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Transcriptome profile of S. cerevisiae treated with tauroursodeoxycholic acid (TUDCA)

ABSTRACT: Transcriptome profile of S. cerevisiae treated with tauroursodeoxycholic acid (TUDCA)

PROVIDER: PRJNA773716 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16532218_1.fastq.gz	Fastqsanger.gz
	SRR16532218_2.fastq.gz	Fastqsanger.gz
	SRR16532219_1.fastq.gz	Fastqsanger.gz
	SRR16532219_2.fastq.gz	Fastqsanger.gz
	SRR16532220_1.fastq.gz	Fastqsanger.gz

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Transcriptome profile of S. cerevisiae treated with tauroursodeoxycholic acid (TUDCA)

Project description:Cells respond to endoplasmic reticulum (ER) stress through activation of signaling pathways such as the Unfolded Protein Response (UPR) which improve the ER folding environment capacity upon changes in misfolded protein burden. Small molecules termed chemical chaperones can attenuate the UPR under stress conditions and improve folding and trafficking of specific mutant proteins. One such compound is the bile acid tauroursodeoxycholic acid (TUDCA). Despite promising results in multiple models of protein folding diseases, TUDCA’s mechanism of action remains unclear. To better define how TUDCA attenuate ER stress, we leveraged the genetically tractable budding yeast, S. cerevisiae. Consistent with properties described for TUDCA, we found it significantly improves growth of yeast subjected to ER stress caused by the N-glycosylation inhibitor tunicamycin (Tm) independently of activity of the UPR. In addition to other data, transcriptomics of strains treated with TUDCA link its ability to resuce Tm-induced stress with cell wall remodeling.

2024-11-13 | GSE186390 | GEO

Tauroursodeoxycholic Acid (TUDCA) Reduces ER Stress and Lessens Disease Activity in Ulcerative Colitis

Project description:Background and Aims: In inflammatory bowel disease, protein misfolding in the endoplasmic reticulum (ER) potentiates epithelial barrier dysfunction and impairs mucosal healing. Tauroursodeoxycholic acid (TUDCA), a naturally occurring bile acid, acts as a chemical chaperone to reduce protein aggregation and colitis severity in preclinical models. We conducted an open label trial evaluating oral TUDCA as therapy in patients with active ulcerative colitis (UC). Methods: Patients with moderate-to-severely active UC (Mayo score ≥6, endoscopic subscore ≥1) received oral TUDCA at 1.75 or 2 g/day for 6 weeks. Exclusion criteria included known hepatic disorders or change in UC therapy within 60 days. Clinical disease activity questionnaires, endoscopy with biopsy, blood, and stool were collected at enrollment and after 6 weeks. The primary outcome measure was change in ER stress markers while safety, tolerability and change in UC disease activity were secondary outcomes. Results: Thirteen participants completed the study with eleven evaluable for clinical response. TUDCA was well-tolerated with transient dyspepsia being the most common side effect. Mucosal biopsies revealed significant reductions in ER stress and inflammation as well as an increase in markers of epithelial restitution. Clinical, endoscopic, and histologic disease activity were significantly improved at week 6 (mean total Mayo Score: 9 to 4.5, p<0.001). Conclusions: Six weeks of oral TUDCA promoted mucosal healing, lessened ER stress, and reduced UC clinical disease activity. TUDCA was safe and well-tolerated in patients with active UC. A randomized controlled trial of adjunctive TUDCA therapy in patients with UC is warranted. ClinicalTrials.gov (NCT04114292).

2025-05-30 | GSE266963 | GEO

Tauroursodeoxycholic acid-induced neural stem cell proliferation

Project description:Tauroursodeoxycholic acid (TUDCA), an endogenous neuroprotective bile acid and a metabolic regulator, stimulates NSC proliferation and enhances adult NSC pool in vitro and in vivo. In this study, we dissected the mechanism triggered by this proliferation-inducing molecule, namely in mediating metabolic reprogramming. Liquid chromatography coupled with mass spectrometry based detection of differential proteomics revealed that TUDCA reduces the mitochondrial levels of the long-chain acyl-CoA dehydrogenase (LCAD), an enzyme crucial for β-oxidation of long-chain fatty acids (FA).

2021-09-09 | PXD017979 | Pride

Tauroursodeoxycholic Acid (TUDCA) Reduces ER Stress and Lessens Disease Activity in Ulcerative Colitis

Project description:Tauroursodeoxycholic Acid (TUDCA) Reduces ER Stress and Lessens Disease Activity in Ulcerative Colitis

| PRJNA1108804 | ENA

Tauroursodeoxycholic acid prevents acute graft-versus-host disease in mice by regulating intestinal apoptosis and inflammation

Project description:The effect of tauroursodeoxycholic acid on the development of acute graft-versus-host disease was tested in a murine allogeneic stem cell transplantation model. TUDCA was shown to reduce acute GVHD by reducing intestinal antigen presentation and following apoptosis and increasing the viability of intestinal epithelial cells.

