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ATF3 Inhibits Cardiac Ferroptosis by Directly Binding FANCD2 in Response to Myocardial Ischemia/Reperfusion Injury

ABSTRACT: ATF3 Inhibits Cardiac Ferroptosis by Directly Binding FANCD2 in Response to Myocardial Ischemia/Reperfusion Injury

PROVIDER: PRJNA798711 | ENA |

REPOSITORIES: ENA

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ATF3 Inhibits Cardiac Ferroptosis by Directly Binding FANCD2 in Response to Myocardial Ischemia/Reperfusion Injury [ChIP-Seq]

Project description:ATF3 Inhibits Cardiac Ferroptosis by Directly Binding FANCD2 in Response to Myocardial Ischemia/Reperfusion Injury [ChIP-Seq]

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ATF3 Inhibits Cardiac Ferroptosis by Directly Binding FANCD2 in Response to Myocardial Ischemia/Reperfusion Injury [RNA-Seq 2]

Project description:ATF3 Inhibits Cardiac Ferroptosis by Directly Binding FANCD2 in Response to Myocardial Ischemia/Reperfusion Injury [RNA-Seq 2]

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ATF3 Inhibits Cardiac Ferroptosis by Directly Binding FANCD2 in Response to Myocardial Ischemia/Reperfusion Injury [RNA-Seq 1]

Project description:ATF3 Inhibits Cardiac Ferroptosis by Directly Binding FANCD2 in Response to Myocardial Ischemia/Reperfusion Injury [RNA-Seq 1]

| PRJNA798718 | ENA

ATF3 Inhibits Cardiac Ferroptosis by Directly Binding FANCD2 in Response to Myocardial Ischemia/Reperfusion Injury [ChIP-Seq]

Project description:We performed ChIP-seq to find the trageted genes regulated by ATF3 in hypoxia/reoxygenation (H/R)using ATF3 antibody for ChIP.

2023-01-01 | GSE193996 | GEO

ATF3 Inhibits Cardiac Ferroptosis by Directly Binding FANCD2 in Response to Myocardial Ischemia/Reperfusion Injury [RNA-Seq 2]

Project description:Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to compare NGS-derived neonatal mouse cells' transcriptome profiling (RNA-seq) to microarray method and to evaluate protocols for optimal high-throughput data analysis, to find the trageted genes regulated by ATF3 in Hypoxia/Reoxygenation(H/R)

2023-01-01 | GSE193999 | GEO

ATF3 Inhibits Cardiac Ferroptosis by Directly Binding FANCD2 in Response to Myocardial Ischemia/Reperfusion Injury [RNA-Seq 1]

Project description:The goals of this study are to compare mice heart tissues' transcriptome profiling (RNA-seq) to microarray and quantitative reverse transcription polymerase chain reaction (qRT–PCR) methods and to evaluate protocols for optimal high-throughput data analysis, and find the potential molecule implicating in myocardial ischemia/reperfusion injury.

2023-01-01 | GSE193997 | GEO

ATF3 Inhibits Cardiac Ferroptosis by Directly Binding FANCD2 in Response to Myocardial Ischemia/Reperfusion Injury

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-01-01 | GSE194000 | GEO

ATF3 coordinates the survival/proliferation of cardiac macrophages to protect against ischemia-reperfusion injury

Project description:Cardiac resident MerTK+ macrophages exert multiple protective roles post-ischemic injury, however, the mechanisms regulating their fate are not fully understood. Here we show that GAS6-inducible transcription factor ATF3 prevents apoptosis of MerTK+ macrophages after ischemia-reperfusion (IR) injury, by repressing the transcription of multiple genes involved in type I interferon expression (Ifih1 and Infb1) and apoptosis (Apaf1). Mice lacking ATF3 in cardiac macrophages or myeloid cells showed excessive loss of MerTK+ cardiac macrophages, poor angiogenesis, and worse heart dysfunction post-IR, which were rescued by the transfer of MerTK+ cardiac macrophages. GAS6 administration improved cardiac repair in an ATF3-dependent manner. Finally, we showed a negative association of GAS6 and ATF3 expression with the risk of major adverse cardiac events in patients with ischemic heart disease. These results indicate that the GAS6-ATF3 axis has a protective role against IR injury by regulating MerTK+ cardiac macrophage survival/proliferation.

