Apoptosis and necrosis induced by ultraviolet radiation in the presence of autologous plasma

Artyukhov, V. G.; Земченкова, О. В.; Basharina, O. V.; Ryazantsev, S. V.; Pashkov, M. V.

doi:10.1134/s1990519x14030043

Cited by 5 publications

(6 citation statements)

References 12 publications

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“…6 Whereas UV-induced apoptosis is a complex event involving different pathways like DNA damage, cell death receptor activation and oxidative stress accompanied by mitochondrial changes and cytochrome c release. 23,24 Here, the induction of apoptosis in lymphocytes by UVA only is dose dependent. Only a high dose of UVA light, whether it is administered in a single high dose or via repetitive low doses, is as efficient as standard ECP to induce adequate cell damage to compensate for the lack of 8-MOP resulting in sufficient apoptosis.…”

Section: Discussionmentioning

confidence: 99%

“…The mode of action of 8‐MOP in the context of ECP is well described, as it covalently binds to DNA and crosslinks pyrimidine bases after UVA light activation, resulting in cell cycle arrest and apoptosis of treated cells 6 . Whereas UV‐induced apoptosis is a complex event involving different pathways like DNA damage, cell death receptor activation and oxidative stress accompanied by mitochondrial changes and cytochrome c release 23,24 . Here, the induction of apoptosis in lymphocytes by UVA only is dose dependent.…”

Section: Discussionmentioning

confidence: 99%

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A simplified extracorporeal photopheresis procedure based on single high‐dose ultraviolet A light irradiation shows similar in vitro efficacy

Buchele

Hackstein

2020

Transfusion

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Background: Extracorporeal photopheresis (ECP) is one of the most widely used and effective cell-based therapies for the treatment of T-cell-mediated diseases. The patients' white blood cells (WBCs) are collected by apheresis and exposed to the photosensitizer 8-methoxypsoralen (8-MOP) and ultraviolet A (UVA) light before retransfusion. The UVA/8-MOP combination has been in use in ECP for more than 4 decades; however, whether ECP can be simplified by UVA light irradiation only has never been analyzed. Study Design and Methods: Peripheral blood mononuclear cells were treated with classical ECP or different UVA light doses only (UVA only). Treatment efficacy was investigated by apoptosis induction in WBC subsets, inhibition of T-cell proliferation, and the ability of monocytes to induce allogeneic T-cell expansion and to respond to lipopolysaccharide and interferon-γ stimulation in vitro. Results: High-dose UVA only treatment (5 J/cm 2) was as efficient as ECP to induce apoptosis within 48 hours. UVA only treatment modulated the composition of the surviving cells by improving monocyte survival and promoting CD8 + T-cell apoptosis. Both ECP and UVA only treatment inhibited anti-CD3/ anti-CD28 triggered T-cell proliferation. Interestingly, whereas ECP-treated monocytes exhibited a markedly reduced capacity to respond to stimulation and to induce allogeneic T-cell proliferation, UVA only treatment preserved monocyte functionality to some degree. Conclusions: High-dose UVA only and standard ECP showed comparable efficacy in inducing apoptosis and inhibiting direct T-cell proliferation. Hence, UVA only treatment can be a simplified alternative to ECP therapy. Furthermore, increased monocyte survival with partially preserved functionality after UVA only treatment may provide a novel method for immunoregulation.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

A simplified extracorporeal photopheresis procedure based on single high‐dose ultraviolet A light irradiation shows similar in vitro efficacy

Buchele

Hackstein

2020

Transfusion

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“…Given that necrosis proceeds more slowly than apoptosis, late death may be a largely due to necrosis [Rode, ]. Though UV cytotoxicity studies suggest that necrosis rarely occurs [e.g., Michael et al, ], it may be present when using higher radiant exposures [Artyukhov et al, ]. It will be important to investigate necrosis further because it may modify the microenvironment of gliomas, thus affecting the cellular responses to UV [Shokrollahi et al, ].…”

