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Transcription profiling of human primary dermal endothelial cells infects with Kaposis sarcoma-associated herpes virus vs. controls

ABSTRACT: Primary human dermal endothelial cells were infected or NOT infected with isolated Kaposi's sarcoma associated herpes virus for 7 days. Total RNA was isolated using Trireagent and subjected to microarray.

ORGANISM(S): Homo sapiens

SUBMITTER: Jay Woo Shin

PROVIDER: E-GEOD-1377 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Lymphatic reprogramming of blood vascular endothelium by Kaposi sarcoma-associated herpesvirus.

Hong Young-Kwon YK Foreman Kimberly K Shin Jay W JW Hirakawa Satoshi S Curry Christine L CL Sage David R DR Libermann Towia T Dezube Bruce J BJ Fingeroth Joyce D JD Detmar Michael M

Nature genetics 20040627 7

Kaposi sarcoma is considered a neoplasm of lymphatic endothelium infected with Kaposi sarcoma-associated herpesvirus. It is characterized by the expression of lymphatic lineage-specific genes by Kaposi sarcoma tumor cells. Here we show that infection of differentiated blood vascular endothelial cells with Kaposi sarcoma-associated herpesvirus leads to their lymphatic reprogramming; induction of approximately 70% of the main lymphatic lineage-specific genes, including PROX1, a master regulator of ...[more]

PMID: 15220917

Similar Datasets

Kaposi's sarcoma-associated herpes virus

Project description:Primary human dermal endothelial cells were infected or NOT infected with isolated Kaposi's sarcoma associated herpes virus for 7 days. Total RNA was isolated using Trireagent and subjected to microarray. Keywords: other

2004-05-08 | GSE1377 | GEO

Homo sapiens

Project description:Kaposi's sarcoma-associated herpes virus

| PRJNA90025 | ENA

Transcription profiling of Kaposi sarcoma, normal skin and primary cells

Project description:Identification of the relationships of Kaposi sarcoma (KS), normal skin to various cell cultures. The effects of KS herpes virus, the infectious cause of KS, on infected endothelial cells are also investigated.

2004-08-01 | E-MEXP-66 | biostudies-arrayexpress

Metabolic reprogramming of Kaposi’s sarcoma associated herpes virus infected B-cells in hypoxia

Project description:Metabolic reprogramming of Kaposi’s sarcoma associated herpes virus infected B-cells in hypoxia

| PRJNA471994 | ENA

K1 and K15 of Kaposi sarcoma-associated herpes virus are functional homologues of latent membrane protein 2A of Epstein-Barr virus

2014-04-01 | GSE53914 | GEO

K1 and K15 of Kaposi sarcoma-associated herpes virus are functional homologues of latent membrane protein 2A of Epstein-Barr virus

Project description:LMP2A of Epstein-Barr virus is a receptor that mimics an activated B cell receptor, BCR. K1 and K15, related receptors of Kaposi sarcoma-associated herpes virus, KSHV, are expressed in virus-associated tumors but their functions are less obvious. We addressed this uncertainty with mutant EBVs encoding the KSHV genes K1 or K15 in lieu of LMP2A and infected primary human B cells with them. K1 and K15 encoded proteins appear to have noncomplementing redundant functions in this model but our findings suggest that both KSHV proteins can replace LMP2AM-bM-^@M-^Ys key activities contributing to the survival, activation and proliferation of B cells. We infected unsorted B cells with the four virus stocks, wt EBV, K1 EBV, K15 EBV or M-NM-^TLMP2A EBV, adjusted to yield similar rates of EBV-activated and growth transformed B cells. Eight days p.i. activated B cells in the lymphocyte gate were collected by FACS sorting and their RNAs analyzed with the aid of the Affymetrix GeneChip Human Gene 1.0 ST Array covering the whole transcriptome of approx. 29,000 annotated human genes. B cell preparations from four different donors were infected and analyzed accordingly.

