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Btg2 Inhibits the UFMylation of Fmo1 thus Restricting Taurine Synthesis and Exacerbating Ferroptosis in Hepatic Ischemia-Reperfusion Injury in Mice

ABSTRACT: Hepatic ischemia‒reperfusion (I/R) injury (HIRI) represents a frequently occurring pathological phenomenon during liver surgery, yet the mechanisms governing HIRI remain inadequately comprehended. This study intends to explore the role of B-cell translocation gene 2 (Btg2) in HIRI.

ORGANISM(S): Mus musculus

PROVIDER: GSE293329 | GEO | 2025/04/03

REPOSITORIES: GEO

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Btg2 Inhibits the UFMylation of Fmo1 thus Restricting Taurine Synthesis and Exacerbating Ferroptosis in Hepatic Ischemia-Reperfusion Injury in Mice

Project description:Hepatic ischemia‒reperfusion (I/R) injury (HIRI) represents a frequently occurring pathological phenomenon during liver surgery, yet the mechanisms governing HIRI remain inadequately comprehended. This study intends to explore the role of B-cell translocation gene 2 (Btg2) in HIRI. We find that Btg2 expression is up-regulated following HIRI. We subsequently develop an HIRl model utilizing hepatocyte-specific Btg2 transgenic over-expression and systemic Btg2 knockout male mice, discovering that Btg2 deletion mitigates inflammation and apoptosis. Furthermore, cellular experiments confirm that Btg2 knockdown alleviates inflammation and mitochondrial stress generated by hypoxia/reoxygenation (H/R). Metabolomics reveals enrichment of taurine metabolism pathway in the Btg2-/- mice. Mechanistically, we demonstrate that Btg2 restricts the UFMylation of flavin-containing monooxygenase 1 (Fmo1), the essential enzyme for taurine synthesis, by the E3 ligase UFM1-specific ligase 1 (Ufl1), consequently facilitating the K48 ubiquitination-mediated degradation of Fmo1. Adeno-associated virus-mediated Fmo1 over-expression inhibits ferroptosis and HIRI significantly in vivo, while adenovirus-mediated Btg2 over-expression mitigates ferroptosis and hypoxia/reoxygenation damage in vitro. Moreover, virtual screening of natural compounds reveals that Daturataturin A inhibits Btg2 and attenuates ferroptosis and HIRI sufficiently. These results propose that Btg2 may constitute a promising therapeutics target for HIRI.

2025-07-25 | PXD066631 |

BTG1 and BTG2 Regulate B Linege Commitment by Modulation of EBF1 Activity

Project description:The human BTG1 and BTG2 genes are targeted by genetic alterations in hematological malignancies. In this study we examined the unique and overlapping functions of Btg1 and Btg2 in mouse B cell development. Mice deficient for Btg1 and Btg2 displayed the strongest phenotype with a decrease in B cell numbers in bone marrow due to impaired B cell commitment and immature B cell differentiation. To determine the underlying mechanism, microarray expression analyis was performed on early (B220+ CD43+) and late (B220+ CD43-) B cells of WT and Btg1;Btg2 dKO mice. Total RNA obtained from sorted B220+ CD43+ ( Hardy fractions ABC) and B220+ CD43- (Hardy fractions DEF) BM cells of WT and Btg1-/-;Btg2-/- mice. In total 4 samples were analyzed and no replicates were included.

2014-03-19 | E-GEOD-55997 | biostudies-arrayexpress

BTG1 and BTG2 Regulate B Linege Commitment by Modulation of EBF1 Activity

2014-03-19 | GSE55997 | GEO

B-cell Translocation Gene 2 Inhibits UFMylation Modification of FMO1 thus Restricting Taurine Synthesis and Exacerbating Ferroptosis in Hepatic Ischemia-Reperfusion Injury

Project description:B-cell Translocation Gene 2 Inhibits UFMylation Modification of FMO1 thus Restricting Taurine Synthesis and Exacerbating Ferroptosis in Hepatic Ischemia-Reperfusion Injury

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RNAseq of cultured neonatal rat ventricular cardiomyocytes treated with siRNA for Btg1 and Btg2 knockdown.

