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In JoVE (1)
Other Publications (5)
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Articles by Shane McAllister in JoVE
Epstein-बर्र वायरस विकास तब्दील Lymphoblastoid सेल लाइन्स की स्थापना
Joyce Hui-Yuen1,2, Shane McAllister1,2, Siva Koganti2, Erik Hill2, Sumita Bhaduri-McIntosh1,2,3,4
1Stony Brook Children's Hospital, State University of New York at Stony Brook, 2Department of Pediatrics, State University of New York at Stony Brook, 3Department of Molecular Genetics, State University of New York at Stony Brook, 4Department of Microbiology, State University of New York at Stony Brook
हम बदल बी सेल Epstein-बर्र वायरस का उपयोग लाइनों पैदा करने के लिए एक विधि का वर्णन. हम भी एक उपन्यास परख है कि बी कोशिकाओं को संक्रमण के बाद तीन दिन के रूप में में जल्दी के रूप में परिवर्तन से गुजरना करने के लिए किस्मत की पहचान कर सकते हैं वर्णन.
Other articles by Shane McAllister on PubMed
Kaposi Sarcoma-associated Herpesvirus (KSHV) Induces Heme Oxygenase-1 Expression and Activity in KSHV-infected Endothelial Cells
Blood. May, 2004 | Pubmed ID: 14726403
Kaposi sarcoma (KS) is the most common AIDS-associated malignancy and is characterized by angiogenesis and the presence of spindle cells. Kaposi sarcoma-associated herpesvirus (KSHV) is consistently associated with all clinical forms of KS, and in vitro infection of dermal microvascular endothelial cells (DMVECs) with KSHV recapitulates many of the features of KS, including transformation, spindle cell proliferation, and angiogenesis. To study the molecular mechanisms of KSHV pathogenesis, we compared the protein expression profiles of KSHV-infected and uninfected DMVECs. This comparison revealed that heme oxygenase-1 (HO-1), the inducible enzyme responsible for the rate-limiting step in heme catabolism, was up-regulated in infected endothelial cells. Recent evidence suggests that the products of heme catabolism have important roles in endothelial cell biology, including apoptosis and angiogenesis. Here we show that HO-1 mRNA and protein are up-regulated in KSHV-infected cultures. Comparison of oral and cutaneous AIDS-KS tissues with normal tissues revealed that HO-1 mRNA and protein were also up-regulated in vivo. Increased HO-1 enzymatic activity in vitro enhanced proliferation of KSHV-infected DMVECs in the presence of free heme. Treatment with the HO-1 inhibitor chromium mesoporphyrin IX abolished heme-induced proliferation. These data suggest that HO-1 is a potential therapeutic target for KS that warrants further study.
Increased Efficiency of Phorbol Ester-induced Lytic Reactivation of Kaposi's Sarcoma-associated Herpesvirus During S Phase
Journal of Virology. Feb, 2005 | Pubmed ID: 15681463
Expression of Kaposi's sarcoma-associated herpesvirus (KSHV) lytic genes is thought to be essential for the establishment and progression of KSHV-induced diseases. The inefficiency of lytic reactivation in various in vitro systems hampers the study of lytic genes in the context of whole virus. We report here increased expression of KSHV lytic genes and increased release of progeny virus when synchronized cultures of body cavity-based lymphoma-1 cells are treated with a phorbol ester during S phase of the cell cycle.
Novel Cellular Genes Essential for Transformation of Endothelial Cells by Kaposi's Sarcoma-associated Herpesvirus
Cancer Research. Jun, 2005 | Pubmed ID: 15958552
Kaposi's sarcoma-associated herpesvirus (KSHV) is involved in the development of lymphoproliferative diseases and Kaposi's sarcoma. The oncogenicity of this virus is reflected in vitro by its ability to transform B cells and endothelial cells. Infection of dermal microvascular endothelial cells (DMVEC) transforms the cells from a cobblestone-like monolayer to foci-forming spindle cells. This transformation is accompanied by dramatic changes in the cellular transcriptome. Known oncogenes, such as c-Kit, are among the KSHV-induced host genes. We previously showed that c-Kit is an essential cellular component of the KSHV-mediated transformation of DMVEC. Here, we test the hypothesis that the transformation process can be used to discover novel oncogenes. When expression of a panel of KSHV-induced cellular transcripts was inhibited with antisense oligomers, we observed inhibition of DMVEC proliferation and foci formation using antisense molecules to RDC1 and Neuritin. We further showed that transformation of KSHV-infected DMVEC was inhibited by small interfering RNA directed at RDC1 or Neuritin. Ectopic expression of Neuritin in NIH 3T3 cells resulted in changes in cell morphology and anchorage-independent growth, whereas RDC1 ectopic expression significantly increased cell proliferation. In addition, both RDC1- and Neuritin-expressing cells formed tumors in nude mice. RDC1 is an orphan G protein-coupled receptor, whereas Neuritin is a growth-promoting protein known to mediate neurite outgrowth. Neither gene has been previously implicated in tumorigenesis. Our data suggest that KSHV-mediated transformation involves exploitation of the hitherto unrealized oncogenic properties of RDC1 and Neuritin.
Pharmacogenomics. Apr, 2005 | Pubmed ID: 16013955
Kaposi's sarcoma (KS) is a multifocal angioproliferative disorder affecting the skin, mucosa and viscera of individuals infected with human herpesvirus-8 (HHV-8; also Kaposi's sarcoma-associated herpesvirus [KSHV]). KS is the most common neoplasm in AIDS patients; the clinical outcome of AIDS-KS is significantly improved by highly active antiretroviral therapy (HAART). However, in Africa, where the severest manifestations of KS occur, there is limited access to these and other effective but expensive drugs. Here we present a review of current efforts to identify novel therapeutic targets for the treatment of KS using functional genomics, with recommendations regarding the development of economically feasible treatments for use in Africa.
The American Journal of Pathology. Oct, 2011 | Pubmed ID: 21820995
Interferon (IFN)-γ is present in lesions of patients with Lyme disease and positively correlates with the severity of manifestations. To investigate the role of IFNγ in the development of Lyme carditis, wild-type and IFNγ-deficient C57BL/6 mice were infected with the causative bacterium, Borrelia burgdorferi. Histological analysis revealed no change in the severity of carditis between wild-type and IFNγ-deficient mice at 14, 21, 25, and 28 days after infection. However, a distinct shift in the types of leukocytes within the hearts of IFNγ-deficient mice was observed at 25 days. In the absence of IFNγ, the number of neutrophils in the heart was increased, whereas the number of T lymphocytes was decreased. Bacterial loads within hearts were the same as in wild-type mice. Macrophages secrete chemokines that recruit immune cells, which could contribute to the accumulation of leukocytes in murine Lyme carditis. The ability of IFNγ and B. burgdorferi to activate murine macrophages was examined, and the two stimuli synergistically induced chemoattractants for mononuclear cells (ie, CXCL9, CXCL10, CXCL11, CXCL16, and CCL12) and decreased those for neutrophils (ie, CXCL1, CXCL2, and CXCL3). IFNγ and B. burgdorferi also synergistically enhanced secretion of CXCL9 and CXCL10 by murine cardiac endothelial cells. These results indicate that IFNγ influences the composition of inflammatory infiltrates in Lyme carditis by promoting the accumulation of leukocytes associated with chronic inflammation and suppressing that of cells that typify acute inflammation.