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3,4-Dimethoxychalcone, a caloric restriction mimetic, enhances the TFEB-mediated autophagy and alleviates pyroptosis and necroptosis after spinal cord injury

ABSTRACT: This study investigated the therapeutic value of a candidate CRM, 3,4-dimethoxychalcone (3,4-DC), in functional recovery after SCI and its underlying mechanism. RNA sequencing was used to identify the mechanisms of 3,4-DC in SCI.

ORGANISM(S): Mus musculus

PROVIDER: GSE210033 | GEO | 2022/08/01

REPOSITORIES: GEO

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3,4-Dimethoxychalcone, a caloric restriction mimetic, enhances TFEB-mediated autophagy and alleviates pyroptosis and necroptosis after spinal cord injury.

Project description:Background: Caloric restriction mimetics (CRMs) mimic the favourable effects of caloric restriction (CR) and have been shown to have therapeutic effects in neuroinflammatory disease. However, whether CRMs improve the functional recovery from spinal cord injury (SCI) and the underlying mechanism of action remain unclear. In this study, we used the CRMs 3,4-dimethoxychalcone (3,4-DC) to evaluate the therapeutic value of CRMs for SCI. Methods: HE, Masson and Nissl staining; footprint analysis; and the Basso mouse scale were used to determine the functional recovery from SCI after 3,4-DC treatment. RNA sequencing was used to identify the mechanisms of 3,4-DC in SCI. Western blotting, qPCR and immunofluorescence were used to detect the levels of pyroptosis, necroptosis, autophagy and the AMPK-TRPML1-calcineurin signalling pathway. We employed a dual-luciferase reporter assay in vitro and applied AAV vectors to inhibit TFEB in vivo to explore the mechanism of 3,4-DC. Results: 3,4-DC reduced glial scar area and motor neuron death and improved functional recovery after SCI. RNA-sequencing results indicated that oxidative stress, pyroptosis, necroptosis, and autophagy may be involved in the ability of 3,4-DC to improve functional recovery. Furthermore, 3,4-DC inhibited pyroptosis and necroptosis by enhancing autophagy. We also found that 3,4-DC enhances autophagy by promoting TFEB activity. A decrease in the TFEB level abolished the protective effect of 3,4-DC. In addition, 3,4-DC partially regulated TFEB activity through the AMPK-TRPML1-calcineurin signalling pathway. Conclusions: 3,4-DC promotes functional recovery by upregulating TFEB-mediated autophagy and inhibiting pyroptosis and necroptosis after SCI, which may have potential clinical application value.

| S-EPMC9830432 | biostudies-literature

3,4-Dimethoxychalcone, a caloric restriction mimetic, enhances the TFEB-mediated autophagy and alleviates pyroptosis and necroptosis after spinal cord injury

Project description:3,4-Dimethoxychalcone, a caloric restriction mimetic, enhances the TFEB-mediated autophagy and alleviates pyroptosis and necroptosis after spinal cord injury

| PRJNA863479 | ENA

Gene expression profiling in zebrafish embryos exposed to 3,4-dichloroaniline (3,4-DCA)

Project description:The zebrafish (Danio rerio) embryo toxicity test (DarT) is considered as an alternative to the acute fish toxicity test. However, DarT rarely reveals information on the mechanisms underlying a toxic effect and is relatively insensitive compared to chronic toxic effects. We hypothesized that, by using gene expression profiles as an additional endpoint, it may be possible to increase the sensitivity and predictive value of DarT. Therefore we exposed zebrafish embryos for 48 h to the reference compound 3,4-dichloroaniline and analyzed gene expression patterns with a 14 k oligonucleotide array. Keywords: differential gene expression upon chemical exposure in zebrafish embryos

2006-11-08 | GSE6228 | GEO

Ascending dorsal column sensory neurons respond to spinal cord injury and downregulate genes related to lipid metabolism

