Melatonin and amfenac modulate calcium entry, apoptosis, and oxidative stress in ARPE-19 cell culture exposed to blue light irradiation (405 nm)

Argun, Mehmet; Tök, Levent; Uğuz, Abdülhadi Cihangir; Çelik, Ömer; Tök, Özlem; Nazıroğlu, Mustafa

doi:10.1038/eye.2014.50

Cited by 36 publications

(22 citation statements)

References 45 publications

(48 reference statements)

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“…Calcium plays an important role in supporting neuronal survival. The accumulation of intracellular Ca 2+ affects mitochondrial depolarization activity , which is essential for ATP synthesis and subsequently controls neuronal survival . In addition, Ghazizadeh and colleagues reported that epilepsy is involved in Ca 2+ entry and oxidative stress‐induced neuronal death .…”

Section: Discussionmentioning

confidence: 99%

Increased Expression of Transient Receptor Potential Vanilloid 4 in Cortical Lesions of Patients with Focal Cortical Dysplasia

et al. 2016

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Section: Discussionmentioning

confidence: 99%

Increased Expression of Transient Receptor Potential Vanilloid 4 in Cortical Lesions of Patients with Focal Cortical Dysplasia

et al. 2016

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“…The activated caspase-8/10 cleaves and activates the effector caspases (caspase-3, -6 and -7), which subsequently target a range of cellular substrates that lead to apoptosis [36]. The intrinsic apoptotic pathway is induced by a variety of intracellular stimuli such as damages mediated by irradiation or chemotherapeutic agents, growth factor deprivation, or oxidative stress [37, 38]. In this pathway, the disruption of the mitochondrial membrane leads to the release of pro-apoptotic proteins from the mitochondrial intermembrane space into the cytoplasm, which relies on the apoptosome including procaspase-9, apoptotic protease activating factor 1 (Apaf-1) and cytochrome c [38–41].…”

Section: Programmed Cell Death In the Treatment Of Osteosarcomamentioning

confidence: 99%

Cell apoptosis, autophagy and necroptosis in osteosarcoma treatment

Yang

et al. 2016

Oncotarget

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Osteosarcoma is the most common primary bone tumor in children and adolescents. Although combined therapy including surgery and multi-agent chemotherapy have resulted in great improvements in the overall survival of patients, chemoresistance remains an obstacle for the treatment of osteosarcoma. Molecular targets or effective agents that are actively involved in cell death including apoptosis, autophagy and necroptosis have been studied. We summarized how these agents (novel compounds, miRNAs, or proteins) regulate apoptotic, autophagic and necroptotic pathways; and discussed the current knowledge on the role of these new agents in chemotherapy resistance in osteosarcoma.

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“…Under many kinds of cellular stresses, unfolded proteins are accumulated in the ER and influence normal ER functions [10,11]. Activation of caspase-12 plays a role in the triggering of apoptosis by the intrinsic ER stress apoptotic pathway, which is mediated by ER through activation of the caspase-9-and caspase-3-dependent pathways.…”

Section: Introductionmentioning

confidence: 99%

Zinc Chloride Inhibits Human Lens Epithelial Cell Migration and Proliferation Involved in TGF-β1 and TNF-α Signaling Pathways in HLE B-3 Cells

Guo

et al. 2014

Biol Trace Elem Res

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Zinc is one of the most abundant essential elements in the human body, which is an essential, coenzyme-like component of many enzymes, and is indispensable to their functions. However, high levels of zinc ions can lead to cell damage. In the present study, we explored the effects of high concentrations of zinc chloride (ZnCl2) on lens epithelial cell proliferation and migration and further investigated the effects of different concentrations of ZnCl2 on caspase-9 and caspase-12, transforming growth factor-beta 1 (TGF-β1), and tumor necrosis factor-alpha (TNF-α). We found that ZnCl2 could inhibit human lens epithelial (HLE) B-3 cell migration and induce apoptosis/necrosis. In addition, ZnCl2 can efficiently decrease the expressions of caspase-9 and caspase-12, increase the expression of TNF-α at both gene and protein levels, and thus induces cell death. Taken together, our results indicate that ZnCl2 can inhibit HLE B-3 cell migration and proliferation by decreasing the expression of TGF-β1 and increasing the expression of TNF-α and finally lead to HLE B-3 cell death.

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Melatonin and amfenac modulate calcium entry, apoptosis, and oxidative stress in ARPE-19 cell culture exposed to blue light irradiation (405 nm)

Cited by 36 publications

References 45 publications

Increased Expression of Transient Receptor Potential Vanilloid 4 in Cortical Lesions of Patients with Focal Cortical Dysplasia

Increased Expression of Transient Receptor Potential Vanilloid 4 in Cortical Lesions of Patients with Focal Cortical Dysplasia

Cell apoptosis, autophagy and necroptosis in osteosarcoma treatment

Zinc Chloride Inhibits Human Lens Epithelial Cell Migration and Proliferation Involved in TGF-β1 and TNF-α Signaling Pathways in HLE B-3 Cells

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