Enhancement of FGF-1 release along with cytosolic proteins from rat astrocytes by hydrogen peroxide

Ito, Jin‐ichi; Nagayasu, Yuko; Hoshikawa, M.; Kato, Koichi; Miura, Yutaka; Asai, Kiyofumi; Hayashi, Hideki; Yokoyama, Shinji; Michikawa, Makoto

doi:10.1016/j.brainres.2013.05.035

Cited by 17 publications

(16 citation statements)

References 38 publications

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“…As a result, oxidative stress will initiate harmful effect on cardiac cells, resulting in myocardial cell death and consequent hypertrophy and fibrosis, finally leading to diabetic dysfunction (cardiomyopathy) [41]. Some studies mentioned that the expression of aFGF was up-regulated by oxidative stress, implying that the increase of aFGF expression was an adaptive response and may show a protective effect against oxidative stress [42]–[44]. Since hyperglycemia is the predominant trigger of diabetic complications, the mechanistic studies here were performed with the H9c2 cells exposed to high glucose for mimicking diabetic hyperglycemia in vitro.…”

Section: Discussionmentioning

confidence: 99%

The Prevention of Diabetic Cardiomyopathy by Non-Mitogenic Acidic Fibroblast Growth Factor Is Probably Mediated by the Suppression of Oxidative Stress and Damage

Zhang

Chen

et al. 2013

PLoS ONE

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BackgroundEmerging evidence showed the beneficial effect of acidic fibroblast growth factor (aFGF) on heart diseases. The present study investigated whether non-mitogenic aFGF (nm-aFGF) can prevent diabetic cardiomyopathy and the underlying mechanisms, if any.Methodology/Principal FindingsType 1 diabetes was induced in mice by multiple intraperitoneal injections of low-dose streptozotocin. Hyperglycemic and age-matched control mice were treated with or without nm-aFGF at 10 µg/kg daily for 1 and 6 months. Blood pressure and cardiac function were assessed. Cardiac H9c2 cell, human microvascular endothelial cells, and rat cardiomyocytes were exposed to high glucose (25 mM) for mimicking an in vitro diabetic condition for mechanistic studies. Oxidative stress, DNA damage, cardiac hypertrophy and fibrosis were assessed by real-time qPCR, immunofluorescent staining, Western blotting, and pathological examination. Nm-aFGF significantly prevented diabetes-induced hypertension and cardiac dysfunction at 6 months. Mechanistic studies demonstrated that nm-aFGF showed the similar preventive effect as the native aFGF on high glucose-induced oxidative stress (increase generation of reactive oxygen species) and damage (cellular DNA oxidation), cell hypertrophy, and fibrotic response (increased mRNA expression of fibronectin) in three kinds of cells. These in vitro findings were recaptured by examining the heart of the diabetic mice with and without nm-aFGF.ConclusionsThese results suggest that nm-aFGF can prevent diabetic cardiomyopathy, probably through attenuation of cardiac oxidative stress, hypertrophy, and fibrosis.

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Section: Discussionmentioning

confidence: 99%

The Prevention of Diabetic Cardiomyopathy by Non-Mitogenic Acidic Fibroblast Growth Factor Is Probably Mediated by the Suppression of Oxidative Stress and Damage

Zhang

Chen

et al. 2013

PLoS ONE

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“…Similarly, H 2 O 2 in concentrations less than 500 μ M enhanced the release of heat shock protein (HSP70, HSP90) and fibroblast growth factor from cultured rat astrocytes, which contributes to neuron survival, neurite outgrowth, and angiogenesis [7] . Hence, H 2 O 2 is probably favorable in both the structural and functional recovery of cutaneous wound.…”