Project description:The goal of this study was to compare the transcriptional effects of sciatic nerve injury and spinal cord injury on lumbar dorsal root ganglion (DRG) and FACS-sorted dorsal column (DC) sensory neurons. We performed RNA-seq of whole DRG from naïve and spinal cord-injured (SCI) mice (1dpi) and compared this with previously published data for sciatic nerve transection. In order to assess changes specifically in DC neurons, we performed RNA-seq from FACS-sorted DC neurons from Thy1-YFP16 transgenic mice in naïve, sciatic nerve injured (SNI), and SCI (1 and 3dpi). We found that DC neurons alter their transcriptome after SCI, but that gene changes after SCI mostly differ from SNI. These transcriptional differences may reflect both growth promoting and growth inhibitory effects on axon regeneration after SCI.

2021-01-19 | GSE149646 | GEO

Transcriptomic analysis of young roots of spruce tianshan treated with 1mMDHAP (3,4 dihydroxyacetophenone)

Project description:In past studies the hypothesis of "self-toxicity of natural regeneration barriers of Spruce tianshan" were proposed, and verified that 3, 4-dihydroxyacetophenone (DHAP) contained in litter of Spruce Tianshan was the direct cause of population regeneration barriers.The molecular basis of DHAP-induced autotoxicity was explored through transcriptomic analysis of young roots of spruce tianshan treated with DHAP (3,4 dihydroxyacetophenone).

2021-01-01 | GSE160134 | GEO

Label free quantitative proteomic analysis on (-)-epicatechin (EC) and 5-(3',4'-dihydroxyphenyl)-γ-valerolactone (3,4-diHPV) treated Caco-2 and Hepa1c1c7 cells

Project description:Epicatechin (EC) is a well-known dietary polyphenol and widely found in various foods, e.g., apple, cocoa, green tea, wine, etc. Its consumption has been associated with attenuation of some chronic diseases. After ingestion of EC, a large portion is passed into the large intestinal lumen where it is extensively degraded into various microbial metabolites. One of the major EC microbial metabolites is 5-(3’,4’-dihydroxyphenyl)-γ-valerolactone (3,4-diHPV). The protein expression profiles of EC or 3,4-diHPV treated Caco-2 and Hepa1c1c7 cells were studied with the help of label-free quantitative proteomics. Compared to the parent compound EC, 3,4-diHPV was able to induce upregulations of more Nrf2-related proteins in both cell lines, and the number of significant differentially expressed proteins (DEPs) induced by 3,4-diHPV in Hepa1c1c7 cells was much higher than the respective EC treatment.

2022-08-12 | PXD033248 | Pride

Ferroptosis, necroptosis, and pyroptosis in anticancer immunity.

Project description:In recent years, cancer immunotherapy based on immune checkpoint inhibitors (ICIs) has achieved considerable success in the clinic. However, ICIs are significantly limited by the fact that only one third of patients with most types of cancer respond to these agents. The induction of cell death mechanisms other than apoptosis has gradually emerged as a new cancer treatment strategy because most tumors harbor innate resistance to apoptosis. However, to date, the possibility of combining these two modalities has not been discussed systematically. Recently, a few studies revealed crosstalk between distinct cell death mechanisms and antitumor immunity. The induction of pyroptosis, ferroptosis, and necroptosis combined with ICIs showed synergistically enhanced antitumor activity, even in ICI-resistant tumors. Immunotherapy-activated CD8+ T cells are traditionally believed to induce tumor cell death via the following two main pathways: (i) perforin-granzyme and (ii) Fas-FasL. However, recent studies identified a new mechanism by which CD8+ T cells suppress tumor growth by inducing ferroptosis and pyroptosis, which provoked a review of the relationship between tumor cell death mechanisms and immune system activation. Hence, in this review, we summarize knowledge of the reciprocal interaction between antitumor immunity and distinct cell death mechanisms, particularly necroptosis, ferroptosis, and pyroptosis, which are the three potentially novel mechanisms of immunogenic cell death. Because most evidence is derived from studies using animal and cell models, we also reviewed related bioinformatics data available for human tissues in public databases, which partially confirmed the presence of interactions between tumor cell death and the activation of antitumor immunity.

