The role of neutrophil gelatinase-associated lipocalin and iron homeostasis in object recognition impairment in aged sepsis-survivor rats

Nikaido, Yoshikazu; Midorikawa, Yoko; Furukawa, Tatsuo; Shimoyama, Shuji; Takekawa, Daiki; Kitayama, Masato; Ueno, Shinji; Kushikata, Tetsuya; Hirota, Kazuyoshi

doi:10.1038/s41598-021-03981-7

Cited by 6 publications

(4 citation statements)

References 46 publications

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“…In pathological conditions, iron accumulation and a ferric/ferrous ion imbalance are the causes of apoptosis, necrosis, autophagy, and fer-roptosis. In fact, the cortex and hippocampus of people with neurodegenerative disorders, such as MS, Alzheimer's disease, and others, exhibit iron buildup [57].…”

Section: Discussionmentioning

confidence: 99%

Experimental Analysis of Tear Fluid and Its Processing for the Diagnosis of Multiple Sclerosis

Tomečková

Tkáčiková

Talian

et al. 2023

Sensors

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A pilot analysis of the tear fluid of patients with multiple sclerosis (MS) collected by glass microcapillary was performed using various experimental methods: liquid chromatography–mass spectrometry, Raman spectroscopy, infrared spectroscopy, and atomic-force microscopy. Infrared spectroscopy found no significant difference between the tear fluid of MS patients and the control spectra; all three significant peaks were located at around the same positions. Raman analysis showed differences between the spectra of the tear fluid of MS patients and the spectra of healthy subjects, which indicated a decrease in tryptophan and phenylalanine content and changes in the relative contributions of the secondary structures of the polypeptide chains of tear proteins. Atomic-force microscopy exhibited a surface fern-shaped dendrite morphology of the tear fluid of patients with MS, with less roughness on both oriented silicon (100) and glass substrates compared to the tear fluid of control subjects. The results of liquid chromatography–mass spectrometry showed downregulation of glycosphingolipid metabolism, sphingolipid metabolism, and lipid metabolism. Proteomic analysis identified upregulated proteins in the tear fluid of patients with MS such as cystatine, phospholipid transfer protein, transcobalamin-1, immunoglobulin lambda variable 1–47, lactoperoxidase, and ferroptosis suppressor protein 1; and downregulated proteins such as haptoglobin, prosaposin, cytoskeletal keratin type I pre-mRNA-processing factor 17, neutrophil gelatinase-associated lipocalin, and phospholipase A2. This study showed that the tear proteome in patients with MS is modified and can reflect inflammation. Tear fluid is not a commonly used biological material in clinico-biochemical laboratories. Experimental proteomics has the potential to become a promising contemporary tool for personalized medicine, and it might be applied in clinical practice by providing a detailed analysis of the tear-fluid proteomic profile of patients with MS.

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Section: Discussionmentioning

confidence: 99%

Experimental Analysis of Tear Fluid and Its Processing for the Diagnosis of Multiple Sclerosis

Tomečková

Tkáčiková

Talian

et al. 2023

Sensors

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“…The interplay between neutrophils and blood-brain barrier integrity is an unavoidable subject in central nervous system diseases. Both systemic circulation and inflammatory factors in the brain milieu can contribute to blood-brain barrier disruption [225]. Under pathological conditions, chemokines and cytokines can drive neutrophil aggregation towards the blood-brain barrier, further exacerbating its integrity [226].…”

Section: Neutrophils and Netsmentioning

confidence: 99%

The Interplay between Ferroptosis and Neuroinflammation in Central Neurological Disorders

Xu,

Jia,

et al. 2024

Antioxidants

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Central neurological disorders are significant contributors to morbidity, mortality, and long-term disability globally in modern society. These encompass neurodegenerative diseases, ischemic brain diseases, traumatic brain injury, epilepsy, depression, and more. The involved pathogenesis is notably intricate and diverse. Ferroptosis and neuroinflammation play pivotal roles in elucidating the causes of cognitive impairment stemming from these diseases. Given the concurrent occurrence of ferroptosis and neuroinflammation due to metabolic shifts such as iron and ROS, as well as their critical roles in central nervous disorders, the investigation into the co-regulatory mechanism of ferroptosis and neuroinflammation has emerged as a prominent area of research. This paper delves into the mechanisms of ferroptosis and neuroinflammation in central nervous disorders, along with their interrelationship. It specifically emphasizes the core molecules within the shared pathways governing ferroptosis and neuroinflammation, including SIRT1, Nrf2, NF-κB, Cox-2, iNOS/NO·, and how different immune cells and structures contribute to cognitive dysfunction through these mechanisms. Researchers’ findings suggest that ferroptosis and neuroinflammation mutually promote each other and may represent key factors in the progression of central neurological disorders. A deeper comprehension of the common pathway between cellular ferroptosis and neuroinflammation holds promise for improving symptoms and prognosis related to central neurological disorders.

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“…Cellular iron concentrations relative to Fe 2+ and Fe 3+ were evaluated using the Iron Detection Assay Kit (ab83366, Abcam) [24]. Cells were homogenized in a 4-10 volume of iron determination buffer.…”

Section: Iron Determinationmentioning

confidence: 99%

YTHDF3-mediated m6A Modification Facilitates Osteosarcoma Progression through the FSP1-CoQ10-NAD(P)H Axis to Suppress Ferroptosis

Liu,

Li,

Zhu

et al. 2024

Arch Med Sci

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IntroductionOsteosarcoma (OS) remains a formidable malignancy, characterized by its relentless nature and limited therapeutic interventions. YTHDF3, a key reader protein recognizing m6A-modified mRNAs, has attracted considerable attention due to its prominent role in cancer biology. This study embarks on an exploration of the intricate interplay between YTHDF3, a vital RNA modification reader protein, m6A RNA modification, and the FSP1-CoQ10-NADPH metabolic pathway in the pathogenesis of OS.Material and methodsFirstly, we procured tissue specimens and corresponding non-cancerous tissues from 10 OS patients and cultured OS cell lines. Then, we established a ferroptosis model in OS cells through treatment with RSL3 to reveal the relation between YTHDF3 and ferroptosis.ResultsClinical evaluation of OS samples revealed a notable upsurge in the expression of YTHDF3 and the concurrent overexpression of ferroptosis-related proteins. In vitro experiments suggested that YTHDF3 potentially facilitated FSP1 mRNA translation through an m6A-dependent mechanism, subsequently inhibiting ferroptosis via the FSP1-CoQ10-NADPH pathway, thereby promoting OS progression.ConclusionsThese compelling findings underscore the promise of targeting the YTHDF3-FSP1 axis as an innovative and potentially transformative therapeutic strategy for the treatment of OS. This study not only enhances our understanding of ferroptosis regulation but also sheds light on the significance of YTHDF3 and FSP1 as potential targets for therapeutic intervention in OS, offering new prospects for cancer treatment strategies.

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The role of neutrophil gelatinase-associated lipocalin and iron homeostasis in object recognition impairment in aged sepsis-survivor rats

Cited by 6 publications

References 46 publications

Experimental Analysis of Tear Fluid and Its Processing for the Diagnosis of Multiple Sclerosis

Experimental Analysis of Tear Fluid and Its Processing for the Diagnosis of Multiple Sclerosis

The Interplay between Ferroptosis and Neuroinflammation in Central Neurological Disorders

YTHDF3-mediated m6A Modification Facilitates Osteosarcoma Progression through the FSP1-CoQ10-NAD(P)H Axis to Suppress Ferroptosis

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