15 results on '"Marie-José Haure"'
Search Results
2. Data from Epidermal Growth Factor Receptor/β-Catenin/T-Cell Factor 4/Matrix Metalloproteinase 1: A New Pathway for Regulating Keratinocyte Invasiveness after UVA Irradiation
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Guy Laurent, Eric Delabesse, Marie Charveron, Addolorata-Maria-Luce Coluccia, Marie-José Haure, Talal Al Saati, Hélène Hernandez-Pigeon, Loïc Ysebaert, Naïs Prade-Houdellier, Amandine Blanc, and Christine Jean
- Abstract
Previous studies have established that UV irradiation results in epidermal growth factor receptor (EGFR) activation in keratinocytes. However, the signaling pathways and cellular effects related to this process remain incompletely elucidated. Herein, we describe for the first time that UVA-mediated EGFR activation results in β-catenin tyrosine phosphorylation at the Y654 residue responsible for the dissociation of E-cadherin/α-catenin/β-catenin complexes. Moreover, UVA induces an EGFR-dependent, but Wnt-independent, β-catenin relocalization from the membrane to the nucleus followed by its association with T-cell factor 4 (TCF4). This newly formed β-catenin/TCF4 complex binds to a specific site on matrix metalloproteinase 1 (MMP1) promoter and governs MMP1 gene and protein expression, as well as cell migration in collagen and gelatin. Altogether, these results suggest that UVA stimulates keratinocyte invasiveness through two coordinated EGFR-dependent processes: loss of cell-to-cell contact due to β-catenin/E-cadherin/α-catenin dissociation and increased cell migration through extracellular matrix component degradation due to β-catenin/TCF4–dependent MMP1 regulation. These events may represent an important step in epidermis repair following UVA injury and their abnormal regulation could contribute to photoaging and photocarcinogenesis. [Cancer Res 2009;69(8):3291–9]
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- 2023
3. ESDR586 - Interest of Silybum marianum extract, Manganese PCA and Lespedeza capitata extract in a new anti-hair loss serum to stimulate hair growth and prolong anagen phase
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Hélène Duplan, Sandrine Bessou-Touya, Nathalie Castex-Rizzi, Sophie Carrère, Valérie Mengeaud, Anaïs Noustens, Marie-José Haure, Camille Mas, Marguerite Lévêque, and Daniel Bacqueville
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- 2022
4. ESDR570 - Targeting JAK/STAT and Wnt/b-catenin pathways and 5a-reductase activity to develop an effective anti-hair loss product
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Sandrine Bessou Touya, Hélène Duplan, Anaïs Noustens, Marie-José Haure, Sylvie Daunes Marion, Sophie Carrère, Marguerite Lévêque, Virginie Turlier, Mélanie Froliger, and Camille Mas
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- 2022
5. Results from in vitro and ex vivo skin aging models assessing the antiglycation and anti-elastase MMP-12 potential of glycylglycine oleamide
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Isabelle Ceruti, Sandrine Bessou-Touya, Nathalie Castex-Rizzi, Marie-José Haure, and Patrick Bogdanowicz
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0301 basic medicine ,Oleamide ,extracellular matrix ,Dermatology ,Matrix metalloproteinase ,matrix metalloproteinase-12 ,Skin Aging ,030207 dermatology & venereal diseases ,03 medical and health sciences ,chemistry.chemical_compound ,0302 clinical medicine ,Glycation ,Medicine ,fibrillin-1 ,skin aging ,Original Research ,biology ,integumentary system ,business.industry ,glycylglycine oleamide ,In vitro ,030104 developmental biology ,Clinical, Cosmetic and Investigational Dermatology ,Biochemistry ,chemistry ,biology.protein ,glycation ,business ,Elastin ,Type I collagen ,Ex vivo - Abstract
Patrick Bogdanowicz,Marie-José Haure,Isabelle Ceruti,Sandrine Bessou-Touya,Nathalie Castex-Rizzi Department of Pharmacology,Pierre Fabre Dermo-Cosmétique, Toulouse,France Background: Glycation is an aging reaction of naturally occurring sugars with dermal proteins. Type I collagen and elastin are most affected by glycation during intrinsic chronological aging. Aim: To study the in vitro and ex vivo assays in human skin cells and explants and the antiaging effects of glycylglycine oleamide (GGO). Materials and methods: The antiglycation effect of GGO was assessed in a noncellular in vitro study on collagen and, ex vivo, by immunohistochemical staining on human skin explants (elastin network glycation). The ability of GGO to contract fibroblasts was assessed in a functional assay, and its anti-elastase (MMP-12) activity was compared to that of oleic acid alone, glycylglycine (GG) alone, and oleic acid associated with GG. Results: In vitro, GGO reduced the glycation of type I collagen. Ex vivo, GGO restored the expression of fibrillin-1 inhibited by glycation. Furthermore, GGO induced a tissue retraction of almost 30%. Moreover, the MMP-12 activity was inhibited by up to 60%. Conclusion: Under the present in vitro and ex vivo conditions, GGO prevents glycation of the major structural proteins of the dermis, helping to reduce the risk of rigidification. By maintaining the elastic function of the skin, GGO may be a promising sparring partner for other topical antiaging agents. Keywords: extracellular matrix, glycylglycine oleamide, glycation, fibrillin-1, matrix metalloproteinase-12, skin aging
