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Resveratrol improves hepatic ischemia-reperfusion injury (HIRI) through inhibiting neutrophils via suppressing ERK signaling pathway

ABSTRACT: Resveratrol improves hepatic ischemia-reperfusion injury (HIRI) through inhibiting neutrophils via suppressing ERK signaling pathway

PROVIDER: PRJNA889405 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21862911_1.fastq.gz	Fastqsanger.gz
	SRR21862911_2.fastq.gz	Fastqsanger.gz
	SRR21862912_1.fastq.gz	Fastqsanger.gz
	SRR21862912_2.fastq.gz	Fastqsanger.gz
	SRR21862913_1.fastq.gz	Fastqsanger.gz

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Resveratrol improves hepatic ischemia-reperfusion injury (HIRI) through inhibiting neutrophils via suppressing ERK signaling pathway

Project description:Methods: Methods: To better understand the role of resveratrol in the regulation of neutrophils activation and function, neutrophils with or without resveratrol in the expose of LPS were compared in a transcriptome sequencing study. Total RNA was isolated from bone marrow and FACS-separated neutrophils. Transcriptome sequencing libraries were generated using NEBNext® Ultra™ RNA Library Prep Kit for Illumina® (NEB, USA) following manufacturer’s recommendations and sequenced on an Illumina Hiseq platform (Illumina, San Diego, CA). Sequences were aligned to the reference genome with TopHat and processed with Cufflinks, which quantifies each transcript in each sample using reference annotations produced bythe University of California Santa Cruz UCSC. Differentially expressed genes with a fold change of >=2.0 and p value<0.01 between resveratrol treated and control neutrophils were submitted to GO and KEGG enrichment analysis, which uses unbiased methods to assess pathway enrichment. Results: Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses revealed that downregulated genes from resveratrol-stimulated neutrophils are involved in neutrophil migration, neutrophil chemotaxis, TNF signaling pathway and cytokine activity, among other. Compared to control neutrophils, neutrophils with resveratrol exhibited downregulated levels of cell survival related genes (Camkk1, Aqp1, Bcl2a1b, etc), cell cycle related genes (Ccnb1, Ccnb2, Cdc20, Cdk1, etc), adhesion and migration related genes (Cass4, Nectin4, Gp5, Gpr35, etc), and cytokines (Csf1, Csf3, Ccl2, Ccl7, Ccl12).

2023-02-09 | GSE215236 | GEO

Repurposing Zafirlukast Confers Renal Protection in Ischemia-Reperfusion Injury via Suppressing Macrophage METosis

Project description:Repurposing Zafirlukast Confers Renal Protection in Ischemia-Reperfusion Injury via Suppressing Macrophage METosis

| PRJNA1288531 | ENA

Repurposing Zafirlukast Confers Renal Protection in Ischemia-Reperfusion Injury via Suppressing Macrophage METosis

Project description:Tacrolimus is widely used to prevent post-transplant acute kidney injury (AKI) but causes severe toxicities (e.g., nephrotoxicity, hyperglycemia). We repurposed zafirlukast (ZFK), an FDA-approved asthma drug, to address this limitation. In a murine kidney ischemia-reperfusion injury (KIRI) model, ZFK significantly attenuated renal dysfunction, reducing serum creatinine and blood urea nitrogen (BUN) to levels comparable to tacrolimus, without inducing metabolic adverse effects. RNA sequencing revealed that ZFK recapitulated tacrolimus’ anti-inflammatory gene signatures while uniquely suppressing macrophage extracellular trap formation (METosis). Mechanistically, ZFK inhibited METosis by downregulating PAD4 and CitH3 expression, confirmed by immunofluorescence and flow cytometry. Single-cell transcriptomics (Tabula Muris and GEO database) identified macrophages as the primary target via CysLT1R antagonism. This study provides the first evidence that ZFK protects against KIRI by targeting METosis, a key driver of sterile inflammation. Given its established safety profile, ZFK could bypass Phase I trials, accelerating clinical translation as a safer alternative to calcineurin inhibitors. Our findings also highlight the broader potential of ZFK in METosis-related diseases (e.g., sepsis, atherosclerosis) and underscore drug repurposing as a strategic approach for rapid therapeutic development.

