Unknown,Transcriptomics,Genomics,Proteomics

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Expression data from HT-29, a human colonic epithelial cell line

ABSTRACT: Gene(s) in epithelial cells can be upregulated or downregulated by different stimuli in a tissue-specific manner. We used genome-wide microarray analysis to profile the expression of genes in HT-29 cells that are upregulated after stimulation with sodium butyrate (NaB) and subsequently downregulated by the addition of ciprofloxacin antibiotic. The specific aim was to evaluate genes that are associated with mucosal immunity. HT-29 cells were stimulated with sodium butyrate (NaB) (n=3), NaB and ciprofloxacin (n=3) or culture media (unstimulated control, n=3) for 24 hours. RNA extracted from these cells were hybridized on Affymetrix microarrays.

ORGANISM(S): Homo sapiens

SUBMITTER: Protim Sarker

PROVIDER: E-GEOD-45220 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Background: Diabetic kidney disease (DKD) is the leading cause of end-stage renal disease worldwide with limited treatment options. The intricate pathogenesis of dysregulated lipid metabolism leading to the development of DKD remains obscure. Lipophagy, which refers to the autophagic degradation of intracellular lipid droplets, has been found to be impaired in DKD, resulting in renal tubule dysfunction and ectopic lipid deposition (ELD). The lipotoxity in renal tubules is closely related to the pathogenesis of DKD. Therefore, it is crucial to develop effective and safe agents that can restore autophagic flux and lipophagy in renal tubules for potential preventive interventions. Purpose: This study seeks to investigate the preventive effect of sodium butyrate (NaB) on ELD in the progression of DKD and elucidate the underlying mechanisms involved.Methods: The beneficial effects of NaB were investigated in glucolipotoxicity (GLT)-stimulated HK-2 cells and the streptozotocin (STZ) injection combined with a high-fat diet induced DKD model mice. Additionally, we managed to silence transcription factor EB (TFEB) in HK-2 cells and establish the renal specific silence model by retrograde ureteral infusion of AAV9-shTFEB in mice. We investigated the expression profile of RNAs in HK-2 cells through. The mechanism of NaB is demonstrated by RNA sequencing (RNA-seq), pulldown MS assay, SPR experiments etc.Results: Our findings revealed that serum butyrate level is reduced in DKD patients and is statistically correlated with urinary protein excretion and eGFR. Sodium butyrate (NaB) dose-dependently improved lipid deposition in HK-2 cells and renal tubular epithelial cells of DKD model mice. This effect may be attributed to the promotion of TFEB dephosphorylation, as NaB can directly interact with PPP2R1A to activate PP2A phosphorylation activity. Therefore, NaB may play a role in improving renal lipid deposition in DKD through the PP2A-TFEB pathway. Conclusion: NaB acts as a PP2A-TFEB axis activator that restores lipophagy to ameliorate ELD and renal dysfunction in DKD.

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Expression data from HT-29, a human colonic epithelial cell line

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