NF-kappa B Transcription Factor and Human Immunodeficiency Virus Type 1 (HIV-1) Activation by Methylene Blue Photosensitization

Piret, Bernard; Legrand-Poels, Sylvie; Sappey, Christine; Piette, Jacques

doi:10.1111/j.1432-1033.1995.00447.x

Cited by 14 publications

(15 citation statements)

References 61 publications

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“…Thus, several protein kinase signalling pathways are activated, some of which (stress kinases) are presumed to lead to apoptosis [130], whereas others are presumed to promote cell survival [131,132]. NF-κB is activated by different photosensitisers used in PDT [133][134][135].…”

Section: Cam-kinase Inhibition As a Mechanism To Sensitise Cells To Cmentioning

confidence: 99%

Calcium/calmodulin-dependent protein kinases as potential targets in cancer therapy

Rodriguez-Mora¹,

LaHair²,

Howe³

et al. 2005

Expert Opinion on Therapeutic Targets

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In this review the authors discuss the expression and activation of a family of protein kinases known as the calcium/calmodulin-dependent kinases (CaM-kinase) and the role that these kinases have in the activation of antiapoptotic signalling pathways. In addition, the authors outline a novel mechanism of activation of these kinases by oxidative stress. Founded on this novel mechanism of activation and the role that these kinases have in activating antiapoptotic signalling pathways, the authors propose that the CaM-kinases would make very good targets for sensitising cancer cells to certain therapeutic treatments. Furthermore, the authors discuss the role that these kinases have in cell transformation and in the regulation of the cell cycle. Based on these roles the authors suggest that inhibition of the CaM-kinases not only has the potential to sensitise cancer cells, but also has the potential to induce cytostasis in these cells.

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Section: Cam-kinase Inhibition As a Mechanism To Sensitise Cells To Cmentioning

confidence: 99%

Calcium/calmodulin-dependent protein kinases as potential targets in cancer therapy

Rodriguez-Mora¹,

LaHair²,

Howe³

et al. 2005

Expert Opinion on Therapeutic Targets

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“…Support for connection between 1 O 2 and Akt activation is indirect. 1 O 2 has been shown to induce activation of NF-jB, a transcription factor that mediates antiapoptotic signaling following many stimuli including oxidant injury (23)(24)(25), and both PI3-K-Akt and MEK-ERK pathways mediate activation of NF-jB by multiple factors (26)(27)(28). In addition, NF-jB was identified to be a target of Akt in the antiapoptotic PDGF signaling (29).…”

Section: Introductionmentioning

confidence: 99%

Singlet Oxygen–induced Activation of Akt/Protein Kinase B is Independent of Growth Factor Receptors¶

Zhuang¹,

Kochevar²

2003

Photochem Photobiol

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Singlet oxygen (1O2)-induced cytotoxicity is believed to be responsible for responses to photodynamic therapy and for apoptosis of T helper cells after UV-A treatment. Other cytotoxic oxidants, such as hydrogen peroxide and peroxynitrite have been shown to stimulate cell survival signaling pathways in addition to causing cell death. Both these oxidants stimulate the Akt/protein kinase B survival signaling pathway through activation of membrane tyrosine kinase growth factor receptors. We evaluated the ability of 1O2 to activate the Akt/protein kinase B pathway in NIH 3T3 cells and examined potential activation pathways. Exposure of fibroblasts to 1O2 elicited a strong and sustained phosphorylation of Akt, which occurred concurrently with phosphorylation of p38 kinase, a proapoptotic signal. Inhibition of phosphatidylinositol-3-OH kinase (PI3-K) completely blocked Akt phosphorylation. Significantly, cell death induced by 1O2 was enhanced by inhibition of PI3-K, suggesting that activation of Akt by 1O2 may contribute to fibroblast survival under this form of oxidative stress. 1O2 treatment did not induce phosphorylation of platelet-derived growth factor receptor (PDGFR) or activate SH-PTP2, a substrate of growth factor receptors, suggesting that PDGFR was not activated. In addition, specific inhibition of PDGFR did not affect Akt phosphorylation elicited by 1O2. Activation of neither focal adhesion kinase (FAK) nor Ras protein, both of which mediate responses to reactive oxygen species, appeared to be pathways for the 1O2-induced activation of the PI3-K-Akt survival pathway. Thus, activation of Akt by 1O2 is mediated by PI3-K and contributes to a survival response that counteracts cell death after 1O2-induced injury. However, unlike the response to other oxidants, activation of the PI3-K-Akt by 1O2 does not involve activation of growth factor receptors, FAK or Ras protein.

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“…Phthalocyanines are oxygen dependent for their photobiological effects, acting via singlet oxygen production as well as other reactive oxygen species (18). On the other hand, other oxygen-dependent photosensitizers, such as methylene blue and rose bengal, can activate the HIV promoter (8).…”

Section: Discussionmentioning

confidence: 99%

“…While cells that are latently infected with HIV are particularly sensitive to Pc 4 phototreatment and undergo apoptosis soon after treatment (7), the question remains whether such treatment can activate latent HIV. Such activation has been shown to occur under oxidative stress and following phototreatment with other sensitizers (8)(9)(10).…”

Section: Introductionmentioning

confidence: 99%

Photosensitized Decontamination of Blood with the Silicon Phthalocyanine Pc 4: No Activation of the Human Immunodeficiency Virus Promoter

Zmudzka

Strickland

Beer

et al. 1997

Photochem & Photobiology

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Photochemical decontamination of red blood cell concentrates (RBCC) with the silicon phthalocyanine Pc 4 and red light is being studied to enhance the viral safety of blood transfusion. Recent reports indicate that treatments with radiation and various phototsensitizing agents can activate the promoter of human immunodeficiency virus (HIV). This raises the possibility that an inadequate, sublethal photochemical treatment of RBCC could induce HIV in latently infected cells. This question has been addressed using HeLa cells stably transfected with the chloramphenicol acetyl transferase gene under the control of the HIV promoter. In control studies, 8-methoxypsoralen (8-MOP) excited by UVA light caused activation of the HIV promoter in a dose- and time-dependent manner. At 0.1 microgram/mL of 8-MOP, maximal activation occurred with 18 J/cm2, 30 h after light exposure, With Pc 4 at 20 nM, over 90% of HeLa cells were killed after 24 h when exposed to 1 J/cm2 of red light. During that time interval and over a wide range of light doses no activation of the HIV promoter occurred. It is concluded that RBCC sterilization with Pc 4 and red light is unlikely to induce HIV production in latently infected cells.

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NF-kappa B Transcription Factor and Human Immunodeficiency Virus Type 1 (HIV-1) Activation by Methylene Blue Photosensitization

Cited by 14 publications

References 61 publications

Calcium/calmodulin-dependent protein kinases as potential targets in cancer therapy

Calcium/calmodulin-dependent protein kinases as potential targets in cancer therapy

Singlet Oxygen–induced Activation of Akt/Protein Kinase B is Independent of Growth Factor Receptors¶

Photosensitized Decontamination of Blood with the Silicon Phthalocyanine Pc 4: No Activation of the Human Immunodeficiency Virus Promoter

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