Summary of project PR001913
This data is available at the NIH Common Fund's National Metabolomics Data Repository (NMDR) website, the Metabolomics Workbench, https://www.metabolomicsworkbench.org, where it has been assigned Project ID PR001913. The data can be accessed directly via it's Project DOI: 10.21228/M8FH9H This work is supported by NIH grant, U2C- DK119886.
See: https://www.metabolomicsworkbench.org/about/howtocite.php
| Project ID: | PR001913 |
| Project DOI: | doi: 10.21228/M8FH9H |
| Project Title: | Attenuation of Helicobacter pylori VacA toxin-induced cell death by modulation of intracellular taurine metabolism |
| Project Type: | Untargeted Metabolomics analysis |
| Project Summary: | Colonization of the human stomach with H. pylori strains producing active forms of a secreted toxin (VacA) is associated with an increased risk of peptic ulcer disease and gastric cancer, compared to colonization with strains producing hypoactive forms of VacA. Previous studies have shown that VacA causes cell vacuolation and mitochondrial dysfunction. In this study, we sought to define the cellular metabolic consequences of VacA intoxication. Untargeted metabolomic analyses revealed that several hundred metabolites were significantly altered in VacA-treated gastroduodenal cells (AGS and AZ-521) compared to control cells. Pathway analysis suggested that VacA caused alterations in taurine and hypotaurine metabolism. Treatment of cells with the purified active s1m1 form of VacA, but not hypoactive s2m1 or Delta_6-27 VacA mutant proteins (defective in membrane channel formation), caused reductions in taurine and hypotaurine levels. Supplementation of the tissue culture medium with taurine or hypotaurine protected AZ-521 cells against VacA-induced cell death. Untargeted global metabolomics of AZ-521 cells or AGS cells intoxicated with VacA in the presence or absence of extracellular taurine showed that taurine was the main intracellular metabolite significantly altered by extracellular taurine supplementation. These results indicate that VacA causes alterations in cellular taurine metabolism and indicate that repletion of taurine is sufficient to attenuate VacA-induced cell death. |
| Institute: | Vanderbilt University |
| Department: | Chemistry |
| Laboratory: | Center for Innovative Technology |
| Last Name: | CODREANU |
| First Name: | SIMONA |
| Address: | 1234 STEVENSON CENTER LANE |
| Email: | SIMONA.CODREANU@VANDERBILT.EDU |
| Phone: | 6158758422 |
Summary of all studies in project PR001913
| Study ID | Study Title | Species | Institute | Analysis(* : Contains Untargted data) | Release Date | Version | Samples | Download(* : Contains raw data) |
|---|---|---|---|---|---|---|---|---|
| ST003067 | Attenuation of Helicobacter pylori VacA toxin-induced cell death by modulation of intracellular taurine metabolism - Study #1 | Homo sapiens | Vanderbilt University | MS* | 2024-06-12 | 1 | 48 | Uploaded data (22.4G)* |
| ST003068 | Attenuation of Helicobacter pylori VacA toxin-induced cell death by modulation of intracellular taurine metabolism _ Study #2 | Homo sapiens | Vanderbilt University | MS* | 2024-06-12 | 1 | 20 | Uploaded data (8.2G)* |
| ST003070 | Attenuation of Helicobacter pylori VacA toxin-induced cell death by modulation of intracellular taurine metabolism - Study #3 | Homo sapiens | Vanderbilt University | MS* | 2024-06-12 | 1 | 40 | Uploaded data (16.4G)* |
| ST003071 | Attenuation of Helicobacter pylori VacA toxin-induced cell death by modulation of intracellular taurine metabolism - Study #4 | Homo sapiens | Vanderbilt University | MS* | 2024-06-12 | 1 | 40 | Uploaded data (17.4G)* |
