project description:CAV1 loss-of-function mutations have been associated with the development of pulmonary arterial hypertension (PAH). CAV1 is an integral component of endothelial caveolae, specialized lipid rafts that attach to the actin cytoskeleton and modulate receptor/signal transduction coupling. CAV1 loss in pulmonary artery endothelial cells produced a proliferative, hypermigratory cellular phenotype with a disrupted cytoskeletal architecture, mirroring known features of PAH pathobiology. Gene expression on Human Pulmonary Arterial Endothelial Cells (PAECs) transfected with non-targeting siRNA control pool or siRNA (ON-TARGET plus CAV1) in the presence or absence of TNF-alpha was evaluated

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Bone Marrow-Derived NGFR-Positive Dendritic Cells Regulate Arterial Remodeling

Project description:It has been proposed that bone marrow contributes to the pathogenesis of arteriosclerosis. Nerve growth factor receptor (NGFR) is expressed in bone marrow stromal cells; it is also present in peripheral blood and ischemic coronary arteries. We hypothesized that bone marrow-derived NGFR-positive (NGFR+) cells regulate arterial remodeling. We found that human NGFR+ mononuclear cells (MNCs) in peripheral blood expressed markers for plasmacytoid dendritic cells (DCs) and were susceptible to apoptosis in response to proNGF secreted by activated arterial smooth muscle cells (SMCs). Bone marrow-specific depletion of NGFR+ cells increased neointimal formation following arterial ligation in mice. Bone marrow-derived NGFR+ cells accumulated in the neointima and underwent apoptosis. In contrast, in a bone marrow-specific NGFR-knockout model, SMCs occupied the neointima with augmented proliferation. NGFR+ cells in the neointima promoted mannose receptor C-type 1-positive antiinflammatory macrophage accumulation and secreted antiinflammatory IL-10, thereby inhibiting SMC proliferation in the neointima. In patients with acute coronary syndrome (ACS), NGFR+ peripheral MNCs increased after ACS onset. Multiple linear regression analysis showed that an insufficient increase in NGFR+ peripheral MNCs in ACS was an adjusted independent risk factor for 9-month intimal progression of a nontargeted lesion. Taken together, these observations imply that bone marrow-derived NGFR+ DCs are suppressors of arteriosclerosis.

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Evaluating the transcriptional regulators of arterial gene expression via a catalogue of characterized arterial enhancers

Project description:The establishment and growth of the arterial endothelium requires the coordinated expression of numerous genes. However, regulation of this process is not yet fully understood. Here, we combined in silico analysis with transgenic models to characterize arterial-specific enhancers associated with eight key arterial identity genes (Acvrl1/Alk1, Cxcr4, Cxcl12, Efnb2, Gja4/Cx37, Gja5/Cx40, Nrp1 and Unc5b). Next, to elucidate the regulatory pathways upstream of arterial gene transcription, we investigated the transcription factors binding each arterial enhancer compared to a similar assessment of non-arterial endothelial enhancers. These results found that binding of SOXF and ETS factors was a common occurrence at both arterial and pan-endothelial enhancers, suggesting neither are sufficient to direct arterial specificity. Conversely, FOX motifs independent of ETS motifs were over-represented at arterial enhancers. Further, MEF2 and RBPJ binding was enriched but not ubiquitous at arterial enhancers, potentially marking an arterial sub-set. Lastly, there was no shared or arterial-specific signature for WNT-associated TCF/LEF, TGFβ/BMP-associated SMAD1/5 and SMAD2/3, shear stress-associated KLF4 or venous-enriched NR2F2. This cohort of well characterized and in vivo-verified enhancers can now provide a platform for future studies into the interaction of different transcriptional and signalling pathways with arterial gene expression.

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