Project description:Total RNA was isolated from n=3 culture wells per siRNA treatment group, from 6 independent primary neonatal rat cardiomyocyte isolations. RNA was pooled to obtain n=3 independent samples per siRNA treatment group for sequencing. The siRNA treatment groups were= siScr (Scramble control), siBtg12 (Btg1/Btg2 double knockdown), siBtg1 (Btg1 single knockdown), siBtg2 (Btg2 single knockdown).

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MicroRNA-409-3p/BTG2 Signaling Axis Improves Impaired Angiogenesis and Wound Healing in Obese Mice

Project description:Wound healing is facilitated by neoangiogenesis, a complex process that is essential to tissue repair in response to injury. MicroRNAs are small, non-coding RNAs that can regulate the wound healing process including stimulation of impaired angiogenesis that is associated with Type-2 diabetes (T2D). Expression of miR-409-3p was significantly increased in the non-healing skin wounds of patients with T2D compared to the non-wounded normal skin, and in the skin of a murine model with T2D. In response to high glucose, neutralization of miR-409-3p markedly improved EC growth and migration in human umbilical vein endothelial cells (HUVECs), promoted wound closure and angiogenesis as measured by increased CD31 in human skin organoids, while overexpression attenuated EC angiogenic responses. Bulk mRNA-Seq transcriptomic profiling revealed BTG2 as a target of miR-409-3p, where overexpression of miR-409-3p significantly decreased BTG2 mRNA and protein expression. A 3′ untranslated region (3′-UTR) luciferase assay of BTG2 revealed decreased luciferase activity with overexpression of miR-409-3p, while inhibition had opposite effects. Mechanistically, in response to high glucose, miR-409-3p deficiency in ECs resulted in increased mTOR phosphorylation meanwhile BTG2 silencing significantly decreased mTOR phosphorylation. Endothelial specific and tamoxifen-inducible miR-409-3p knock out mice (MiR-409IndECKO) with hyperglycemia that underwent dorsal skin wounding showed significant improvement of wound closure, increased blood flow, granulation tissue thickness (GTT), and CD31 that correlated with increased BTG2 expression. Taken together, our results show that miR-409-3p is a critical mediator of impaired angiogenesis in diabetic skin wound healing.

2025-01-31 | GSE252852 | GEO

TIS21/BTG2/PC3 and cyclin D1 are key determinants of nuclear diacylglycerol kinase-zeta-dependent cell cycle arrest

Project description:In addition to lipid second messengers derived from the plasma membrane, increasing evidence supports the existence of nuclear lipid-dependent signaling networks. Diacylglycerol is a key second messenger, generated at the nuclear level, which is metabolized by diacylglycerol kinases (DGKs). It has been demonstrated that nuclear DGK-ζ negatively regulates cell cycle progression. The aim of this study was to identify key determinants of nuclear DGK-ζ-dependent cell cycle arrest in C2C12 mouse myoblasts. Using DNA microarrays, Real-Time RT-PCR and western blot, we demonstrated that nuclear DGK-ζ downregulated the expression of cyclin D1 and increased the expression of TIS21/BTG2/PC3, a transcriptional regulator of cyclin D1 with a strong anti-proliferative function. Overexpression of TIS21/BTG2/PC3 blocked the cells in G1 phase of the cell cycle and decreased the levels of Ser807/811 phosphorylated retinoblastoma protein, similarly to overexpression of DGK-ζ. Moreover, during myogenic differentiation of C2C12 cells, we showed an increase of TIS21/BTG2/PC3 expression and a decrease in cyclin D1 levels. siRNA downregulation of TIS21/BTG2/PC3 impaired myogenic differentiation by opposing cell cycle arrest. In summary, these data identify TIS21/BTG2/PC3 and cyclin D1 as downstream effectors of the nuclear DGK-ζ and highlight the importance of this DGK isoform in the regulation of myoblast proliferation and differentiation.

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mRNA destabilization by BTG1 and BTG2 maintains T cell quiescence

Project description:mRNA destabilization by BTG1 and BTG2 maintains T cell quiescence

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mRNA destabilization by BTG1 and BTG2 maintains T cell quiescence [mTAIL-seq]

Project description:mRNA destabilization by BTG1 and BTG2 maintains T cell quiescence [mTAIL-seq]

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mRNA destabilization by BTG1 and BTG2 maintains T cell quiescence [RNA-seq]

Project description:mRNA destabilization by BTG1 and BTG2 maintains T cell quiescence [RNA-seq]

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