Apoptosis Versus Cell Differentiation

Lanneau, David; Thonel, Aurélie de; Maurel, Sébastien; Didelot, Céline; Garrido, Carmen

doi:10.4161/pri.1.1.4059

Cited by 197 publications

(96 citation statements)

References 103 publications

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“…In this experiment the antiapoptotic function of HSP-90 activated by microwaves radiation is sufficient for it not to cause cell death by activation of enzymatic pathways. It is known that microwaves may trigger injury in the cellular cytoplasm [59] and that HSP-90, an intracellular protein ensures the stability of different proteins [27], although the role of this chaperone is unknown in relation to necrosis.…”

Section: Discussionmentioning

confidence: 99%

“…Other stress-related stimuli such as fever, convulsions [20], drugs (amphetamine or LSD) [21], injury and neurodegenerative diseases [22] cause modifications in the basal levels of HSP-90. An increase in HSP-90 in neuronal subpopulations [23] and/or its activation in new non neuronal glial and microglial cell populations [24] indicates participation by this protein in neuroprotective mechanisms [25], oxidative stress [26] and anti-apoptic activity [27,28].…”

Section: Introductionmentioning

confidence: 99%

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EXPOSURE TO 2.45 GHz MICROWAVE RADIATION PROVOKES CEREBRAL CHANGES IN INDUCTION OF HSP-90 Î±/Î² HEAT SHOCK PROTEIN IN RAT.

Jorge-Mora¹,

Álvarez-Folgueiras²,

Leiro³

et al. 2010

PIER

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Abstract-Physical agents such as non-ionizing continuous-wave 2.45 GHz radiation may cause damage that alters cellular homeostasis and may trigger activation of the genes that encode heat shock proteins (HSP). We used Enzyme-Linked ImmunoSorbent Assay (ELISA) and immunohistochemistry to analyze the changes in levels of HSP-90 and its distribution in the brain of Sprague-Dawley rats, ninety minutes and twenty-four hours after acute (30min) continuous exposure to 2.45 GHz radiation in a the Gigahertz Transverse Electromagnetic (GTEM cell). In addition, we studied further indicators of neuronal insult: dark neurons, chromatin condensation and nucleus fragmentation, which were observed under optical conventional or fluorescence microscopy after DAPI staining. The cellular distribution of protein HSP-90 in the brain increased with each corresponding SAR (0.034 ± 3.10 −3 , 0.069 ± 5.10 −3 , 0.27 ± 21.10 −3 W/kg), in hypothalamic nuclei, limbic cortex and somatosensorial cortex after exposure to the radiation. At twenty-four hours post-irradiation, levels of HSP-90 protein remained high in all hypothalamic nuclei for all SARs, and in the parietal cortex, except the limbic system, HSP-90 levels were lower than in non-irradiated rats, almost half the levels in rats exposed to the highest power radiation. Non-apoptotic cellular nuclei and a some dark neurons were found ninety minutes and twenty-four hours after maximal SAR exposure. The results suggest that acute exposure to electromagnetic fields triggered an imbalance in anatomical HSP-90 levels but the anti-apoptotic mechanism is probably sufficient to compensate the non-ionizing stimulus. Further studies are required to determine the regional effects of chronic electromagnetic pollution on heat shock proteins and their involvement in neurological processes and neuronal damage.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

EXPOSURE TO 2.45 GHz MICROWAVE RADIATION PROVOKES CEREBRAL CHANGES IN INDUCTION OF HSP-90 Î±/Î² HEAT SHOCK PROTEIN IN RAT.

Jorge-Mora¹,

Álvarez-Folgueiras²,

Leiro³

et al. 2010

PIER

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“…HSPs may also determine the cell fate by orchestrating the decision of apoptosis vs differentiation 45. Indeed, in our two week model apoptosis has been elicited by a chemical agent already at the beginning of culture when differentiation just begins (our unpublished observation).…”

Section: Discussionmentioning

confidence: 83%

“…Constitutive heat shock proteins such as HSP70 are present during the mouse myoblast differentiation period,43 while HSP90 inhibition affected protein kinases regulating pathways required for myoblast differentiation 44. Multiple transduction proteins, which are essential for differentiation, are client proteins of HSP90 45. In porcine satellite cells, a mild heat shock increased transcription and translation of HSP90, HSP70, HSP25/27, while in fused satellite cells, protein synthesis rates were significantly increased, and degradation rates decreased 46.…”

