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You searched for +publisher:"Rutgers University" +contributor:("Medina, Daniel"). Showing records 1 – 2 of 2 total matches.

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Rutgers University

1. Vengsarkar, Diana S., 1970-. Adaptation of colon cancer cells to histone deacetylase inhibitors generates cell lines with a non-malignant phenotype.

Degree: MS, Microbiology and Molecular Genetics, 2016, Rutgers University

Histones are subject to various covalent post-translational modifications that can influence specific changes in chromatin structure and levels of transcription. The Polycomb (PcG) and Trithorax (TrxG) group systems are classic epigenetic systems that mediate transcriptional repression and activation, respectively, through mutually-exclusive modifications of histone H3 at lysine 27 (H3K27) in the gene promoter region. The Polycomb Repressive Complex 2 (PRC2) mediates transcriptional silencing by trimethylating H3K27 while TrxG proteins mediate transcriptional activation by acetylating H3K27. Histone deacetylases (HDACs) 1 and 2 are associated with the PRC2 complex and their overexpression has been linked to a variety of cancers. The Rabson Laboratory adapted SW480 colon cancer cells to the pan-HDAC inhibitor vorinostat. Vorinostat-adapted cells (SH80) showed a near elimination of tumorigenicity in tumor xenografts, global changes in mRNA expression, and an upregulation of PRC2 target genes. The overarching goal of this research was to determine which changes were necessary to generate the non-malignant phenotype of SH80. First, we used H3K27 trimethylation and acetylation status to evaluate changes at PRC2 targets as a function of i) vorinostat concentration and ii) acute treatment versus adaptation with vorinostat. Second, we investigated if selective inhibition of HDACs 1, 2, and 3 would be sufficient to generate the non-malignant phenotype by adapting SW480 cells to the inhibitor CI-994 and evaluating changes in proliferation, colony formation, and gene expression at PRC2 targets. Three PRC2 target genes were identified that had striking changes in mRNA expression as a function of vorinostat concentration and/or adaptation that correlated with H3K27 modifications and may be important to generating the non-malignant phenotype: TSPAN8, STMN2, and EDN3. Cells adapted to 12 µM CI-994 showed a substantial reduction in colony formation, suggesting that targeted inhibition of HDACs 1, 2, and 3 may reduce tumorigenicity. Changes in mRNA expression in CI-994 adapted cells were similar to SH80 cells, indicating that inhibition of HDACs 1, 2, and 3 leads to altered expression of PRC target genes. Substantial changes in gene expression were observed for TSPAN8, STMN2, and EDN3, further reinforcing the idea that these genes may be of particular importance to the non-malignant phenotype. Advisors/Committee Members: Rabson, Arnold B (chair), Scotto, Kathleen W (internal member), Medina, Daniel J (outside member).

Subjects/Keywords: Colon (Anatomy) – Cancer; Histones

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

Vengsarkar, Diana S., 1. (2016). Adaptation of colon cancer cells to histone deacetylase inhibitors generates cell lines with a non-malignant phenotype. (Masters Thesis). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/50237/

Chicago Manual of Style (16th Edition):

Vengsarkar, Diana S., 1970-. “Adaptation of colon cancer cells to histone deacetylase inhibitors generates cell lines with a non-malignant phenotype.” 2016. Masters Thesis, Rutgers University. Accessed April 11, 2021. https://rucore.libraries.rutgers.edu/rutgers-lib/50237/.

MLA Handbook (7th Edition):

Vengsarkar, Diana S., 1970-. “Adaptation of colon cancer cells to histone deacetylase inhibitors generates cell lines with a non-malignant phenotype.” 2016. Web. 11 Apr 2021.

Vancouver:

Vengsarkar, Diana S. 1. Adaptation of colon cancer cells to histone deacetylase inhibitors generates cell lines with a non-malignant phenotype. [Internet] [Masters thesis]. Rutgers University; 2016. [cited 2021 Apr 11]. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/50237/.