| S-EPMC7418434 | biostudies-literature

Transcription profiling by array of Lotus japonicus leaves in response to treatment with the nitrification inhibitor DMPP (3,4-dimethylpirazole phosphate)

Project description:Transcriptomic profiling was carried out for leaves of Lotus japonicus plants grown in the presence or absence of 10 mg/L-1 of the nitrification inhibitor DMPP (3,4-dimethylpirazole phosphate).

2019-07-01 | E-MTAB-7268 | biostudies-arrayexpress

Autophagy, ferroptosis, pyroptosis, and necroptosis in tumor immunotherapy.

Project description:In recent years, immunotherapy represented by immune checkpoint inhibitors (ICIs) has led to unprecedented breakthroughs in cancer treatment. However, the fact that many tumors respond poorly or even not to ICIs, partly caused by the absence of tumor-infiltrating lymphocytes (TILs), significantly limits the application of ICIs. Converting these immune "cold" tumors into "hot" tumors that may respond to ICIs is an unsolved question in cancer immunotherapy. Since it is a general characteristic of cancers to resist apoptosis, induction of non-apoptotic regulated cell death (RCD) is emerging as a new cancer treatment strategy. Recently, several studies have revealed the interaction between non-apoptotic RCD and antitumor immunity. Specifically, autophagy, ferroptosis, pyroptosis, and necroptosis exhibit synergistic antitumor immune responses while possibly exerting inhibitory effects on antitumor immune responses. Thus, targeted therapies (inducers or inhibitors) against autophagy, ferroptosis, pyroptosis, and necroptosis in combination with immunotherapy may exert potent antitumor activity, even in tumors resistant to ICIs. This review summarizes the multilevel relationship between antitumor immunity and non-apoptotic RCD, including autophagy, ferroptosis, pyroptosis, and necroptosis, and the potential targeting application of non-apoptotic RCD to improve the efficacy of immunotherapy in malignancy.

| S-EPMC9208265 | biostudies-literature

ZBP1 is a cytosolic RNA virus sensor driving activation of the NLRP3 inflammasome, pyroptosis, necroptosis and apoptosis

Project description:The innate immune system recognizes nucleic acids as a signature of microbial infection and initiates host-protective responses, including the production of type I IFN and proinflammatory cytokines. Z-DNA binding protein 1 (ZBP1, also known as DLM-1 or DAI) was previously identified as a dsDNA binding protein, triggering DNA-mediated activation of innate immune responses. However, mice or cells lacking ZBP1 produce normal levels of type I IFN in response to dsDNA. Therefore, the classification of ZBP1 as a true DNA sensor remains to be resolved. Here, we report that the single stranded RNA virus, influenza A virus (IAV) is a trigger of the cytosolic sensor ZBP1. Sensing of IAV infection by ZBP1 engages a novel NLRP3 inflammasome pathway that is not defined by the conventions of the canonical and non-canonical NLRP3 inflammasome pathways. Surprisingly, IAV-induced cell death was not prevented by the absence of the NLRP3 inflammasome. Instead, we identified parallel contributions from pyroptosis, necroptosis and apoptosis in the execution of ZBP1-dependent cell death, mediated by the kinase RIPK3. Overall, the ability of ZBP1 to sense IAV infection signifies a point of divergence for IAV-induced programmed cell death pathways and inflammasome activation. We used microarrays to explore the gene expression profiles differentially expressed in influenza-infected bone marrow derived macrophages (BMDM) isolated from Ifnar1-/- and wild-type mice.

2016-08-11 | E-GEOD-77611 | biostudies-arrayexpress

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