Agmatine protects Müller cells from high-concentration glucose-induced cell damage via N-methyl-D-aspartic acid receptor inhibition

Han, Ning; Yu, Li; Song, Zhidu; Luo, Lifu; Wu, Yue

doi:10.3892/mmr.2015.3540

Cited by 17 publications

(6 citation statements)

References 42 publications

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“…31) Lee et al found that HG could inhibit mTORC1 activity. 33) Our results verified this report by revealing that mTOR signaling pathway may be associated with HGinduced apoptosis in HK-2 cells. However, these effects were alleviated in the presence of miR-15b-5p mimics, demonstrating that miR-15b-5p mimics activated mTOR signaling pathway via increasing the level of p-Akt, p-mTOR and p-p70S6K.…”

Section: Discussionsupporting

confidence: 89%

High Glucose-Induced Apoptosis in Human Kidney Cells Was Alleviated by miR-15b-5p Mimics

Shen¹,

Fang²,

Guo³

et al. 2019

Biological & Pharmaceutical Bulletin

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MicroRNAs were involved in a wide range of biological processes of diabetic nephropathy (DN). It is reported that miR-15b-5p was downregulated in the patients with DN. However, the mechanisms underlying the regulatory effects of miR-15b-5p on patients with diabetes remain unclear. Thus, this study aimed to investigate the role of miR-15b-5p during high glucose (HG)-induced apoptosis in human kidney cells. Quantitative real-time (qRT)-PCR was used to detect the level of miR-15b-5p. CCK-8 assay, EdU staining assays and flow cytometry were used to detect cell proliferation, apoptosis respectively in vitro. In addition, Western blotting was used to determine active caspase-3, cleaved poly(ADP-ribose) polymerase (PARP), phosphorylated (p)-AKT, p-mammalian target of rapamycin (mTOR), p-S6, p-c-Jun N terminal kinase (JNK), p-p38 and p-extracellular signal-regulated kinase (ERK) proteins levels. The expression of miR-15b-5p in patients with DN were dramatically decreased compared with health persons. Similarly, HG down-regulated the expression of miR-15b-5p in HK-2 cells. In contrast, miR-15b-5p mimics alleviated HG-induced apoptosis in HK-2 cells via decreasing the expressions of active caspase 3 and cleaved PARP. EdU detection further confirmed that miR-15b-5p mimics attenuated the anti-proliferation effect of HG in HK-2 cells. Furthermore, HGinduced Akt/mTOR pathway downregulation and JNK upregulation were markedly reversed by miR-15b-5p mimics in cells. The data suggested that miR-15b-5p mimics protects HK-2 cells from HG-induced apoptosis. The anti-apoptotic effects of miR-15b-5p may due to the activation of the Akt/mTOR pathway as well as inactivation of JNK. Taken together, miR-15b-5p might be a potential therapeutic target for the treatment of patients with DN.

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Section: Discussionsupporting

confidence: 89%

High Glucose-Induced Apoptosis in Human Kidney Cells Was Alleviated by miR-15b-5p Mimics

Shen¹,

Fang²,

Guo³

et al. 2019

Biological & Pharmaceutical Bulletin

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“…Agmatine (decarboxylated arginine) is an endogenous polyamine synthesized via decarboxylation of l -arginine by arginine decarboxylase. 10 , 11 As shown in a previous study, agmatine has oxygen radical-scavenging effects (antioxidant activity), protects mitochondrial function, and confers resistance to cellular apoptosis. 12 The agmatine-induced protection of mitochondria is presumed to be a key mechanism of action, and agmatine effectively inhibits ROS-induced activation of BAX.…”

Section: Introductionmentioning

confidence: 82%

Protective Effect of Agmatine Against Cisplatin- Induced Cellular Apoptosis in an Auditory Cell Line

Park¹,

Lee²,

Jung³

et al. 2022

Int Adv Otol

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Background: The aims of this study were to evaluate the protective effects of agmatine against cisplatin-induced cellular apoptosis in an auditory cell line and to prove the protective mechanism of agmatine. Methods: The House Ear Institute-Organ of Corti 1 cells were co-treated with agmatine at different concentrations and 15 µM of cisplatin for 48 hours. Cell viability and proliferation were measured. Annexin V-fluorescein isothiocyanate /propidium iodide staining was performed to analyze apoptosis. The levels of intracellular reactive oxygen species were measured using flow cytometry. The expression of BCL2-associated X protein and the enzymatic activity of caspase-3 was measured to examine the pathway of apoptosis induction. Results: In normal conditions, the maximal protective effect occurred with 10 mM of agmatine. However, in the presence of cisplatin, the maximal protective effect was observed from 8 mM of agmatine. Thus, 8 mM was chosen as the ideal agmatine concentration for the analysis of protective effects against cisplatin-induced cytotoxicity. Agmatine exerted a significant protective effect against 15 µM of cisplatin when applied for 48 hours and reduced the proportion of necrotic and late apoptotic cells. Agmatine did not significantly reduce the cisplatin-induced increase in reactive oxygen species but decreased the expression of BCL2-associated X protein and the activity of caspase-3. Conclusion: Agmatine protected against cisplatin-induced cellular apoptosis in an auditory cell line. These effects were mediated by the protection of mitochondrial function and inhibition of apoptosis.

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“…These alterations lead to the activation of cell death pathways. Apoptosis is described due to a decrease in Bcl-2 and an increase in Bax (bcl2 associated X) and caspase-3 levels [173][174][175]. Recently, several studies have shown the activation of pyroptosis and mitophagy/autophagy pathways [169,[176][177][178][179][180].…”

Section: Müller Cells In Drmentioning

confidence: 99%

Contribution of Müller Cells in the Diabetic Retinopathy Development: Focus on Oxidative Stress and Inflammation

et al. 2022

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Diabetic retinopathy is a neurovascular complication of diabetes and the main cause of vision loss in adults. Glial cells have a key role in maintenance of central nervous system homeostasis. In the retina, the predominant element is the Müller cell, a specialized cell with radial morphology that spans all retinal layers and influences the function of the entire retinal circuitry. Müller cells provide metabolic support, regulation of extracellular composition, synaptic activity control, structural organization of the blood–retina barrier, antioxidant activity, and trophic support, among other roles. Therefore, impairments of Müller actions lead to retinal malfunctions. Accordingly, increasing evidence indicates that Müller cells are affected in diabetic retinopathy and may contribute to the severity of the disease. Here, we will survey recently described alterations in Müller cell functions and cellular events that contribute to diabetic retinopathy, especially related to oxidative stress and inflammation. This review sheds light on Müller cells as potential therapeutic targets of this disease.

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Agmatine protects Müller cells from high-concentration glucose-induced cell damage via N-methyl-D-aspartic acid receptor inhibition

Cited by 17 publications

References 42 publications

High Glucose-Induced Apoptosis in Human Kidney Cells Was Alleviated by miR-15b-5p Mimics

High Glucose-Induced Apoptosis in Human Kidney Cells Was Alleviated by miR-15b-5p Mimics

Protective Effect of Agmatine Against Cisplatin- Induced Cellular Apoptosis in an Auditory Cell Line

Contribution of Müller Cells in the Diabetic Retinopathy Development: Focus on Oxidative Stress and Inflammation

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