Council of Science Editors:

Vengsarkar, Diana S. 1. Adaptation of colon cancer cells to histone deacetylase inhibitors generates cell lines with a non-malignant phenotype. [Masters Thesis]. Rutgers University; 2016. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/50237/


Rutgers University

2. Ibironke, Olufunmilola, 1978-. Air pollution particulate matter effects on adaptive human antimycobacterial immunity.

Degree: PhD, Physiology and Integrative Biology, 2019, Rutgers University

Tuberculosis (TB) and air pollution both contribute significantly to the global burden of disease. Epidemiological studies provide evidence that indoor (household) air pollution increases the risk of new infections with Mycobacterium tuberculosis (M.tb) and development of TB. The mechanisms by which exposure to ‘real-world’-derived urban ambient (outdoor) particulate matter (PM) adversely affects M.tb-specific human host T cell functions in vitro have not been studied. In this thesis research, we explored the effects of air pollution PM2.5 (≤2.5 µm, median aerodynamic diameter) collected in the Iztapalapa municipality of Mexico City on M.tb-specific T cell functions in human peripheral blood mononuclear cells (PBMC). Upon in vitro exposure, PM2.5 was observed in clusters of free, non-membrane-bound particle agglomerates in the cytoplasm of the exposed cells. PM2.5 exposure did not alter the expression of activation marker CD54 on antigen presenting cells (APC), however, increased the expression of CD80 while decreasing the constitutively expressed CD86 on monocytes during M.tb infection. Exposure to PM2.5 of M.tb-infected PBMC led to an increase of intracellular growth of M.tb, indicating loss of M.tb growth controlling capacity of the cells that occurred independent of PM-induced changes to PBMC viability. Exposure of PBMC to PM2.5 also altered M.tb-specific T-cell immune responses by (1) decreasing the surface expression of early T cell activation markers CD69 and CD25 on T cells, (2) inhibiting the intracellular expression of both interferon-gamma (IFN-γ) and tumor necrosis factor alpha (TNF-α), and (3) decreasing the expression of T-box transcription factor TBX21 (T-bet) known to directly regulate the expression of IFN-γ. In contrast, PM2.5 exposure increased the intracellular expression of the anti-inflammatory cytokine interleukin 10 (IL-10) and the phosphorylation of transcription factor STAT-3. The observed PM2.5-induced decrease in the expression of human pro-inflammatory M.tb-specific T cell cytokines, and the loss of intracellular M.tb growth control are associated with the increased expression of anti-inflammatory cytokine IL-10 and decreased expression of transcription factor T-bet. Together, the findings of this study suggest that the PM2.5-induced decrease of critical human host immune cell functions against M.tb represents the mechanistic correlate of epidemiological observations that outdoor air pollution exposure is associated with increases in the incidence of TB and with adversely modified TB treatment outcomes.

Advisors/Committee Members: Fan, Huizhou (chair), Langer, Jerome (internal member), Haimovich, Beatrice (internal member), Medina, Daniel (internal member), School of Graduate Studies.

Subjects/Keywords: Air  – Pollution; Tuberculosis

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

Ibironke, Olufunmilola, 1. (2019). Air pollution particulate matter effects on adaptive human antimycobacterial immunity. (Doctoral Dissertation). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/60169/

Chicago Manual of Style (16th Edition):

Ibironke, Olufunmilola, 1978-. “Air pollution particulate matter effects on adaptive human antimycobacterial immunity.” 2019. Doctoral Dissertation, Rutgers University. Accessed April 11, 2021. https://rucore.libraries.rutgers.edu/rutgers-lib/60169/.

MLA Handbook (7th Edition):

Ibironke, Olufunmilola, 1978-. “Air pollution particulate matter effects on adaptive human antimycobacterial immunity.” 2019. Web. 11 Apr 2021.

Vancouver:

Ibironke, Olufunmilola 1. Air pollution particulate matter effects on adaptive human antimycobacterial immunity. [Internet] [Doctoral dissertation]. Rutgers University; 2019. [cited 2021 Apr 11]. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/60169/.

Council of Science Editors:

Ibironke, Olufunmilola 1. Air pollution particulate matter effects on adaptive human antimycobacterial immunity. [Doctoral Dissertation]. Rutgers University; 2019. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/60169/

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