Intermittent hypoxia-generated ROS contributes to intracellular zinc regulation that limits ischemia/reperfusion injury in adult rat cardiomyocyte

Lien, Chih-Feng; Lee, Wen-Sen; Wang, I-Chieh; Chen, Tsung-I; Chen, Tzu-Lin; Yang, Kun‐Ta

doi:10.1016/j.yjmcc.2018.03.014

Cited by 24 publications

(19 citation statements)

References 44 publications

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“…Reduced cell necroptosis results in inhibition of ROS and increased antioxidative capacity, which can limit the irreversible damage to the cells. Decreased ROS can also inhibit inflammatory signaling, and contribute to the attenuation of local and systematic inflammation (37). A physiological ROS level is essential to induce an anti-ROS response and maintain cellular homeostasis (37).…”

Section: Discussionmentioning

confidence: 99%

“…Decreased ROS can also inhibit inflammatory signaling, and contribute to the attenuation of local and systematic inflammation (37). A physiological ROS level is essential to induce an anti-ROS response and maintain cellular homeostasis (37). Notably, the ROS pathway is a double-edged sword; it helps pulmonary alveolar cells survive protein synthesis-associated stress; however, when cellular injury is too severe, it leads to inflammation and changes that ultimately damage these cells ( Fig.…”

Section: Discussionmentioning

confidence: 99%

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Necrostatin‑1 protects mice from acute lung injury by suppressing necroptosis and reactive oxygen species

et al. 2020

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acute lung injury (ali) is characterized by tissue damage and inflammatory cytokine secretion; however, the therapeutic options available to treat ALI remain limited. Necrostatin-1 (Nec-1) has the ability to attenuate cell necroptosis in various inflammatory diseases. The present study evaluated the protective effects of Nec-1 on a mouse model of lipopolysaccharide-induced ALI. Histological alterations in the lungs were evaluated through hematoxylin and eosin staining, and the expression levels of cytokines in the bronchoalveolar lavage fluid and lung tissues were determined by ELISA. In addition, accumulated production of reactive oxygen species was determined by staining with DCFH-DA probes, western blotting and immunofluorescence. The results revealed that treatment with the necroptosis inhibitor, Nec-1, exerted significant protective effects on ALI-induced inflammation and necroptosis. The key proteins involved in necroptosis were markedly reduced, including receptor-interacting serine/threonine-protein kinase (riP)1 and RIP3. Notably, antioxidant proteins were upregulated by Nec-1, which may attenuate oxidative stress. Furthermore, treatment with Nec-1 markedly suppressed necroptosis in the pulmonary alveoli RLE-6TN cell line. Taken together, these data revealed a novel association between ALI and necroptosis, and suggested that necroptosis inhibitors may be used as effective anti-inflammatory drugs to treat ALI.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Necrostatin‑1 protects mice from acute lung injury by suppressing necroptosis and reactive oxygen species

et al. 2020

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“…Simulated I/R in cultured cardiomyocytes was performed using a modified protocol described previously [21]. Briefly, cardiomyocytes were stabilized at 37 °C in Normal Tyrode (NT) buffer (140 mM NaCl, 4.5 mM KCl, 2.0 mM CaCl 2 , 1.2 mM MgCl 2 , 11 mM glucose, and 10 mM HEPES, with pH adjusted to 7.4 using NaOH) for 10 min, transferred to 100% N 2 -saturated ischemia buffer (123 mM NaCl, 8 mM KCl, 2.5 mM CaCl 2 , 0.9 mM NaH 2 PO 4 , 0.5 mM MgSO 4 , 20 mM Na-lactate, and 20 mM HEPES with pH adjusted to 6.0 using NaOH) for 6 h, and then reperfused with a culture medium for 12 h in a 5% CO 2 incubator.…”

Section: Methodsmentioning

confidence: 99%

Intermittent Hypoxia Prevents Myocardial Mitochondrial Ca2+ Overload and Cell Death during Ischemia/Reperfusion: The Role of Reactive Oxygen Species