2025-07-13 | GSE302105 | GEO

RNA sequencing of mouse cardiac neutrophils after myocardial ischemia and reperfusion injury model

Project description:We performed bulk RNA-seq of cardiac neutrophils from the heart of WT and Cd300a-/- mice 3 days after myocardial ischemia and reperfusion.

2025-06-28 | GSE263749 | GEO

Repurposing Zafirlukast Confers Renal Protection in Ischemia-Reperfusion Injury via Suppressing Macrophage METosis [RNA-Seq]

2025-07-14 | GSE302163 | GEO

Repurposing Zafirlukast Confers Renal Protection in Ischemia-Reperfusion Injury via Suppressing Macrophage METosis [RNA-Seq]

Project description:Repurposing Zafirlukast Confers Renal Protection in Ischemia-Reperfusion Injury via Suppressing Macrophage METosis [RNA-Seq]

| PRJNA1289122 | ENA

Transcriptional changes during hepatic ischemia-reperfusion in the rat

Project description:Ischemia-reperfusion (IR) injury, a ubiquitous consequence of liver transplantation, is a cause of early graft rejection and increased morbidity. At present, there are no effective strategies to reduce hepatic IR injury. Molecular mechanisms that promote cell survival under these circumstances are largely undefined. We examined changes in global gene expression at early reperfusion times to identify potential IR-mediated protective responses. Using a rat model of 30 minutes of 70% warm ischemia followed by reperfusion, RNA for microarray analysis was extracted from the non-ischemic and the ischemic-reperfused lobes at four reperfusion times: 0 (no reperfusion), 0.5, 2, and 6 hours. Differentially expressed genes and pathway analyses were used to identify IR-induced events. The transcriptome of the reperfused lobes was unique and discrete at each reperfusion time, showing no evidence of sustained changes of the gene expression alterations seen at 30 minutes of reperfusion. At all reperfusion times, a significant portion of gene expression changes in the reperfused lobes were present in the non-ischemic lobes. However, the earliest reperfusion time, 30 minutes, showed a marked increase in the expression of a set of immediate-early genes (c-Fos, c-Jun, Atf3, Egr1) that was exclusive to the reperfused lobe. Similarities of gene expression changes in the reperfused and the non-ischemic lobes at each time suggest that hemodynamics and/or circulating factors are potent stimuli in an IR model. However, early reperfusion events appear to reflect a cell-autonomous response that may be protective, thereby representing potential targets to ameliorate IR injury.

2019-12-16 | GSE117915 | GEO

Mouse kidney ischemia-reperfusion injury time course

Project description:Time course experiments involving bilateral renal ischemia reperfusion injury (IRI) in C57BL/6J mice (0 hr control, 20 min bilateral ischemia without reperfusion, 4, 16, 24, 36, 48, and 72 hrs post IRI). This dataset also includes IRI at 48 hrs and 72 hrs in Azin1 A-to-I locked and Azin1 A-to-I uneditable mice.

2024-09-30 | GSE267650 | GEO

Vitamin B12 alleviates myocardial ischemia/reperfusion injury

Project description:To examine the protective effect of B12 on myocardial ischemia/reperfusion injury and figure out the mechanism of B12.

2024-01-01 | GSE225105 | GEO

Resveratrol exerts antiviral activity against pseudorabies virus through regulation of the OPN-ERK/JNK-IL-1β signaling axis

Project description:We analyzed the changes in the cellular proteome after PRV infection in resveratrol-treated PK-15 cells using TMT quantitative proteomics combined with LC-MS/MS. The results identified the differential proteins osteopontin (iOPN) and interleukin-1 receptor accessory protein (IL-1RAP), which have significant biological implications. The regulation of OPN-IL-1β signaling by PRV infection was further studied through the OPN-ERK/JNK-IL-1β signaling axis

2025-02-19 | PXD060943 |

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