The NADPH oxidase inhibitor DPI can abolish hypoxia-induced apoptosis of human kidney proximal tubular epithelial cells through Bcl2 up-regulation via ERK activation without ROS reduction

Song, Han-Jung; Han, Il-Yong; Kim, Yeonye; Kim, Young Hwan; Choi, Il‐Whan; Seo, Su‐Kil; Jung, So Young; Park, SaeGwang; Kang, Mi Seon

doi:10.1016/j.lfs.2015.02.004

Cited by 32 publications

(19 citation statements)

References 44 publications

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“…Furthermore, monensin reduced the levels of G 1 /S phase transition-associated proteins, including cyclin A, cyclin D1, cyclin E, CDK2, CDK4 and CDK6, in a dose-dependent manner ( Figure 1C and D). These results show that monensin inhibits cellular proliferation of PC-3 cells via G 1 arrest, similar to previous reports (19).…”

Section: Monensin Induces G 1 Cell-cycle Arrest By Down-regulating Cysupporting

confidence: 93%

Monensin Induces PC-3 Prostate Cancer Cell Apoptosis via ROS Production and Ca2+ Homeostasis Disruption

Kim

et al. 2016

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Section: Monensin Induces G 1 Cell-cycle Arrest By Down-regulating Cysupporting

confidence: 93%

Monensin Induces PC-3 Prostate Cancer Cell Apoptosis via ROS Production and Ca2+ Homeostasis Disruption

Kim

et al. 2016

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“…Several studies depicted that CoCl 2 could alter protein expression of Bcl-2 family [33] and trigger caspase-cascade apoptosis [34]. In our study, CoCl 2 treatment suppressed the expression of anti-apoptotic proteins Bcl-2 and Bcl-X L .…”

Section: Discussionsupporting

confidence: 65%

Lutein Attenuates Both Apoptosis and Autophagy upon Cobalt (II) Chloride-Induced Hypoxia in Rat Műller Cells

Fung

Law

2016

PLoS ONE

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Retinal ischemia/reperfusion injury is a common feature of various retinal diseases such as glaucoma and diabetic retinopathy. Lutein, a potent anti-oxidant, is used to improve visual function in patients with age-related macular degeneration (AMD). Lutein attenuates apoptosis, oxidative stress and inflammation in animal models of acute retinal ischemia/hypoxia. Here, we further show that lutein improved Műller cell viability and enhanced cell survival upon hypoxia-induced cell death through regulation of intrinsic apoptotic pathway. Moreover, autophagy was activated upon treatment of cobalt (II) chloride, indicating that hypoxic injury not only triggered apoptosis but also autophagy in our in vitro model. Most importantly, we report for the first time that lutein treatment suppressed autophagosome formation after hypoxic insult and lutein administration could inhibit autophagic event after activation of autophagy by a pharmacological approach (rapamycin). Taken together, lutein may have a beneficial role in enhancing glial cell survival after hypoxic injury through regulating both apoptosis and autophagy.

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“…Song et al reported that diphenyleneiodonium reduced cellular apoptosis in kidney proximal tubular epithelial cells without a reduction in ROS owing to the upregulation of Bcl2 [19]. Cellular apoptosis was reduced by maintaining mitochondrial membrane permeabilization through Bcl2 family regulation; the results of our present study are considered to be similar to those of that study.…”

Section: Discussionsupporting

confidence: 90%

Protective effect of agmatine against cisplatin-induced apoptosis in an auditory cell line

Park

Lee

et al. 2020

Preprint

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23Objectives: Agmatine, an endogenous metabolite of arginine, is known to have 24 antioxidant activity, protect mitochondrial function, and confer resistance to cellular 25 apoptosis. The aim of this study was to evaluate the protective effects of agmatine 26 against cisplatin-induced cellular apoptosis in an auditory cell line. 27 Methods: HEI-OC1 cells were co-treated with agmatine at different concentrations and 28 15 µM cisplatin for 48 h. Cell viability was measured and annexin V-FITC/propidium 29 iodide (PI) staining was performed to analyze apoptosis. The levels of intracellular 30 reactive oxygen species (ROS) were measured using flow cytometry. The expression 31 of BAX (Bcl2-associated X protein) and the enzymatic activity of caspase-3 were 32 measured to examine the pathway of apoptosis induction. 33 Results: Co-treatment with 8 mM agmatine protected HEI-OC1 cells against cisplatin-34 induced cell apoptosis. Agmatine exerted a significant protective effect against 15 µM 35 cisplatin when applied for 48 h and reduced the proportion of necrotic and late 36 apoptotic cells. Agmatine did not reduce the cisplatin-induced increase in ROS but 37 decreased the expression of BAX and the activity of caspase-3. 38 Conclusions: Agmatine protected against cisplatin-induced cellular apoptosis in an 39 auditory cell line. These effects were mediated by the protection of mitochondrial 40 function and inhibition of apoptosis. 128 ChemiDOC touch imaging system (Bio-Rad, Hercules, CA). The relative band 129 densities were computed using ImageJ software (Imagej.nih.gov/ij/index.html).

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The NADPH oxidase inhibitor DPI can abolish hypoxia-induced apoptosis of human kidney proximal tubular epithelial cells through Bcl2 up-regulation via ERK activation without ROS reduction

Cited by 32 publications

References 44 publications

Monensin Induces PC-3 Prostate Cancer Cell Apoptosis via ROS Production and Ca2+ Homeostasis Disruption

Monensin Induces PC-3 Prostate Cancer Cell Apoptosis via ROS Production and Ca2+ Homeostasis Disruption

Lutein Attenuates Both Apoptosis and Autophagy upon Cobalt (II) Chloride-Induced Hypoxia in Rat Műller Cells

Protective effect of agmatine against cisplatin-induced apoptosis in an auditory cell line

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