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- 2016
6. A new dermocosmetic containing retinaldehyde, delta-tocopherol glucoside and glycylglycine oleamide for managing naturally aged skin: results from in vitro to clinical studies
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Christine Coutanceau, Daniel Bacqueville, Hélène Duplan, Laure Duprat, Sandrine Bessou-Touya, Marie-José Haure, Valérie Mengeaud, Nathalie Castex-Rizzi, Patrick Bogdanowicz, and Céline Rouvrais
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0301 basic medicine ,Oleamide ,formulation ,Human skin ,Dermatology ,Pharmacology ,Skin Aging ,Extracellular matrix ,030207 dermatology & venereal diseases ,03 medical and health sciences ,chemistry.chemical_compound ,0302 clinical medicine ,Dermis ,delta-tocopherol glucoside ,Medicine ,preclinical aged skin model ,Original Research ,integumentary system ,biology ,business.industry ,glycylglycine oleamide ,Fibulin ,030104 developmental biology ,medicine.anatomical_structure ,Biochemistry ,chemistry ,Clinical, Cosmetic and Investigational Dermatology ,statistics ,retinaldehyde ,biology.protein ,business ,Elastin ,Ex vivo - Abstract
Céline Rouvrais,1,* Daniel Bacqueville,2,* Patrick Bogdanowicz,2,* Marie-José Haure,2 Laure Duprat,2 Christine Coutanceau,3 Nathalie Castex-Rizzi,2 Hélène Duplan,2 Valérie Mengeaud,1 Sandrine Bessou-Touya2 1Clinical Skin Research Center, 2Department of Pharmacology, Pierre Fabre Dermo-Cosmétique, Toulouse, 3Laboratoire Dermatologique Avène, Lavaur, France *These authors contributed equally to this work Introduction: Natural aging of skin tissues, the addition of the cumulative action of the time and radiation exposure result in skin atrophy, wrinkles and degeneration of the extracellular matrix (ECM). The aim of the study was to investigate the beneficial effect of a combination containing retinaldehyde (RAL), delta-tocopherol glucoside (delta-TC) and glycylglycine oleamide (GGO) and of a dermocosmetic containing the combination. Materials and methods: The protective effect of the combination was assessed through invitro gene expression of ultraviolet (UV)-irradiated fibroblasts. A skin aging assay using UV light on ex vivo skin samples and a clinical study conducted in 36 women aged from 35 to 55years with a minimum of level 4 to a maximum of level 6 on the crow’s feet photoscale assessed the antiaging effect of the dermocosmetic. Results: When added to UV-irradiated fibroblasts, the combination substantially improved the ECM in activating the elastin fiber production (fibrillin 2, fibulin 1 and 5 and lysyl oxidase-like2) as well as that of proteins involved in the cellular ECM interactions (integrin β1, paxillin and actin a2). An ex vivo photodamaged human skin model showed that the dermocosmetic formulation containing the combination of the active ingredients protected the elastic network against UV-induced alterations including both elastin and fibrillin-rich fibers in the dermis. A daily application of the dermocosmetic for 2months on naturally aged skin resulted in a statistically significant improvement (p
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- 2017
7. UVA-activated synthesis of metalloproteinases 1, 3 and 9 is prevented by a broad-spectrum sunscreen
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Patrick Bogdanowicz, Guy Laurent, Jean-Jacques Fournié, Nathalie Castex-Rizzi, Christine Jean, and Marie-José Haure
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Regulation of gene expression ,medicine.medical_specialty ,Photoaging ,Immunology ,Chromosomal translocation ,Dermatology ,General Medicine ,Matrix metalloproteinase ,Biology ,medicine.disease ,Molecular biology ,HaCaT ,Cell culture ,Gene expression ,medicine ,Immunology and Allergy ,Radiology, Nuclear Medicine and imaging ,sense organs ,Immunostaining - Abstract
Background Specific sunscreens against ultraviolet (UV) A and B radiations are essential to prevent matrix degradation and the activation of intracellular signaling pathways involved in photoaging and photocarcinogenesis. Matrix degradation results from UVA-induced production of matrix metalloproteinases (MMP) and activation of intracellular pathways in fibroblasts and keratinocytes. In particular, in keratinocytes, UVA radiation induces β-catenin nuclear translocation and stimulates MMP gene transcription. