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铁死亡相关基因乳铁传递蛋白在年龄相关性听力损失中的鉴定与实验验证

Identification and experimental validation of ferroptosis-related gene lactotransferrin in age-related hearing loss.

作者信息

Zeng Chaojun, Gu Xi, Chen Yuqing, Lin Yanchun, Chen Junying, Chen Zhifeng, Chen Chenyu, Yao Guangnan, Lin Chang

机构信息

Department of Otorhinolaryngology Head and Neck Surgery, The First Affiliated Hospital, Fujian Medical University, Fuzhou, China.

Department of Otorhinolaryngology Head and Neck Surgery, National Regional Medical Center, Binhai Campus of the First Affiliated Hospital, Fujian Medical University, Fuzhou, China.

出版信息

Front Aging Neurosci. 2024 Jan 11;16:1309115. doi: 10.3389/fnagi.2024.1309115. eCollection 2024.

DOI:10.3389/fnagi.2024.1309115
PMID:38282692
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10809180/
Abstract

OBJECTIVE: To reveal the relationship between ARHL and ferroptosis and screen ferroptosis-related genes (FRGs) in ARHL. METHODS: Bioinformatics were used to analyze the hub genes and molecular mechanism of ferroptosis in the aging cochleae. Senescence β-galactosidase staining, iron content detection, and micro malondialdehyde (MDA) assay kits were used to measure β-galactosidase activity, and expression of Fe and MDA, respectively. Fluorescence microscope was used for immunofluorescence assay of hub genes. Western blot was used to verify the expression of hub genes in HEI-OC1 cells, cochlear explants, and cochleae of C57BL/6J mice. Data were expressed as mean ± SD of at least three independent experiments. RESULTS: The analysis of bioinformatics confirmed that lactotransferrin (LTF) is the hub gene and CEBPA-miR-130b-LTF network is the molecular mechanism for cochlear ferroptosis. Compared with the control group, the experiments proved that the indicators of ferroptosis, including Fe, MDA, and LTF were differentially expressed in aging HEI-OC1 cells, aging cochlear explants, and aging cochleae. CONCLUSION: These results demonstrate that ferroptosis plays an important role in ARHL, and LTF is a potential therapeutic target for ARHL via regulating cochlear ferroptosis.

摘要

目的：揭示年龄相关性听力损失（ARHL）与铁死亡之间的关系，并筛选ARHL中铁死亡相关基因（FRGs）。 方法：运用生物信息学分析衰老耳蜗中铁死亡的关键基因和分子机制。采用衰老β-半乳糖苷酶染色、铁含量检测及微量丙二醛（MDA）检测试剂盒分别测定β-半乳糖苷酶活性、铁和MDA的表达。利用荧光显微镜对关键基因进行免疫荧光检测。采用蛋白质免疫印迹法验证关键基因在HEI-OC1细胞、耳蜗外植体及C57BL/6J小鼠耳蜗中的表达。数据以至少三个独立实验的平均值±标准差表示。 结果：生物信息学分析证实乳铁蛋白（LTF）是关键基因，CEBPA-miR-130b-LTF网络是耳蜗铁死亡的分子机制。与对照组相比，实验证明在衰老的HEI-OC1细胞、衰老的耳蜗外植体和衰老的耳蜗中，包括铁、MDA和LTF在内的铁死亡指标存在差异表达。 结论：这些结果表明铁死亡在ARHL中起重要作用，LTF通过调节耳蜗铁死亡是ARHL的一个潜在治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fffe/10809180/c7f6f72a22d9/fnagi-16-1309115-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fffe/10809180/6758902eac43/fnagi-16-1309115-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fffe/10809180/4806bc658381/fnagi-16-1309115-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fffe/10809180/8edfcc6d33ea/fnagi-16-1309115-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fffe/10809180/9c5935eafd0d/fnagi-16-1309115-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fffe/10809180/48f8721c7f13/fnagi-16-1309115-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fffe/10809180/c7f6f72a22d9/fnagi-16-1309115-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fffe/10809180/6758902eac43/fnagi-16-1309115-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fffe/10809180/4806bc658381/fnagi-16-1309115-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fffe/10809180/8edfcc6d33ea/fnagi-16-1309115-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fffe/10809180/9c5935eafd0d/fnagi-16-1309115-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fffe/10809180/48f8721c7f13/fnagi-16-1309115-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fffe/10809180/c7f6f72a22d9/fnagi-16-1309115-g006.jpg

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引用本文的文献

[1]
Targeting Programmed Cell Death in Acquired Sensorineural Hearing Loss: Ferroptosis, Necroptosis, and Pyroptosis.

Neurosci Bull. 2025-4-22

[2]
Ferroptosis and hearing loss: from molecular mechanisms to therapeutic interventions.

J Enzyme Inhib Med Chem. 2025-12

[3]
Improving understanding of ferroptosis: Molecular mechanisms, connection with cellular senescence and implications for aging.

Heliyon. 2024-10-24

[4]
The miR-182-5p/GPX4 Pathway Contributes to Sevoflurane-Induced Ototoxicity via Ferroptosis.

Int J Mol Sci. 2024-6-20

[5]
Ferrostatin-1 inhibits fibroblast fibrosis in keloid by inhibiting ferroptosis.

PeerJ. 2024

本文引用的文献

[1]
lncRNA-associated ceRNA network revealing the potential regulatory roles of ferroptosis and immune infiltration in Alzheimer's disease.

Front Aging Neurosci. 2023-2-16

[2]
Ferroptosis in AS progression: role of miRNA.

Eur Rev Med Pharmacol Sci. 2022-11

[3]
Relationship between miRNA and ferroptosis in tumors.

Front Pharmacol. 2022-11-4

[4]
Sirtuin 7 mitigates renal ferroptosis, fibrosis and injury in hypertensive mice by facilitating the KLF15/Nrf2 signaling.

Free Radic Biol Med. 2022-11-20

[5]
Tumor necrosis factor-α mediated inflammation versus apoptosis in age-related hearing loss.

Front Aging Neurosci. 2022-9-7

[6]
miR-130b/301b Is a Negative Regulator of Beige Adipogenesis and Energy Metabolism In Vitro and In Vivo.

Diabetes. 2022-11-1

[7]
Emerging Mechanisms and Targeted Therapy of Ferroptosis in Neurological Diseases and Neuro-oncology.

Int J Biol Sci. 2022-6-27

[8]
Ferroptosis turns 10: Emerging mechanisms, physiological functions, and therapeutic applications.

Cell. 2022-7-7

[9]
LDL receptor-related protein 1 (LRP1), a novel target for opening the blood-labyrinth barrier (BLB).

Signal Transduct Target Ther. 2022-6-10

[10]
The Lactoferrin Phenomenon-A Miracle Molecule.

Molecules. 2022-5-4

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