Summary of project PR001756
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 PR001756. The data can be accessed directly via it's Project DOI: 10.21228/M8QT46 This work is supported by NIH grant, U2C- DK119886.
See: https://www.metabolomicsworkbench.org/about/howtocite.php
| Project ID: | PR001756 |
| Project DOI: | doi: 10.21228/M8QT46 |
| Project Title: | Role of cilia in mitochondrial function |
| Project Summary: | Autosomal dominant polycystic kidney disease (ADPKD), the most common potentially lethal genetic disease in humans and the fourth leading cause of kidney disease, exhibits features of both a ciliary and metabolic disorder. Our previous research revealed that cells overexpressing Exoc5 with elongated cilia demonstrate enhanced recovery from oxidative stress. To investigate the connection between primary cilia and metabolism, we conducted an unbiased metabolomics screen. Global metabolic profiling was performed on canine MDCK cells (Control, Exoc5 ciliary targeting sequence mutation (CTS-mut), Exoc5 knockdown (KD), Exoc5 overexpression (OE)) and murine cells (Ift88 knockout (KO), Ift88 rescue). Knockdown (KD) or ciliary targeting sequence mutation (CTS-mut) in Exoc5, a central exocyst component, resulted in cilia loss. Similarly, Ift88 knockout (KO) resulted in cilia loss. For each experimental group, we cultivated six independent replicates of Exoc5 OE, KD, CTS-mut, and control MDCK cells, as well as six independent replicates of murine Ift88 KO and rescue cells. Cell pellets were obtained from the cultures, and we analyzed the global metabolic profiles for all 36 cell pellets. The most significant findings from the metabolomics screen indicated defects in tryptophan metabolism. This discovery suggests a potential link between primary cilia function and tryptophan-related metabolic pathways. Further exploration of these findings may shed light on the underlying mechanisms and implications for ADPKD pathogenesis and metabolic disturbances. |
| Institute: | Medical University of South Carolina |
| Department: | Medicine |
| Last Name: | Lipschutz |
| First Name: | Josh |
| Address: | 96 Jonathan Lucas St, Charleston, SC 29425 |
| Email: | lipschut@musc.edu |
| Phone: | 843-792-7659 |
Summary of all studies in project PR001756
| Study ID | Study Title | Species | Institute | Analysis(* : Contains Untargted data) | Release Date | Version | Samples | Download(* : Contains raw data) |
|---|---|---|---|---|---|---|---|---|
| ST002809 | Role of cilia in mitochondrial function | Mouse / canine | Medical University of South Carolina | MS | 2024-06-01 | 1 | 36 | Not available |