2021-12-21 | GSE124426 | GEO

Glucocorticoid receptor-dependent therapeutic efficacy of tauroursodeoxycholic acid in preclinical models of Spinocerebellar ataxia type 3

Project description:Spinocerebellar ataxia type 3 (SCA3) is an adult-onset neurodegenerative disease caused by a polyglutamine expansion in the ataxin-3 (ATXN3) gene. No effective treatment is available for this disorder, other than symptomatic approaches. Bile acids have shown therapeutic efficacy in neurodegenerative disease models. Here, we pinpointed tauroursodeoxycholic acid (TUDCA) as an efficient therapeutic, improving the motor and neuropathological phenotype of SCA3 nematode and mouse models. Surprisingly, transcriptomic and functional in vivo data showed that TUDCA acts in neuronal tissue through the glucocorticoid receptor (GR), but independently of its canonical receptor, the FXR. TUDCA was also predicted to bind to the GR, similarly to corticosteroid molecules. GR levels were decreased in disease-affected brain regions, likely due to increased protein degradation as a consequence of ATXN3 dysfunction, being restored by TUDCA treatment. Lastly, based on results of a cohort of pre-symptomatic and symptomatic SCA3 patients, we demonstrated that peripheral expression of GR and FKBP5 might be indicators of clinical conversion and disease progression, respectively. We have established a novel in vivo mechanism for the neuroprotective effects of TUDCA in SCA3, and propose this readily available drug for a clinical trial in SCA3 patients.

2024-03-01 | GSE252250 | GEO

Tauroursodeoxycholic acid ameliorates renal injury induced by COL4A3 mutation

Project description:COL4A3/A4/A5 mutations have been identified as critical causes of Alport syndrome and other genetic chronic kidney diseases. However, the underlying pathogenesis remains unclear, and specific treatments are lacking. Here, we constructed a transgenic Alport syndrome mouse model by generating a mutation (Col4a3 p.G799R) identified previously from one large Alport syndrome family into mice. We observed that the mutation caused a pathological decrease in intracellular and secreted collagen IV α3α4α5 heterotrimers. The mutant collagen IV α3 chains abnormally accumulated in the endoplasmic reticulum and exhibited defective secretion, leading to persistent endoplasmic reticulum stress in vivo and in vitro. RNA-seq analysis revealed that the MyD88/p38 MAPK pathway plays key roles in mediating subsequent inflammation and apoptosis signaling activation. Treatment with tauroursodeoxycholic acid, a chemical chaperone drug that functions as an endoplasmic reticulum stress inhibitor, effectively suppressed endoplasmic reticulum stress, promoted secretion of the α3 chains, and inhibited the activation of the MyD88/p38 MAPK pathway. Tauroursodeoxycholic acid treatment significantly improved renal function in vivo. These results partly clarified the pathogenesis of renal injuries associated with Alport syndrome, especially in glomeruli, and suggested that tauroursodeoxycholic acid might be useful for the early clinical treatment of Alport syndrome.

2024-08-28 | GSE261588 | GEO

Effect of TUDCA on the artery which suffered from the atherosclerosis in ApoE-/- mice

Project description:Cholesterol efflux capacity dysfunction in macrophages is thought to be important in atherosclerosis. However, the molecular mechanism underlying this dysfunction remains unclear. Our previous analysis found that the increase of endoplasmic reticulum stress in macrophages during atherosclerotic plaque formation. Here we extended our analysis to ApoE-/- mice fed a high fat diet, some of which were treated with tauroursodeoxycholic acid (TUDCA) and collected the arteries of mice among these three groups (NFD, HFD and HFD+TUDCA) to perform the Bulk-RNA sequencing. There was significantly high expression of matrix metalloproteinase family (MMP9, MMP25, MMP8, MMP12, MMP13 and MMP3), CD68, inflammasome (IL1b, IL18bp, ifi44, ifi204 and Nlrp3), ER stress (Hspa5) and cholesterol transporters (ABCA1 and ABCG1) in the HFD group compared with the NFD group, however, TUDCA rescued the high expression of the above DEGs to different degrees. As shown by the expression levels of ifi204, Nlrp3, Il1b, and Il18, inflammasome activation was evident in the arteries of the HFD group compared to the NFD group. The ER stress inhibitor TUDCA not only decreased expression of the ER stress-related gene Hspa5 but also down-regulated inflammasome activation (as seen with the expression levels of ifi204, ifi44, NLRP3 and IL1b) in the artery of TUDCA treated mice compared with mice without drugs.

2024-03-05 | GSE260610 | GEO

Tauroursodeoxycholic Acid (TUDCA) Reduces ER Stress and Disease Activity in Ulcerative Colitis

Project description:TUDCA Reduces Ulcerative Colitis Severity

| PRJEB73884 | ENA

Tauroursodeoxycholic Acid (TUDCA) Reduces ER Stress and Lessens Disease Activity in Ulcerative Colitis

Project description:TUDCA Reduces Ulcerative Colitis Severity

| PRJEB73763 | ENA