2023-11-07 | GSE247139 | GEO

Sophoridine derivative 6j inhibits liver cancer cell proliferation via ATF3 mediated ferroptosis

Project description:Liver cancer is one of the most lethal malignancies with an annual death of over 830,000 cases. Although targeted therapeutic drugs have achieved certain clinical efficacy, only sorafenib and lenvatinib are currently marketed as first-line targeted drugs to treat patients with advanced liver cancer. Therefore, developing more drugs are urgently needed. Ferroptosis is an iron-dependent programmed cell death (PCD) distinct from known PCDs including apoptosis, necrosis, and autophagy. Targeting ferroptosis is recognized as a promising potential therapeutic modality for liver cancer. Activating transcription factor 3 (ATF3) is an important ferroptosis inducer and targeting ATF3 offers a potential means to cancer therapy. In the present study, we reported for the first time a sophoridine derivative 6j with promising anti-liver cancer effects in vitro and in vivo. Compound 6j could induce liver cancer cells ferroptosis by promoting the accumulation of intracellular Fe2+, reactive oxygen species (ROS), and MDA. Inhibition of ferroptosis by ferrostatin-1 alleviated 6j induced accumulation of Fe2+, ROS, and MDA and restored cell viability. Further study revealed that compound 6j upregulated the expression of ATF3 via ER stress and knockdown of ATF3 by RNA interference attenuated 6j induced ferroptosis and cell proliferation inhibition. This study would provide new insights for the design of ferroptosis inducers and the development of anti-liver cancer drugs.

2023-08-23 | GSE237138 | GEO

Circ_0008146 exacerbates ferroptosis via regulating miR-342-5p/ACSL4 axis after cerebral ischemia-reperfusion in mice

Project description:Background: Characterized by high incidence, mutilation, and death rate, acute ischemic stroke (AIS) has threatened people’s health seriously. Therefore, there is an urge need for early diagnosis and effective treatment of AIS. The purpose of this study was to clarify the regulatory role and potential molecular mechanism of miR-342-5p and circRNA_0008146 in AIS. Materials and Methods: Small RNA sequencing analysis was performed to screen differentially expressed miRNAs between the AIS and control group. Middle cerebral artery occlusion/reperfusion (MCAO/R) models were constructed in C57BL/6J mice. The circRNA_0008146 and miRNA expression levels were detected by quantitative real-time PCR. Assay kits were used to determine Fe2+ levels and assess a battery of oxidative stress indicators, including ROS, MDA, LPO, SOD, and GSH/GSSG. The content of ACSL4 was measured by Western blot. The neurobehavioral manifestation was evaluated using the modified Neurological Severity (mNSS) Score, rotarod test, and corner test. TTC staining was employed to detect cerebral infarction volume. Nissl staining was adapted to detect histological change and neuronal damage. Results: RNA sequencing analysis revealed miR-342-5p was significantly downregulated in the plasma of AIS patients. MiR-342-5p inhibited oxidative stress and RSL3-induced ferroptosis after cerebral ischemic-reperfusion injury in vivo by targeting ferroptosis-related gene ACSL4. CircRNA_0008146 acted as a sponge of miR-342-5p, and overexpression of circRNA_0008146 increased brain damage in stroke mice. CircRNA_0008146 contributed to ferroptosis in cerebral infraction via sponging miR-342-5p to regulate ACSL4. Conclusion: CircRNA_0008146/miR-342-5p/ACSL4 axis regulate ferroptosis after cerebral ischemia-reperfusion, which may be a potential therapeutic target for ischemic stroke.

2024-08-08 | GSE254322 | GEO

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