Chang

Lien

Lee

et al. 2019

Cells

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It has been documented that reactive oxygen species (ROS) contribute to oxidative stress, leading to diseases such as ischemic heart disease. Recently, increasing evidence has indicated that short-term intermittent hypoxia (IH), similar to ischemia preconditioning, could yield cardioprotection. However, the underlying mechanism for the IH-induced cardioprotective effect remains unclear. The aim of this study was to determine whether IH exposure can enhance antioxidant capacity, which contributes to cardioprotection against oxidative stress and ischemia/reperfusion (I/R) injury in cardiomyocytes. Primary rat neonatal cardiomyocytes were cultured in IH condition with an oscillating O2 concentration between 20% and 5% every 30 min. An MTT assay was conducted to examine the cell viability. Annexin V-FITC and SYTOX green fluorescent intensity and caspase 3 activity were detected to analyze the cell death. Fluorescent images for DCFDA, Fura-2, Rhod-2, and TMRM were acquired to analyze the ROS, cytosol Ca2+, mitochondrial Ca2+, and mitochondrial membrane potential, respectively. RT-PCR, immunocytofluorescence staining, and antioxidant activity assay were conducted to detect the expression of antioxidant enzymes. Our results show that IH induced slight increases of O2−· and protected cardiomyocytes against H2O2- and I/R-induced cell death. Moreover, H2O2-induced Ca2+ imbalance and mitochondrial membrane depolarization were attenuated by IH, which also reduced the I/R-induced Ca2+ overload. Furthermore, treatment with IH increased the expression of Cu/Zn SOD and Mn SOD, the total antioxidant capacity, and the activity of catalase. Blockade of the IH-increased ROS production abolished the protective effects of IH on the Ca2+ homeostasis and antioxidant defense capacity. Taken together, our findings suggest that IH protected the cardiomyocytes against H2O2- and I/R-induced oxidative stress and cell death through maintaining Ca2+ homeostasis as well as the mitochondrial membrane potential, and upregulation of antioxidant enzymes.

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“…Despite continued concerns about their suitability to measure ionic movement in the native cardiovascular system and, in particular, their ability to do that without undesirable off-target effects, fluorescent chemical dyes have become commonplace since their initial discovery over the last 30 years ( Figure 1 ). In fact, many subtypes of cation indicator have been produced to detect zinc (FluoZin-3 or RhodZin-3) [ 48 ], Mg 2+ (Furaptra [ 49 ], Mag-fura2 [ 50 ] and Mag-Indo1 [ 51 ]), and H + (SNARF-1) [ 52 ], although detailed off-target studies have not been conducted in cardiomyocytes at this point.…”

Section: Chemical Dyesmentioning

confidence: 99%

Fluorescent, Bioluminescent, and Optogenetic Approaches to Study Excitable Physiology in the Single Cardiomyocyte

Robinson

Daniels

2018

Cells

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This review briefly summarizes the single cell application of classical chemical dyes used to visualize cardiomyocyte physiology and their undesirable toxicities which have the potential to confound experimental observations. We will discuss, in detail, the more recent iterative development of fluorescent and bioluminescent protein-based indicators and their emerging application to cardiomyocytes. We will discuss the integration of optical control strategies (optogenetics) to augment the standard imaging approach. This will be done in the context of potential applications, and barriers, of these technologies to disease modelling, drug toxicity, and drug discovery efforts at the single-cell scale.

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Intermittent hypoxia-generated ROS contributes to intracellular zinc regulation that limits ischemia/reperfusion injury in adult rat cardiomyocyte

Cited by 24 publications

References 44 publications

Necrostatin‑1 protects mice from acute lung injury by suppressing necroptosis and reactive oxygen species

Necrostatin‑1 protects mice from acute lung injury by suppressing necroptosis and reactive oxygen species

Intermittent Hypoxia Prevents Myocardial Mitochondrial Ca2+ Overload and Cell Death during Ischemia/Reperfusion: The Role of Reactive Oxygen Species

Fluorescent, Bioluminescent, and Optogenetic Approaches to Study Excitable Physiology in the Single Cardiomyocyte

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