Early Alterations of Actin in Cultured Human Keratinocytes and Fibroblasts Exposed to Long‐wavelength Radiations. Possible Involvement in the Uva‐induced Perturbations of Endocytotic Processes

Djavaheri‐Mergny, Mojgan; Pieraggi, M T; Mazière, Cécile; Santús, René; Lageron, A; Salvayre, Robert; Dubertret, Louis; Mazière, J.C.

doi:10.1111/j.1751-1097.1994.tb05000.x

Cited by 28 publications

(14 citation statements)

References 36 publications

(1 reference statement)

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“…This result suggests that UVA might affect melanoma tumor angiogenesis, via enhanced VEGF expression, and this hypothesis will be studied further in a separate project. Finally, UVA radiation exposure has caused decrease the G-actin and cofilin gene expression levels agreeing with earlier studies that have shown that UVA radiation decreases actin expression in human fibroblasts and keratinocytes [21], and in mouse and hamster fibroblasts [22]. …”

Section: Discussionsupporting

confidence: 90%

Ultraviolet-A radiation induces changes in cyclin G gene expression in mouse melanoma B16-F1 cells

Pastila

Leszczyński

2007

Cancer Cell Int

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BackgroundWe have previously shown that ultraviolet-A (UVA) radiation enhances metastatic lung colonization capacity of B16-F1 melanoma cells. The aim of this study was to examine changes in expression profile of genes in mouse melanoma B16-F1 cells exposed to UVA radiation.ResultsB16-F1 melanoma cells were exposed to a single UVA radiation dose of 8 J/cm2 and mRNA was isolated 4 h after the end of UVA exposure. Atlas™ Mouse Cancer 1.2 cDNA expression arrays were used for the large-scale screening to identify the genes involved in the regulation of carcinogenesis, tumor progression and metastasis. Physiologically relevant UVA dose induced differential expression in 9 genes in the UVA exposed melanoma cells as compared to the unexposed control cells. The expression of seven genes out of nine was upregulated (HSC70, HSP86, α-B-crystallin, GST mu2, Oxidative stress induced protein OSI, VEGF, cyclin G), whereas the expression of two genes was down-regulated (G-actin, non-muscle cofilin). The gene expression of cyclin G was mostly affected by UVA radiation, increasing by 4.85-folds 4 hour after exposure. The analysis of cyclin G protein expression revealed 1.36-fold increase at the 6 hour time point after UVA exposure. Cell cycle arrest in G2/M phase, which is known to be regulated by cyclin G, occurred at 4-h hour time-point, peaking 8 hours after the end of UVA irradiation, suggesting that cyclin G might play a role in the cell cycle arrest.ConclusionOur results suggest that UVA radiation-induces changes in the expression of several genes. Some of these changes, e.g. in expression of cyclin G, possibly might affect cell physiology (cell cycle arrest).

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Section: Discussionsupporting

confidence: 90%

Ultraviolet-A radiation induces changes in cyclin G gene expression in mouse melanoma B16-F1 cells

Pastila

Leszczyński

2007

Cancer Cell Int

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“…Alterations in cell adhesion have been described in cultured cells exposed to light (Bolognani et al, 1994;Djavaheri-Mergny et al, 1994). Photosensitization also induced changes in cell anchorage to certain extracellular components, which are associated to a low expression of b1-integrin in ovarian cancer cells (Runnels et al, 1999) and in fibroblasts (Margaron et al, 1996) after Verteporfin phototreatment.…”

Section: Discussionmentioning

confidence: 96%

Loss of E‐cadherin mediated cell–cell adhesion as an early trigger of apoptosis induced by photodynamic treatment

Galaz

Espada

Stockert

et al. 2005

Journal Cellular Physiology

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Photodynamic treatment with different photosensitizers (PSs) can result in the specific induction of apoptosis in many cell types. It is commonly accepted that this apoptotic response depends on the mitochondrial accumulation of the PS. Accumulation in other cellular organelles, such as lysosomes or the Golgi complex, and subsequent photodamage resulting in an apoptotic process has been also described. However, the role played by cell adhesion in apoptosis induced in epithelial cells after photodynamic treatment is not well characterized. Here, we have used a murine keratinocyte line, showing a strong dependence on E-cadherin for cell-cell adhesion and survival, to analyze the relevance of this adhesion complex in the context of zinc(II)-phthalocyanine (ZnPc) photodynamic treatment. We report that under apoptotic conditions, ZnPc phototreatment induces a rapid disorganization of the E-cadherin mediated cell-cell adhesion, which largely preceded both the detachment of cells from the substrate, via beta-1 integrins and the induction of apoptotic mitochondrial markers. Therefore, the alteration in E-cadherin, alpha- and beta-catenins adhesion proteins preceded the release of cytochrome c (cyt c) from mitochondria to the cytosol and the activation of caspase 3. In addition, blocking E-cadherin function with a specific antibody (Decma-1) induced apoptosis in this cell system. These results strongly suggest that the E-cadherin adhesion complex could be the primary target of ZnPc phototreatment, and that loss of E-cadherin mediated cell adhesion after early photodamage triggers an apoptotic response.

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“…This structural rearrangement may be responsible for the detachment of cells from adjacent surface, the cell body retraction and, as a consequence, the loss of contact between neighbouring cells. Previously, it was reported that UVA irradiation can lead to a markedly decreased actin reactivity with fluorescein‐labelled phalloidin (41). This effect was suggested to be a consequence of alternating actin polymerization and thus in the organization of actin filaments.…”

Section: Discussionmentioning

confidence: 99%

Structural alterations provoked by narrow‐band ultraviolet B in immortalized keratinocytes: assessment by atomic force microscopy

Reich

Lehmann

Meurer

et al. 2007

Experimental Dermatology

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We applied atomic force microscopy (AFM) to visualize ultrastructural changes of the keratinocyte morphology after narrow-band ultraviolet B (NB-UVB) irradiation. Immortalized human keratinocytes were cultured under standard conditions, irradiated with NB-UVB light at doses ranging from 50 to 800 mJ/cm2 and imaged by AFM mounted on an inverted optical microscope. It was observed, that NB-UVB irradiation provoked dose-dependent alterations of the keratinocyte morphology. While the surface of non-irradiated cells exhibited homogenously distributed crest-like shaped protrusions (height 0.16 +/- 0.05 microm), cells irradiated with a dose of 800 mJ/cm2 in addition showed round shaped protrusions (height 0.14 +/- 0.06 microm) distributed predominantly around the nucleus and bleb-like protrusions irregularly distributed on the cell surface (height 0.95 +/- 0.29 microm). These irradiated cells easily detached from the supporting glass surface, showed impaired contact with adjacent keratinocytes and significantly rearranged their cytoskeleton network. We hypothesize that these structural and functional alterations reflect ongoing apoptosis in UVB treated cells.

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Early Alterations of Actin in Cultured Human Keratinocytes and Fibroblasts Exposed to Long‐wavelength Radiations. Possible Involvement in the Uva‐induced Perturbations of Endocytotic Processes

Cited by 28 publications

References 36 publications

Ultraviolet-A radiation induces changes in cyclin G gene expression in mouse melanoma B16-F1 cells

Ultraviolet-A radiation induces changes in cyclin G gene expression in mouse melanoma B16-F1 cells

Loss of E‐cadherin mediated cell–cell adhesion as an early trigger of apoptosis induced by photodynamic treatment

Structural alterations provoked by narrow‐band ultraviolet B in immortalized keratinocytes: assessment by atomic force microscopy

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