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Targeting STAT3 with Conditional Knockout or PROTAC Technology Alleviates Renal Injury by Limiting Pyroptosis [RNA-seq]

ABSTRACT: Targeting STAT3 with Conditional Knockout or PROTAC Technology Alleviates Renal Injury by Limiting Pyroptosis [RNA-seq]

PROVIDER: PRJNA1192256 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31551359_1.fastq.gz	Fastqsanger.gz
	SRR31551359_2.fastq.gz	Fastqsanger.gz
	SRR31551360_1.fastq.gz	Fastqsanger.gz
	SRR31551360_2.fastq.gz	Fastqsanger.gz
	SRR31551361_1.fastq.gz	Fastqsanger.gz

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Targeting STAT3 with Conditional Knockout or PROTAC Technology Alleviates Renal Injury by Limiting Pyroptosis [RNA-seq]

Project description:The role of signal transducer and activator of transcription protein 3 (STAT3) in AKI remains controversial. Our study demonstrated an upregulation of total STAT3 protein in AKI mouse models induced by cecal ligation and puncture (CLP) or ischemia-reperfusion (I/R), correlating with patient biopsy results. This increase may be attributed to histone H3K27 acetylation. STAT3 knockout in renal tubular epithelial cells significantly reduced AKI injury and inflammation in mice. Mechanistically, STAT3 induces the transcription of tripartite motif-containing protein 21 (TRIM21), triggering a cascade that activates gasdermin D (GSDMD), resulting in pyroptosis. Administration of the novel proteolysis-targeting chimera (PROTAC) compound E034, which selectively targets STAT3 for ubiquitination and degradation, significantly alleviated renal injury in a low-dose, single-dose regimen, underscoring its substantial therapeutic potential with infrequent dosing requirements. In the context of renal injury, PROTAC emerges as a promising modality by specifically targeting the STAT3/TRIM21/GSDMD axis, which our study has identified as a potential therapeutic target, thereby potentially endowing novel and clinically significant therapeutic strategies.

2025-06-16 | GSE283160 | GEO

Targeting STAT3 with Conditional Knockout or PROTAC Technology Alleviates Renal Injury by Limiting Pyroptosis [ChIP-seq]

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Targeting STAT3 with Conditional Knockout or PROTAC Technology Alleviates Renal Injury by Limiting Pyroptosis [ChIP-seq]

Project description:Targeting STAT3 with Conditional Knockout or PROTAC Technology Alleviates Renal Injury by Limiting Pyroptosis [ChIP-seq]

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Development of MDM2-targeting PROTAC technology for advancing bone regeneration

Project description:MDM2 inhibitor remarkably induced biomineralization in hDPSCs but it remained the problem that p53 activation is insufficient due to MDM2-p53 autoregulatory feedback loop. To overcome the limitation of the MDM2 inhibitors, we applied proteolysis targeting chimera (PROTAC), a technology that degrades a protein of interest (POI) by intracellular ubiquitin-proteasome system. Hence, we propose a strategy to induce hard tissue regeneration by MDM2-targeting PROTAC technology. We selected Nutlin-3 of POI ligand among various MDM2 inhibitors based on the screening process, and the selected CRBN of E3 ligase ligand. The MDM2-PROTAC synthesis platform was designed by each ligand combination. By performing the degradation test for selected compounds, we evaluated the characteristics of the developed MDM2 PROTAC such as the maximal degradation concentration (DCmax), the half of maximal degradation concentration (DC50), and half-lifetime. To investigate gene expression profiling of MDM2-targeting small molecules, we conducted RNA-sequencing under MDM2 PROTAC and Nutlin-3 (POI ligand) treated conditions. We not only confirmed a robust effect on biomineralization by MDM2-targeting small molecules but also demonstrated the potent osteogenic differentiation ability of MDM2 PROTAC when compared to an MDM2 inhibitor. MDM2-PROTAC significantly increased mRNA levels of osteogenic differentiation marker genes. Also, the significant bone generation effect of MDM2 PROTAC was validated in an ovariectomy (OVX)-induced osteoporosis animal model. Through these results, it is expected that a new therapeutic modality for hard tissue regeneration will be possible, and the application range of the PROTAC system can be expanded.

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Project description:Macrophages are involved in the pathophysiology of many diseases as critical cells of the innate immune system. Pyroptosis is a form of macrophage death that induces cytokinesis of phagocytic substances in the macrophages, thereby defending against infection. Dimethyl itaconate (DI) is an analog of itaconic acid with anti-inflammatory effects. However, the effect of dimethyl itaconate on macrophage pyroptosis has not been elucidated clearly. Thus, the present study aimed to analyze the effect of DI treatment on a macrophage pyroptosis model (Lipopolysaccharide, LPS+Adenosine Triphosphate, ATP). The results showed that 0.25 mM DI ameliorated macrophage pyroptosis and downregulated interleukin (IL)-1β expression. Then, real-time quantitative polymerase chain reaction (RT-qPCR) was used to confirm the result of RNA-sequencing of the upregulated oxidative stress-related genes (Gclc and Gss) and downregulated inflammation-related genes (IL-12β and IL-1β). In addition, Gene Ontology (GO) enrichment analysis showed that differential genes were associated with transcript levels and DNA replication. Kyoto encyclopedia of genes and genomes (KEGG) enrichment showed that signaling pathways, such as tumor necrosis factor (TNF), Jak, Toll-like receptor and IL-17, were altered after DI treatment. N-acetyl-L-cysteine (NAC) reversed the DI effect on the LPS+ATP-induced macrophage pyroptosis and upregulated the IL-1β expression. Oxidative stress-related protein Nrf2 is involved in the DI regulation of macrophage pyroptosis. Taken together, these findings suggested that DI alleviates the pyroptosis of macrophages through oxidative stress.

2021-10-16 | GSE185895 | GEO

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2023-12-11 | PXD046949 | Pride

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Project description:Pyroptosis is a type of lytic cell death executed by members of the gasdermin family. It has been demonstrated that induction of pyroptosis can effectively inhibit tumor growth, which implicates a new strategy for clinical tumor therapy, especially for those tumors (such as melanoma) that are insensitive or resistant to the induction of apoptosis.By means of a chemical compound DBIC, designed and identified by our group recently, to induce GSDMC-mediated pyroptosis in melanoma cells.

2025-07-07 | GSE273365 | GEO

Regulation of pyroptosis in radiation induces mouse intestine cells

Project description:Pyroptosis is a recently discovered form of lytic cell death that is characterized by cell swelling and formation of pores and large bubbles on the plasma membrane. We find radiation could induce pyroptosis in human colorectal cancer HCT116 cells, and irradiation induces pyroptosis in mouse normal intestine MODEK cells only after 36 hours and over 8.0 Gy. In view of the significant pyroptosis effect of MODE-K cells, we selected 4Gy and 12Gy, 24h and 48h for experiments. After ONT full-length transcriptome sequencing, the cell pyroptosis model can screen out the differential genes related to cell pyroptosis, which is helpful to further explore the mechanism of pyroptosis of MODE-K cells.

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2024-07-27 | PXD053939 | Pride

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