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Cystathionine-β-Synthase Promotes Colon Carcinogenesis

ABSTRACT: Purpose: The goal of this study is to investigate the role of CBS enzyme in colorectal carcinogenesis Methods: RNA-Seq transcriptome analysis of CBS-overexpression in NCM356 cels compared to control vector cells

ORGANISM(S): Homo sapiens

PROVIDER: GSE91000 | GEO | 2017/12/07

SECONDARY ACCESSION(S): PRJNA356616

REPOSITORIES: GEO

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Cystathionine beta synthase (CBS) Over expression vs PLenti6 Expression Vector Human Bronchial Epithelial Cells (HBEC)

Project description:Cystathionine Beta Synthase (CBS), an enzyme that utilizes a methionine precursor to generate glutathione (GSSH), has been implicated in the mitigation of ROS production in COPD lung. Additionally, post-translational modification analysis on mouse and human cells treated with cigarette smoke showed the unique presence of mono- and di-methylated histone H3 lysine 27 that was not seen in controls, suggesting that cigarette smoke could lead to loss of Polycomb Repressive Complex 2 (PRC2) activity. To elucidate CBS as a potential upstream target for PRC2 inhibition, we overexpressed CBS in Human Bronchial Epithelial Cells (HBECs), grew them as 2D cultures, then conducted bulk RNA seq analysis.

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Endogenous Elevation of Homocysteine Induces Retinal Neuron Death in the Cystathionine-b-Synthase Mutant Mice

Project description:The effects of endogenous elevation of homocysteine on retinal gene expression were screened by microarray analysis, which was performed in triplicate (i.e., three different paired RNA samples) with RNA isolated from neural retinas of cbs+/- HM at 5-weeks after a methionine diet and age-matched wildtype mice. The microarray chips used in this study permitted the screening of 36,212 genes. Of particular interest were those genes in cbs+/- HM mice whose expression levels changed by at least a factor of 2 (increased or decreased expression) compared with the wild-type in each of the replicate experiments. Using these selection criteria, we identified 1219 genes. They were categorized into six functional groups: (1) proapoptosis, (2) antiapoptosis, (3) cell cycle, (4) antioxidant, (5) calcium signaling, and (6) axon growth/guidance, with the remaining genes with marked changes in expression placed in a miscellaneous group. After categorization, relevant genes were further narrowed by SAM analysis; q < 0.06 was considered significant. Microarrays were performed in triplicate as biological repeats and reverse fluoro (i.e., three different paired RNA samples) with RNA isolated from neural retinas of cbs+/- HM at 5-weeks after a methionine diet and age-matched wildtype mice after a methionine diet.

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Endogenous Elevation of Homocysteine Induces Retinal Neuron Death in the Cystathionine-b-Synthase Mutant Mice

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Neurobehavioral dysfunction in a mouse model of Down syndrome: upregulation of cystathionine β-synthase, H2S overproduction, altered protein persulfidation, synaptic dysfunction, endoplasmic reticulum stress, and autophagy

Project description:Down syndrome (DS) is a genetic condition where the person is born with an extra chromosome 21. DS is associated with accelerated aging; people with DS are prone to age-related neurological conditions including an early-onset Alzheimer’s disease. Using the Dp(17)3Yey/ + mice, which overexpresses a portion of mouse chromosome 17, which encodes for the transsulfuration enzyme cystathionine β-synthase (CBS), we investigated the functional role of the CBS/hydrogen sulfide (H2S) pathway in the pathogenesis of neurobehavioral dysfunction in DS. The data demonstrate that CBS is higher in the brain of the DS mice than in the brain of wild-type mice, with primary localization in astrocytes. DS mice exhibited impaired recognition memory and spatial learning, loss of synaptosomal function, endoplasmic reticulum stress, and autophagy. Treatment of mice with aminooxyacetate, a prototypical CBS inhibitor, improved neurobehavioral function, reduced the degree of reactive gliosis in the DS brain, increased the ability of the synaptosomes to generate ATP, and reduced endoplasmic reticulum stress. H2S levels in the brain of DS mice were higher than in wild-type mice, but, unexpectedly, protein persulfidation was decreased. Many of the above alterations were more pronounced in the female DS mice. There was a significant dysregulation of metabolism in the brain of DS mice, which affected amino acid, carbohydrate, lipid, endocannabinoid, and nucleotide metabolites; some of these alterations were reversed by treatment of the mice with the CBS inhibitor. Thus, the CBS/H2S pathway contributes to the pathogenesis of neurological dysfunction in DS in the current animal model.

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