Unknown,Transcriptomics,Genomics,Proteomics

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Copy number variation analysis of 16HBE14o- and T84 cell lines

ABSTRACT: The aim of the project was to detect genomic regions that were normal, duplicated or deleted in these cell lines for transcription factors NFKBp50, NFkBp65, HIF1a and FAS gene which we studied. It is not clear the effects of copy number variations on allele specific assembly or disruption of master regulator transcription factors. Thus, the CNV analysis verified that 16HBE cell line, though transformed with defective simian virus, had normal copy number variations thus was a suitable source for nuclear extract to study the afore mentioned TFs. T84 showed duplications and large genomic deletions for TFs: NFkBp50 and p65. 16HBE and T84 are both epithelial cell lines type from human. 16HBE is derived from bronchial epithelium, while the T84 is derived from the colon carcinoma.

INSTRUMENT(S): Agilent

ORGANISM(S): Homo sapiens

SUBMITTER: Awah Chidiebere

PROVIDER: E-MTAB-4194 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Neutrophil accumulation in crypt abscesses is a pathological hallmark of ulcerative colitis. Based on recent evidence that mucosal metabolic changes influence disease outcomes, we hypothesized that transmigrating neutrophils influence the transcriptional profile of intestinal epithelia. Microarray studies revealed a cohort of hypoxia-responsive genes regulated by neutrophil-epithelial crosstalk. Real-time O2 sensing indicated that transmigrating neutrophils rapidly deplete microenvironmental O2 sufficient enough to stabilize intestinal epithelial cell hypoxia-inducible factor (HIF). Utilizing HIF reporter mice in a TNBS colitis model, we investigated the relative contribution of neutrophils and the respiratory burst to M-bM-^@M-^\inflammatory hypoxiaM-bM-^@M-^] in vivo. Gp91phox-null mice, which mirror human chronic granulomatous disease, developed accentuated colitis compared to control with exaggerated neutrophil infiltration and diminished inflammatory hypoxia. In conclusion, transcriptional imprinting of host tissue by infiltrating neutrophils modulates the host response to inflammation. Likewise, the respiratory burst contributes fundamentally to localized O2 depletion, resultant microenvironmental hypoxia and effective inflammatory resolution. Two models were employed, direct and indirect. The M-bM-^@M-^\DirectM-bM-^@M-^] migration model entailed establishing a chemotactic gradient (using fMLP) across monolayers of T84 intestinal epithelial cells grown on the underside of permeable supports (3um pore). Neutrophils (PMN) were induced to migrate in the physiologically relevant the physiologically relevant basolateral-to-apical direction. Following migration, T84s were rested in complete media and 2hrs later harvested for RNA isolation. In the Indirect model, PMN were applied to T84s as with the direct model. After migration, conditioned supernatants were collected, cells pelleted and supernatants filtered through 0.2um pore. Conditioned supernatants were transferred to naive T84 monolayers for 2hrs, followed by RNA harvest. Each model was exposed to neutrophils (PMN) or not. All monolayers contained chemotactic peptide fMLP on the apical side. Total of 12 samples, 4 conditions in triplicate: Direct migration without neutrophils (T84 +fMLP -PMN), Direct migration with neutrophils (T84 +fMLP +PMN), Indirect migration without neutrophils (T84 +fMLP -PMN), Indirect migration with neutrophils (T84 +fMLP +PMN)

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Copy number variation analysis of 16HBE14o- and T84 cell lines

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