Summary of Study ST002809

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.

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Study IDST002809
Study TitleRole of cilia in mitochondrial function
Study Typecultured cells
Study SummaryAutosomal 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
DepartmentMedicine
Last NameLipschutz
First NameJosh
Address96 Jonathan Lucas St, Charleston, SC 29425
Emaillipschut@musc.edu
Phone8437927659
Submit Date2023-08-03
Analysis Type DetailLC-MS
Release Date2024-06-01
Release Version1
Josh Lipschutz Josh Lipschutz
https://dx.doi.org/10.21228/M8QT46
ftp://www.metabolomicsworkbench.org/Studies/ application/zip

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Factors:

Subject type: Mammal; Subject species: Mouse/canine (Factor headings shown in green)

mb_sample_id local_sample_id Genotype
SA301573MUSC-00285EXOC5_KD
SA301574MUSC-00286EXOC5_KD
SA301575MUSC-00288EXOC5_KD
SA301576MUSC-00283EXOC5_KD
SA301577MUSC-00287EXOC5_KD
SA301578MUSC-00284EXOC5_KD
SA301579MUSC-00278EXOC5_KO
SA301580MUSC-00277EXOC5_KO
SA301581MUSC-00279EXOC5_KO
SA301582MUSC-00280EXOC5_KO
SA301583MUSC-00282EXOC5_KO
SA301584MUSC-00281EXOC5_KO
SA301585MUSC-00294EXOC5_OE
SA301586MUSC-00293EXOC5_OE
SA301587MUSC-00292EXOC5_OE
SA301588MUSC-00289EXOC5_OE
SA301589MUSC-00290EXOC5_OE
SA301590MUSC-00291EXOC5_OE
SA301591MUSC-00304IFT88_KO
SA301592MUSC-00301IFT88_KO
SA301593MUSC-00305IFT88_KO
SA301594MUSC-00303IFT88_KO
SA301595MUSC-00302IFT88_KO
SA301596MUSC-00306IFT88_KO
SA301597MUSC-00307IFT88_KO_WT
SA301598MUSC-00309IFT88_KO_WT
SA301599MUSC-00312IFT88_KO_WT
SA301600MUSC-00311IFT88_KO_WT
SA301601MUSC-00310IFT88_KO_WT
SA301602MUSC-00308IFT88_KO_WT
SA301603MUSC-00295WT
SA301604MUSC-00296WT
SA301605MUSC-00297WT
SA301606MUSC-00298WT
SA301607MUSC-00299WT
SA301608MUSC-00300WT
Showing results 1 to 36 of 36
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