Netrin‐1 upregulates GPX4 and prevents ferroptosis after traumatic brain injury via the UNC5B/Nrf2 signaling pathway

Zhang, Yuanda; Jin, Lufan; Zhao, Dongxu; Ruan, Cijie; Zhou, Jun; Tan, Haoyuan; Bao, Yang

doi:10.1111/cns.13997

Cited by 15 publications

(11 citation statements)

References 38 publications

(60 reference statements)

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“…Furthermore, NRXN3 is a gene associated with obesity [29], and we speculated that NRXN3 takes part in the metabolism process of lipids. Meanwhile, UNC5B is a crucial regulator of ferroptosis in osteosarcoma cells [30] and traumatic brain injury mice [31]. Thus, these four hub DEGs identified in LNCaP and PC3 cells under erastin exposure exhibit to play an essential role in cellular growth and ferroptosis process of PCa cells, and maybe the FRGs and the potential therapy of targeted genes of PCa.…”

Section: Discussionmentioning

confidence: 92%

Identification and validation of ferroptosis related genes in prostate cancer cells under erastin exposure

Huang

Jiang

et al. 2023

Preprint

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Few studies are focusing on the mechanism of erastin acts on prostate cancer(PCa) cells, and essential ferroptosis-related genes (FRGs) that can be PCa treatment targets are rarely known. In the current study, in vitro assays were performed to evaluate the ferroptotic levels of PCa cells under erastin treatment. RNA-seq was used to measure the expression of differentially expressed genes (DEGs) in erastin-induced PCa cells. A series of bioinformatic analyses were applied to analyze the pathways, module, transcription factors, and expression levels of DEGs. Erastin inhibited the expression of ferroptosis marker SLC7A11 and cell survivability in both PCa cells. After treatment with erastin, the concentration level of MDA and Fe2+ significantly increased, whereas GSH and GSSG significantly decreased in PCa cells. A total of 295 overlapping DEGs were screened and identified in two cells under erastin exposure and significantly enriched for association with some pathways. The expression levels of four hub FRGs, including TMEFF2, CLU, NRXN3, and UNC5B, were significantly different in PCa and normal tissues. TMEFF2 was the gene co-expressed with SLC7A11 and GPX4. In both PCa cells, the expression levels of SLC7A11 and cell growth were inhibited after the knockdown of TMEFF2. The concentration of Fe2+ significantly increased in two TMEFF2 downregulated cells. In conclusion, FRGs and their correlations with ferroptosis in PCa were identified and validated. Our results showed that these FRGs play a crucial role in PCa, and offered the potential therapeutic target genes for the investigation and treatment of PCa.

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Section: Discussionmentioning

confidence: 92%

Identification and validation of ferroptosis related genes in prostate cancer cells under erastin exposure

Huang

Jiang

et al. 2023

Preprint

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“…However, knockdown of GPX4 counteracted the effects of NTN1 recombinant. 43 Ferroptosis is a new non-necrotic and non-apoptotic PCD that kills cells through iron-dependent LPO. The critical pathological mechanisms of ferroptosis have been implicated as iron accumulation, LPO production and oxidative damage.…”

Section: Discussionmentioning

confidence: 99%

Fucoxanthin ameliorates traumatic brain injury by suppressing the blood–brain barrier disruption

Zhang,

Hu,

Bai

et al. 2023

iScience

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“…Fluoro-Jade B (FJB) staining: Cell death was evaluated by staining with FJB ( Zhang et al ., 2023 ). Cryostat sections were washed with distilled water and rehydrated with alcohol series (100% ethanol for 3 min, 70% ethanol for 1 min, and 30% ethanol for 1 min) and water.…”

Section: Methodsmentioning

confidence: 99%

Lysophosphatidic Acid Receptor 1 Plays a Pathogenic Role in Permanent Brain Ischemic Stroke by Modulating Neuroinflammatory Responses

Tiwari,

Basnet,

Choi

2024

Biomol Ther (Seoul)

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Lysophosphatidic acid receptor 1 (LPA 1 ) plays a critical role in brain injury following a transient brain ischemic stroke. However, its role in permanent brain ischemic stroke remains unknown. To address this, we investigated whether LPA 1 could contribute to brain injury of mice challenged by permanent middle cerebral artery occlusion (pMCAO). A selective LPA 1 antagonist (AM152) was used as a pharmacological tool for this investigation. When AM152 was given to pMCAO-challenged mice one hour after occlusion, pMCAO-induced brain damage such as brain infarction, functional neurological deficits, apoptosis, and blood-brain barrier disruption was significantly attenuated. Histological analyses demonstrated that AM152 administration attenuated microglial activation and proliferation in injured brain after pMCAO challenge. AM152 administration also attenuated abnormal neuroinflammatory responses by decreasing expression levels of pro-inflammatory cytokines while increasing expression levels of anti-inflammatory cytokines in the injured brain. As underlying effector pathways, NF-κB, MAPKs (ERK1/2, p38, and JNKs), and PI3K/Akt were found to be involved in LPA 1 -dependent pathogenesis. Collectively, these results demonstrate that LPA 1 can contribute to brain injury by permanent ischemic stroke, along with relevant pathogenic events in an injured brain.

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Netrin‐1 upregulates GPX4 and prevents ferroptosis after traumatic brain injury via the UNC5B/Nrf2 signaling pathway

Cited by 15 publications

References 38 publications

Identification and validation of ferroptosis related genes in prostate cancer cells under erastin exposure

Identification and validation of ferroptosis related genes in prostate cancer cells under erastin exposure

Fucoxanthin ameliorates traumatic brain injury by suppressing the blood–brain barrier disruption

Lysophosphatidic Acid Receptor 1 Plays a Pathogenic Role in Permanent Brain Ischemic Stroke by Modulating Neuroinflammatory Responses

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