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Effect of hemoglobin or hemin on human pulmonary microvascular endothelial cells

ABSTRACT: Effect of hemoglobin or hemin on human pulmonary microvascular endothelial cells

PROVIDER: PRJNA1027872 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26383606_1.fastq.gz	Fastqsanger.gz
	SRR26383606_2.fastq.gz	Fastqsanger.gz
	SRR26383607_1.fastq.gz	Fastqsanger.gz
	SRR26383607_2.fastq.gz	Fastqsanger.gz
	SRR26383608_1.fastq.gz	Fastqsanger.gz

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Project description:Human herpesvirus-8 (HHV-8) is the causative agent of Kaposiâs sarcoma and is associated with the angioproliferative disorders primary effusion lymphoma (PEL) and multicentric Castlemanâs disease (MCD). We have previously described evidence of HHV-8 infection within the pulmonary vasculature of patients with idiopathic pulmonary arterial hypertension (IPAH). We speculated that viral infection of the pulmonary microvascular endothelial cells could cause the angioproliferative phenotype characteristic of severe pulmonary arterial hypertension (PAH). We now demonstrate the ability of HHV-8 to infect human pulmonary microvascular endothelial cells (HPMVECs) in vitro, confirming both latent and lytic infection. HHV-8 infection of HPMVECs resulted in significant changes of gene expression including alterations of pathways integral to both cellular apoptosis and angiogenesis. This infection also results in alterations of genes integral to the bone morphogenic protein (BMP) pathway, including down regulation of bone morphogenic protein receptor 1a (BMPR1a) and bone morphogenic protein 4 (BMP4). Other genes previously implicated in the development of PAH are also altered in expression by HHV-8 infection. These include increased expression of Interleukin-6 (IL-6) and the matrix metalloproteinases (MMP)-1, MMP-2 and MMP-10. Lastly, cells infected with HHV-8 apoptosis resistant. Infection of pulmonary microvascular endothelial cells with human herepesvirus-8 results in alteration of the BMP pathway as well as an anti-apoptotic phenotype, consistent with the development of plexiform lesions characteristic of pulmonary arterial hypertension. Experiment Overall Design: â¢ Direct comparison of HHV8-infected and mock-infected human pulmonary microvascular endothelial cells. Experiment Overall Design: â¢ Triplicate infection and mock infection samples were prepared. One hybridization per sample, 6 total hybridizations Experiment Overall Design: â¢ Single channel hybridization (no reference).

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Effect of hemoglobin or hemin on human pulmonary microvascular endothelial cells

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