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KSHV Requires vCyc to Overcome Replicative Senescence in Primary Human Lymphatic Endothelial Cells

ABSTRACT: KSHV Requires vCyc to Overcome Replicative Senescence in Primary Human Lymphatic Endothelial Cells

PROVIDER: PRJNA562924 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10043644_1.fastq.gz	Fastqsanger.gz
	SRR10043644_2.fastq.gz	Fastqsanger.gz
	SRR10043645_1.fastq.gz	Fastqsanger.gz
	SRR10043645_2.fastq.gz	Fastqsanger.gz
	SRR10043646_1.fastq.gz	Fastqsanger.gz

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KSHV Requires vCyc to Overcome Replicative Senescence in Primary Human Lymphatic Endothelial Cells

Project description:We performed high throughput RNA-sequencing on KSHV-infected blood and lymphatic HMVECs at 48hpi as well as WTKSHV- or KSHVDvcyc-infected lymphatic HMVECS at 1wpi to identify differences in gene expression induced by KSHV in these two cell types and gene expression changes that require the KSHV latent gene vcyclin.

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KSHV requires vCyclin to overcome replicative senescence in primary human lymphatic endothelial cells.

Project description:Kaposi's Sarcoma Herpesvirus (KSHV) is present in the main tumor cells of Kaposi's Sarcoma (KS), the spindle cells, which are of endothelial origin. KSHV is also associated with two B-cell lymphomas, Primary Effusion Lymphoma (PEL) and Multicentric Castleman's Disease. In KS and PEL, KSHV is primarily latent in the infected cells, expressing only a few genes. Although KSHV infection is required for KS and PEL, it is unclear how latent gene expression contributes to their formation. Proliferation of cancer cells occurs despite multiple checkpoints intended to prevent dysregulated cell growth. The first of these checkpoints, caused by shortening of telomeres, results in replicative senescence, where cells are metabolically active, but no longer divide. We found that human dermal lymphatic endothelial cells (LECs) are more susceptible to KSHV infection than their blood-specific endothelial cell counterparts and maintain KSHV latency to higher levels during passage. Importantly, KSHV infection of human LECs but not human BECs promotes their continued proliferation beyond this first checkpoint of replicative senescence. The latently expressed viral cyclin homolog is essential for KSHV-induced bypass of senescence in LECs. These data suggest that LECs may be an important reservoir for KSHV infection and may play a role during KS tumor development and that the viral cyclin is a critical oncogene for this process.

| S-EPMC7326280 | biostudies-literature

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Project description:Kaposi sarcoma is the most common cancer in AIDS patients and is typified by red skin lesions. The disease is caused by the KSHV virus (HHV8) and is recognizable by its distinctive red skin lesions. The lesions are KSHV infected spindle cells, most commonly the lymphatic endothelial and blood vessel endothelial cells (LEC and BEC), plus surrounding stroma. The effects of KSHV infection of LECs were assayed using Affymetrix hgu133plus2 chips at 6 and 72 hours post infection. There were n=4 each of lymphatic endothelial cells (LEC) following 6 hours of culture, LEC following 6 hours post KSHV infection, LEC following 72 hours of culture, and LEC following 72 hours post KSHV infection.

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Lymphatic endothelial cells (LEC) transfected with the KSHV microRNA cluster

Project description:Kaposi sarcoma is the most common cancer in AIDS patients and is typified by red skin lesions. The disease is caused by the KSHV virus (HHV8) and is recognisable by its distinctive red skin lesions. The lesions are KSHV-infected spindle cells, most commonly the lymphatic endothelial and blood vessel endothelial cells (LEC and BEC), plus surrounding stroma. The KSHV virus expresses multiple microRNA in a single cluster. Here we test the effects of this KSHV microRNA cluster in LEC cells using Affymetrix hgu133plus2 chips.

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Project description:Kaposi sarcoma is the most common cancer in AIDS patients and is typified by red skin lesions. The disease is caused by the KSHV virus (HHV8) and is recognisable by its distinctive red skin lesions. The lesions are KSHV-infected spindle cells, most commonly the lymphatic endothelial and blood vessel endothelial cells (LEC and BEC), plus surrounding stroma. The KSHV virus expresses multiple microRNA in a single cluster. Here we test the effects of this KSHV microRNA cluster in LEC cells using Affymetrix hgu133plus2 chips. Experiment Overall Design: There are n=3 of: 1. LEC control with empty vector pSIN-MCS (LEC), 2. LEC transfected with the same vector containing the KSHV microRNA cluster.

2009-10-10 | E-GEOD-16355 | biostudies-arrayexpress

The profile of cellular and KSHV microRNAs in KSHV infected lymphatic endothelial cells (6 and 72 hours post infection)

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2009-09-30 | E-GEOD-16357 | biostudies-arrayexpress

KSHV infection of Endothelial Colony Forming Cells

Project description:We performed high throughput RNA-sequencing on KSHV-infected blood and lymphatic Endothelial Colony-Forming Cells at 48hpi to identify differences in gene expression induced by KSHV in these two cell types.

2022-11-28 | GSE207589 | GEO

KSHV vIRF3 promotes angiogenesis of lymphatic endothelial cells (LECs)

Project description:Herein, we report viral interferon regulatory factor 3 (vIRF3) as a pro-angiogenic factor together with HDAC5 that coordinates with LEC transcriptome, thus resulting in hyper-sprouting formation and ultimately leading to abnormal lymphangiogenesis. Overexpression of vIRF3 in LECs but not blood endothelial cells (BECs) exhibited a unique KSHV-associated angiogenic effect, evidenced by elongated spindle shape, sprouting, and tube formation. Furthermore, using vIRF3 knockout recombinant KSHV, we confirmed that vIRF3 is a critical factor of KSHV-mediated lymphangiogenesis in primary LECs.

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