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A phosphoproteomic and transcriptomic analysis of carnosine’s action on signaling in glioblastoma

ABSTRACT: Previous studies demonstrated that carnosine affects signaling molecules of different pathways in a number of experimental models. However, the primary targets of carnosine are still unknown and its effect on complex signal transduction has not been revealed. This is especially the case for pathways that could be responsible for the anti-neoplastic effect of the dipeptide. Therefore, we performed a phosphoprotein antibody array and RNA-seq experiments with U87 glioblastoma cells treated with 50 mM carnosine for 24h, in order to obtain a precise and coherent picture of carnosine’s influence on signal transduction in single tumor cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE110767 | GEO | 2019/05/01

REPOSITORIES: GEO

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A phosphoproteomic and transcriptomic analysis of carnosine’s action on signaling in glioblastoma U87-MG cells

Project description:Previous studies demonstrated that carnosine affects signaling molecules of different pathways in a number of experimental models. However, the primary targets of carnosine are still unknown and its effect on complex signal transduction has not been revealed. This is especially the case for pathways that could be responsible for the anti-neoplastic effect of the dipeptide. Therefore, we performed a phosphoprotein antibody array and RNA-seq experiments with U87 glioblastoma cells treated with 50 mM carnosine for 24h, in order to obtain a precise and coherent picture of carnosine’s influence on signal transduction in single tumor cells.

2019-11-30 | E-MTAB-6455 | biostudies-arrayexpress

RNA-Sequencing of carnosine treated wild-type BDF1 (WT) and transgenic Thy1-aSyn mice

Project description:Mitochondrial dysfunction plays a central role in the pathogenesis of neurodegenerative diseases such as Parkinson’s disease (PD). This study tested the hypothesis that the dipeptide carnosine would exert a beneficial effect in the Thy1-aSyn mouse model of PD, which displays mitochondrial dysfunction. Mitochondrial function and gene expression were evaluated in the midbrain after two months of carnosine administration by intranasal (IN) or drinking water routes of exposure. IN carnosine attenuated transcriptional changes in the midbrain in Thy1-aSyn mice. Additionally, IN-carnosine increased expression of mitochondria complexes and enhanced mitochondrial function, suggesting a potential neuroprotective role for IN-carnosine in PD.

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Carnosine effect in scaffold free human dermis spheroids model

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Phosphoproteomic analysis of TCR signaling with inhibitors

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Iron scavenging and suppression of collagen cross-linking underlie antifibrotic effects of carnosine in the heart with obesity

Project description:Oral consumption of histidyl dipeptides such as l-carnosine has been suggested to promote cardiometabolic health, although therapeutic mechanisms remain incompletely understood. We recently reported that oral consumption of a carnosine analog suppressed markers of fibrosis in liver of obese mice, but whether antifibrotic effects of carnosine extend to the heart is not known, nor are the mechanisms by which carnosine is acting. Here, we investigated whether oral carnosine was able to mitigate the adverse cardiac remodeling associated with diet induced obesity in a mouse model of enhanced lipid peroxidation (i.e., glutathione peroxidase 4 deficient mice, GPx4+/−), a model which mimics many of the pathophysiological aspects of metabolic syndrome and T2 diabetes in humans. Wild-type (WT) and GPx4+/− male mice were randomly fed a standard (CNTL) or high fat high sucrose diet (HFHS) for 16 weeks. Seven weeks after starting the diet, a subset of the HFHS mice received carnosine (80 mM) in their drinking water for duration of the study. Carnosine treatment led to a moderate improvement in glycemic control in WT and GPx4+/− mice on HFHS diet, although insulin sensitivity was largely unchanged. Interestingly, while our transcriptomic analysis revealed that carnosine therapy had no significant impact on global gene expression in the heart, carnosine substantially upregulated cardiac GPx4 expression in both WT and GPx4+/− mice on HFHS diet. Carnosine also significantly reduced protein carbonyls and iron levels in myocardial tissue from both genotypes on HFHS diet. Importantly, we observed a robust antifibrotic effect of carnosine therapy in hearts from mice on HFHS diet, which further in vitro experiments suggest is due to carnosine’s ability to suppress collagen-cross-linking. Collectively, this study reveals antifibrotic potential of carnosine in the heart with obesity and illustrates key mechanisms by which it may be acting.

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Gene expression profile in Caco-2 cells treated with carnosine

Project description:To reveal the effects of carnosine on Caco-2 cells, we have employed whole genome microarray to detect genes that showed significantly different expression when exposed to carnosine. Caco-2 cells were treated with 1 mM carnosine for 3 days. Caco-2 cells were treated with 1 mM carnosine for 3 days. Three independent experiments were performed.

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Gene expression profile in Caco-2 cells treated with carnosine

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Project description:As a first step towards identifying the target genes of EGFR activity in glioma cells, genome-wide expression analyses were performed using the Affymetrix GeneChip Human Genome U133A array. To accomplish this, mRNA expression levels of these genes were measured in the glioblastoma cell lines, U87 and U178, engineered with EGFR by retrovirus transduction (termed U87-EGFR and U178-EGFR respectively), with or without 20 ng/mL EGF treatment for 3 h. U87 and U178 cells engineered to express EGFR were stimulated with or without EGF. The experiment was replicated twice for each U87 and U178 cells.

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