ArticleJournal of visualized experiments : JoVE2010
Identifying dysregulated genes induced by Kaposi's sarcoma-associated herpesvirus (KSHV).
Article in Journal of visualized experiments : JoVE, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 6 citations in OpenAlex.
- Galectin-3 as a Potential Prognostic Biomarker for COVID-19 Disease: A Case-Control Study.Cureus · 2022Article
- Mesangial cells, specialized renal pericytes and cytomegalovirus infectivity: Implications for HCMV pathology in the glomerular vascular unit and post-transplant renal disease.Journal of translational science · 2019Article
- Placental pericytes and cytomegalovirus infectivity: Implications for HCMV placental pathology and congenital disease.American journal of reproductive immunology (New York, N.Y. : 1989) · 2017Article
- Retinal pericytes and cytomegalovirus infectivity: implications for HCMV-induced retinopathy and congenital ocular disease.Journal of neuroinflammation · 2015Article
- Infection and upregulation of proinflammatory cytokines in human brain vascular pericytes by human cytomegalovirus.Journal of neuroinflammation · 2012Article
- KSHV Down-regulates Tropoelastin in Both anJournal of oncobiomarkersArticle
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Currently KS is the most predominant HIV/AIDS related malignancy in Southern Africa and hence the world. It is characterized as an angioproliferative tumor of vascular endothelial cells and produces rare B cell lymphoproliferative diseases in the form of pleural effusion lymphomas (PEL) and some forms of multicentric Castleman's disease. Only 1-5% of cells in KS lesions actively support lytic replication of Kaposi's sarcoma-associated herpesvirus (KSHV), the etiological agent associated with KS, and it is clear that cellular factors must interact with viral factors in the process of oncogenesis and tumor progression. Identifying novel host-factor determinants which contribute to KS pathology is essential for developing prognostic markers for tumor progression and metastasis as well as for developing novel therapeutics for the treatment of KS. The accompanying video details the methods we use to identify host cell gene expression programs altered in dermal microvascular endothelial cells (DMVEC) after KSHV infection and in KS tumor tissue. Once dysregulated genes are identified by microarray analysis, changes in protein expression are confirmed by immunoblot and dual labeled immunofluorescence. Changes in transcriptional expression of dysregulated genes are confirmed in vitro by quantitative real-time polymerase chain reaction (qRT-PCR). Validation of in vitro findings using archival KS tumor tissue is also performed by dual labeled immunochemistry and tissue microarrays. Our approach to identifying dysregulated genes in the KS tumor tissue microenvironment will allow the development of in vitro and subsequently in vivo model systems for discovery and evaluation of potential novel therapeutic for the treatment of KS.
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