Hepatic miR-93 promotes the pathogenesis of metabolic dysfunction-associated steatotic liver disease by suppressing SIRT1
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ABSTRACT:
PROVIDER: PRJNA1162804 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR30723365_1.fastq.gz | Fastqsanger.gz | |||
| SRR30723365_2.fastq.gz | Fastqsanger.gz | |||
| SRR30723366_1.fastq.gz | Fastqsanger.gz | |||
| SRR30723366_2.fastq.gz | Fastqsanger.gz | |||
| SRR30723367_1.fastq.gz | Fastqsanger.gz |
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Project description:The molecular mechanisms underlying the pathogenesis of metabolic dysfunction-associated steatotic liver disease (MASLD) remain largely unclear. Emerging evidence suggests that microRNAs (miRNAs) play a critical role in transcriptional regulation by targeting genes involved in MASLD and other metabolic disorders, this study aims to elucidate the role of miR-93 in lipid metabolism and its impact on MASLD progression.
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Project description:Background: Postoperative cognitive dysfunction (POCD) is a debilitating neurological complication in surgical patients. Current research has focused mainly on microglial activation, but less is known about the resultant neuronal synaptic changes. Recent studies have suggested that silent information regulator 1 (SIRT1) plays a critical role in several different neurological disorders via its involvement in microglial activation. In this study, we evaluate the effects of SIRT1 activation in a POCD mouse model. Methods: Exploratory laparotomy was performed in mice aged 12-14 months under sevoflurane anesthesia to establish our animal POCD model. Transcriptional changes in the hippocampus after anesthesia and surgery were evaluated by RNA sequencing. SIRT1 expression was verified by Western Blot. Mice were treated with SIRT1 agonist SRT1720 or vehicle after surgery. Changes in microglia morphology, microglial phagocytosis, presence of dystrophic neurites, and dendritic spine density were evaluated. Cognitive performance was evaluated using the Y maze and Morris water maze. Results: SIRT1 expression levels were downregulated in POCD. Exposure to anesthesia and surgery lead to alteration in microglia morphology, increased synaptic engulfment, dendritic spine loss, and cognitive deficits. These effects were alleviated by SRT1720 administration. Conclusion: This study suggests an important neuroprotective role for SIRT1 in POCD pathogenesis. Increasing SIRT1 function represents a promising therapeutic strategy for prevention and treatment of POCD.
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Project description:Sirtuin-1 (Sirt1), a class III histone/protein deacetylase is central to cellular metabolism, stress responses and aging, but its contributions to various host immune functions have been little investigated. To study the role of Sirt1 in T-cell functions, we undertook targeted deletions by mating mice with a floxed Sirt1 gene to mice expressing CD4-cre or Foxp3-cre recombinase, respectively. We found that Sirt1 deletion left conventional T-effector cell activation, proliferation and cytokine production largely unaltered. However, Sirt1 targeting promoted the expression and acetylation of Foxp3, a key transcription factor in T-regulatory (Treg) cells, and increased Treg suppressive functions in vitro and in vivo. Consistent with these data, mice with targeted deletions of Sirt1 in either CD4+ T-cells or Foxp3+ Treg cells exhibited prolonged survival of MHC-mismatched cardiac allografts. Allografts in Sirt1 targeted recipients showed long-term preservation of myocardial histology and infiltration by Foxp3+ Treg cells. Comparable results were seen in wild-type allograft recipients treated with Sirt1 inhibitors, such as EX-527 and splitomicin. Hence, Sirt1 may inhibit Treg functions and its targeting may have therapeutic value in autoimmunity and transplantation.
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Project description:SIRT1 chromatin interactome analysis was performed to identify SIRT1 molecular targets involved in replication initiation from cells containing either WT or H363Y SIRT1. Co-IP-MS of pT530 SIRT1 from chromatin extracts was performed. Files are: 1422 WT SIRT1 untreated U2OS; 1423 WT SIRT1 H2O2 treated, U2OS; 1424 H363Y SIRT1 untreated U2OS; 1425 H363Y SIRT1 H2O2 U2OS; 1426 KO SIRT1 untreated U2OS; 1427 KO SIRT1 H2O2 U2OS; 1428 WT SIRT1 untreated HEK; 1429 WT SIRT1 H2O2 HEK; 1430 WT SIRT1 untreated HCT116; 1431 WT SIRT1 H2O2 HCT116; 1432 WT SIRT1 untreated K562; 1433 WT SIRT1 H2O2 K562. Each sample has 9 fractions.
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