Section: Discussionmentioning

confidence: 99%

Effects of Ultraviolet Radiation on Glioma: Systematic Review

Pronin

Koh

Hughes

2017

J of Cellular Biochemistry

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Glioblastoma multiforme is the most aggressive primary brain tumor. Treatment is largely palliative, with current strategies unable to prevent inevitable tumor recurrence. Implantable micro-electromechanical systems are becoming more feasible for the management of several human diseases. These systems may have a role in detecting tumor recurrence and delivering localized therapies. One potential therapeutic tool is ultraviolet (UV) light. This systematic review assesses the effects of UV light on glioma cells. A total of 47 publications are included. The large majority were in vitro experiments conducted on human glioblastoma cell lines in monolayer. In these cells, UV light was shown to induce apoptosis and the expression of genes or activation of proteins that modulate cell death, repair, and proliferation. The nature and magnitude of cellular response varied by UV wavelength, dose, cell line, and time after irradiation. UVC (wavelength 100-280 nm) was most effective at inducing apoptosis, and this effect was dose dependent. The included studies had varied methodologies, complicating reconciliation of results. Further work will be required to determine the best regime of UV irradiation for therapeutic use. J. Cell. Biochem. 118: 4063-4071, 2017. © 2017 Wiley Periodicals, Inc.

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“…ER expression and autocrine estrogen production or treatment by estradiol increase apoptosis rate in many types of ER positive cancers ( 31 ). In a similar study on human lymphocytes, necrosis and apoptosis induction have assayed by flow cytometry after UV exposure and results have shown high dose of UV exposure cause necrosis and apoptosis signaling activation started after first hours of UV exposure ( 20 ). Our data has shown that cell cycle period of ER negative cells was shorter than ER positive cells and its sensitivity to UV exposure was different in comparison with ER positive cell line, This might be in accordance with tumor cell behavior in vivo, considering the fact that the ER negative cancers were often more aggressive and nonresponsive to chemotherapy ( 7 ) and these were more metastatic than ER positive cells.…”

Section: Discussionmentioning

confidence: 99%

“…DNA damage caused by UV (Ultra Violet) radiation has induced pro apoptotic and cell cycle arrest checkpoints expression ( 18 ). Low dose of UV-B has caused to DNA damage and apoptosis ( 19 ), high dose of UV lead to necrosis ( 20 ). Cell death was strikingly polymorphic; it could proceed via necrosis (as in complement-mediated cell death) or apoptosis.…”

Section: Introductionmentioning

confidence: 99%

Apoptosis/Necrosis Induction by Ultraviolet, in ER Positive and ER Negative Breast Cancer Cell Lines

et al. 2015

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Background:Ultraviolet (UV) light exposure has been one of the major inducers of apoptosis. UV exposure has caused pyrimidine dimers and DNA fragmentation which might lead to cell cycle arrest and apoptosis signals activation. UV induced apoptosis has investigated in MDA-MB 468 as an ER negative breast adenocarcinoma and MCF-7 as an ER positive breast cancer cell line. Apoptosis induction rate by UV might be different in these two types of cells due to different biological characteristics of the cell.Objectives:In this paper we have evaluated serial dose of UV-B exposure on ER positive and ER negative breast cancer cell lines and its effect on apoptosis or necrosis induction in these cells.Materials and Methods:MDA-MB468 and MCF-7 cell lines have cultured for 24 hours and UV exposure has carried out at 290 nm at dose of 154 J/m2 to 18 KJ/m2 using UV lamp. UV exposed cells have incubated in cell culture condition for 24 or 48 hours following UV exposure and the cells have stained and analyzed by flow cytometry for apoptosis evaluation by Annexin V/PI method.Results:Apoptosis rate (PI and Annexin V double positive cells) after 24 hours incubation was higher in 24 hours in comparison with 48 hours incubation in both cell lines. The frequency of PI positive MDA-MB 468 cells was higher than PI and Annexin V double positive cells after 48 hours. PI positive MDA-MB 468 cells were significantly higher than MCF-7 cells in 24 hours incubation time.Conclusions:The results have shown that MDA-MB 468 cells were more sensitive to UV exposure and DNA fragmentation and necrosis pathway was dominant in these cells.

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Apoptosis and necrosis induced by ultraviolet radiation in the presence of autologous plasma

Cited by 5 publications

References 12 publications

A simplified extracorporeal photopheresis procedure based on single high‐dose ultraviolet A light irradiation shows similar in vitro efficacy

A simplified extracorporeal photopheresis procedure based on single high‐dose ultraviolet A light irradiation shows similar in vitro efficacy

Effects of Ultraviolet Radiation on Glioma: Systematic Review

Apoptosis/Necrosis Induction by Ultraviolet, in ER Positive and ER Negative Breast Cancer Cell Lines

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