Section: Discussionmentioning

confidence: 99%

Influence of hyperthermal regimes on experimental teratoma development in vitro

Bojanac

Rogosic

Sinčić

et al. 2018

Int J Experimental Path

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SummaryWe screened for the impact of hyperthermal regimes varying in the cumulative equivalent minutes at 43°C (CEM43°C) and media composition on tumour development using an original teratoma in vitro model. Rat embryos (three germ layers) were microsurgically isolated and cultivated at the air‐liquid interface. During a two week period, ectodermal, mesodermal and endodermal derivatives developed within trilaminar teratomas. Controls were grown at 37°C. Overall growth was measured, and teratoma survival and differentiation were histologically assessed. Cell proliferation was stereologically quantified by the volume density of Proliferating Cell Nuclear Antigen. Hyperthermia of 42°C, applied for 15 minutes after plating (CEM43°C 3.75 minutes), diminished cell proliferation (P ˂ .0001) and enhanced differentiation of both myotubes (P ˂ .01) and cylindrical epithelium (P ˂ .05). Hyperthermia of 43°C applied each day for 30 minutes during the first week (CEM43°C 210 minutes) impaired overall growth (P ˂ .01) and diminished cell proliferation (P ˂ .0001). Long‐term hyperthermia of 40.5°C applied for two weeks (CEM43°C 630 minutes) significantly impaired survival (P ˂ .005). Long‐term hyperthermia of 40.5°C applied from the second day when differentiation of tissues begins (CEM43°C 585 minutes) impaired survival (P ˂ .0001), overall growth (P ˂ .01) and cartilage differentiation (P ˂ .05). No teratomas survived extreme regimes: 43°C for 24 hours (CEM43°C 1440 minutes), hyperthermia in the scant serum‐free medium (CEM43°C 630 minutes) or treatment with an anti‐HSP70 antibody before long‐term hyperthermia 40.5°C from the second day (CEM43°C 585 minutes). This in vitro research provided novel insights into the impact of hyperthermia on the development of experimental teratomas from their undifferentiated sources and are thus of potential interest for future therapeutic strategies in corresponding in vivo models.

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“…104 In case of a cell death stimulus, HSPs are overexpressed and have strong anti-apoptotic properties by associating to different key proteins of the apoptosis transduction signaling pathway. 105 HSPs can also be extracellular (membrane-bound or free after secretion). 106,107 HSP27, 108 HSP70 109 and HSP90 110 have been found secreted in the extracellular media, and some of them, as already mentioned above, have been shown to be present in extracellular vesicles, notably in exosomes.…”

Section: Heat Shock Proteins and Exosomesmentioning

confidence: 99%

Exosomes in cancer theranostic: Diamonds in the rough

Cordonnier

Chanteloup

Isambert

et al. 2017

Cell Adhesion & Migration

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During the last 10 years, exosomes, which are small vesicles of 50-200 nm diameter of endosomal origin, have aroused a great interest in the scientific and clinical community for their roles in intercellular communication in almost all physiological and pathological processes. Most cells can potentially release these nanovesicles that share with the parent cell a similar lipid bilayer with transmembrane proteins and a panel of enclosed soluble proteins such as heat shock proteins and genetic material, thus acting as potential nanoshuttles of biomarkers. Exosomes surface proteins allow their targeting and capture by recipient cells, while the exosomes' content can modify the physiological state of recipient cells. Tumor derived exosomes by interacting with other cells of the tumor microenvironment modulate tumor progression, angiogenic switch, metastasis, and immune escape. Targeting tumor-derived exosomes might be an interesting approach in cancer therapy. Furthermore, because a key issue to improve cancer patients' outcome relies on earlier cancer diagnosis (metastases, as opposed to the primary tumor, are responsible for most cancer deaths) exosomes have been put forward as promising biomarker candidates for cancer diagnosis and prognosis. This review summarizes the roles of exosomes in cancer and clinical interest, focusing on the importance of exosomal heat shock proteins (HSP). The challenges of clinical translation of HSPexosomes as therapeutic targets and biomarkers for early cancer detection are also discussed.

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Apoptosis Versus Cell Differentiation

Cited by 197 publications

References 103 publications

EXPOSURE TO 2.45 GHz MICROWAVE RADIATION PROVOKES CEREBRAL CHANGES IN INDUCTION OF HSP-90 Î±/Î² HEAT SHOCK PROTEIN IN RAT.

EXPOSURE TO 2.45 GHz MICROWAVE RADIATION PROVOKES CEREBRAL CHANGES IN INDUCTION OF HSP-90 Î±/Î² HEAT SHOCK PROTEIN IN RAT.

Influence of hyperthermal regimes on experimental teratoma development in vitro

Exosomes in cancer theranostic: Diamonds in the rough

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