Section: Cell Proliferation Stagementioning

confidence: 99%

“…For example, in relatively high concentrations, H 2 O 2 displays its strong ability of oxidization and proinflammation to disinfect wound tissue; however, in comparatively low concentrations, H 2 O 2 assists in removing cell and pathogen debris and promotes secretion of cytokines which help tissue regeneration [5][6][7] . Hence, in this review, the role of H 2 O 2 in cutaneous wound healing and its potential as a chronic wound healing agent are discussed.…”

mentioning

confidence: 99%

Hydrogen Peroxide: A Potential Wound Therapeutic Target

Zhu¹,

Wang²,

Lu³

et al. 2017

Med Princ Pract

109

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Hydrogen peroxide (H2O2) is a topical antiseptic used in wound cleaning which kills pathogens through oxidation burst and local oxygen production. H2O2 has been reported to be a reactive biochemical molecule synthesized by various cells that influences biological behavior through multiple mechanisms: alterations of membrane potential, generation of new molecules, and changing intracellular redox balance, which results in activation or inactivation of different signaling transduction pathways. Contrary to the traditional viewpoint that H2O2 probably impairs tissue through its high oxidative property, a proper level of H2O2 is considered an important requirement for normal wound healing. Although the present clinical use of H2O2 is still limited to the elimination of microbial contamination and sometimes hemostasis, better understanding towards the sterilization ability and cell behavior regulatory function of H2O2 within wounds will enhance the potential to exogenously augment and manipulate healing.

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“…Under pathological conditions such as DN, there are reports of upregulation of bFGF [9] . Concomitantly, some studies have shown that aFGF is upregulated by OS [28] . The increase in the expression of FGFs may reflect an adaptive response to protect the tissues against OS.…”

Section: Mafgf Treatment Inhibits Glucose-induced Apoptosismentioning

confidence: 99%

“…Current evidences indicate elevation of several vasoactive factors in early DN [1,28,29] . We found that diabetes caused an increase of angiotensinogen (AGT) mRNA expression after 1 month ( p < 0.05) and 6 months, along with an increase of endothelial NO synthase (eNOS; p < 0.05) and VEGF at 1 month followed by a significant ( p < 0.05) decrease after 6 months.…”

Section: Mafgf Treatment Prevented Vasoactive Factor Alterations In Dnmentioning

confidence: 99%

Prevention of Diabetic Nephropathy by Modified Acidic Fibroblast Growth Factor

Peña

Chen²,

Feng³

et al. 2017

Nephron

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Background/Aims: Oxidative stress (OS) contributes to all chronic diabetic complications, including diabetic nephropathy (DN). Acidic fibroblast growth factor (aFGF) has shown to confer protection from OS. However, it also has potent angiogenic activity. We hypothesized that a modified human aFGF (maFGF), with antioxidant properties but devoid of angiogenic activity, has preventative action in DN. Methods: Streptozotocin-induced diabetic mice were treated with maFGF (intraperitoneally) daily for 1 or 6 months and were compared with untreated diabetic and non-diabetic controls. Microalbuminuria was assessed to determine functional damage. Renal cortical tissues were examined for multiple extracellular matrix proteins, vasoactive factors and OS markers. For mechanistic studies, immortalized mouse podocytes and human microvascular endothelial cells were exposed to high (25 mM) or low glucose (5 mM). OS, vasoactive factors, fibrosis and apoptosis-related gene expression were tested by real-time qPCR and Enzyme-Linked Immunosorbent Assay. Nitric oxide (NO) analyses were also performed. Results: maFGF did not affect body weight and glycemia but prevented renal hypertrophy and functional changes in DN. It also prevented diabetes-induced DNA damage, nitrosative stress, vasoactive factors, angiotensinogen and endothelial NO synthase alterations. Although it failed to prevent transforming growth factor (TGF)-β1 mRNA upregulation, it prevented fibronectin production. Similar results were obtained in vitro. Decreased NO production in vivo and in vitro was also prevented by maFGF. Conclusions: maFGF treatment prevents DN. This prevention probably involves NO production.

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Enhancement of FGF-1 release along with cytosolic proteins from rat astrocytes by hydrogen peroxide

Cited by 17 publications

References 38 publications

The Prevention of Diabetic Cardiomyopathy by Non-Mitogenic Acidic Fibroblast Growth Factor Is Probably Mediated by the Suppression of Oxidative Stress and Damage

The Prevention of Diabetic Cardiomyopathy by Non-Mitogenic Acidic Fibroblast Growth Factor Is Probably Mediated by the Suppression of Oxidative Stress and Damage

Hydrogen Peroxide: A Potential Wound Therapeutic Target

Prevention of Diabetic Nephropathy by Modified Acidic Fibroblast Growth Factor

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