2014-04-01 | E-GEOD-53914 | biostudies-arrayexpress

Unveiling the Role of KSHV-Infected Human Mesenchymal Stem Cells in Kaposi's Sarcoma Initiation

Project description:Kaposi's sarcoma (KS) may derive from Kaposi's Sarcoma Herpesvirus (KSHV)-infected human Mesenchymal Stem Cells (hMSCs) that migrate to sites characterized by inflammation and angiogenesis, promoting the initiation of KS. By analyzing the RNA sequences of KSHV-infected primary hMSCs, we have identified specific cell subpopulations, mechanisms, and conditions involved in the initial stages of KSHV-induced transformation and reprogramming of hMSCs into KS progenitor cells. Under pro-angiogenic environmental conditions, KSHV can reprogram hMSCs to exhibit gene expression profiles more similar to KS tumors, activating cell cycle progression, cytokine signaling pathways, and endothelial differentiation indicating the involvement of KSHV infection in inducing the Mesenchymal-to-Endothelial (MEndT) transition of hMSCs. This finding underscores the significance of this condition in facilitating KSHV-induced proliferation and reprogramming of hMSCs towards MEndT and closer to KS gene expression profiles, providing further evidence of these cell subpopulations as precursors of KS cells that thrive in a pro-angiogenic environment.

2024-07-08 | GSE260925 | GEO

Transcription profiling of mouse hemangioendothelioma cell lines EOMA and Py-4-1 models for kaposiform hemangioendotheliomas

Project description:Kaposiâs sarcoma (KS) is the most frequently occurring malignant tumor in patients infected with the human immunodeficiency virus. Recent studies have revealed that infection of vascular endothelial cells with Kaposi's sarcoma-associated herpes virus in vitro results in a lymphatic re-programming of these cells, with potent induction of the lymphatic marker genes podoplanin and VEGFR-3 which is mediated by upregulation of the transcription factor Prox1. However, the potential effects of Prox1 expression on the biology of KS and, in particular, on the aggressive and invasive behavior of KS tumors in vivo have remained unknown. We stably expressed Prox1 cDNA in the two mouse hemangioendothelioma cell lines EOMA and Py-4-1, well-established murine models for kaposiform hemangioendothelioma. Surprisingly, we found that expression of Prox1 was sufficient to induce a more aggressive behavior of tumors growing in syngenic mice, leading to enhanced local invasion into the muscular layer and to cellular anaplasia. This enhanced malignant phenotype was associated with upregulation of several genes involved in proteolysis, cytoskeletal reorganisation and migration. Together, these results indicate that Prox1 plays an important, previously unanticipated role in mediating the aggressive behavior of vascular neoplasms such as Kaposi's sarcoma. Experiment Overall Design: Total cellular RNA was extracted from two stably Prox1-expressing Py-4-1 cell clones and from two control-transfected Py-4-1 cell clones.

2008-10-18 | E-GEOD-8171 | biostudies-arrayexpress

Epigenetic reprogramming of Kaposi’s sarcoma-associated herpesvirus during hypoxic reactivation

Project description:Chromatin Immuno-precipitaion sequencing was performed using H3-Ac, H3K4Me3, H3K9Me3, H3K27Me3, LANA, RTA and DNA Polymerase 1 alpha antibodies to investigate its enrichment on Kaposi's sarcoma associated herpesvirus (KSHV) genome in BC3 cells under normoxic or hypoxic conditions

2022-08-15 | GSE202670 | GEO

Prox-1 promotes invasion of kaposiform hemangioendotheliomas

Project description:Kaposi’s sarcoma (KS) is the most frequently occurring malignant tumor in patients infected with the human immunodeficiency virus. Recent studies have revealed that infection of vascular endothelial cells with Kaposi's sarcoma-associated herpes virus in vitro results in a lymphatic re-programming of these cells, with potent induction of the lymphatic marker genes podoplanin and VEGFR-3 which is mediated by upregulation of the transcription factor Prox1. However, the potential effects of Prox1 expression on the biology of KS and, in particular, on the aggressive and invasive behavior of KS tumors in vivo have remained unknown. We stably expressed Prox1 cDNA in the two mouse hemangioendothelioma cell lines EOMA and Py-4-1, well-established murine models for kaposiform hemangioendothelioma. Surprisingly, we found that expression of Prox1 was sufficient to induce a more aggressive behavior of tumors growing in syngenic mice, leading to enhanced local invasion into the muscular layer and to cellular anaplasia. This enhanced malignant phenotype was associated with upregulation of several genes involved in proteolysis, cytoskeletal reorganisation and migration. Together, these results indicate that Prox1 plays an important, previously unanticipated role in mediating the aggressive behavior of vascular neoplasms such as Kaposi's sarcoma. Keywords: Overexpression of Prox1 in Py-4-1 cell line.

2008-08-04 | GSE8171 | GEO

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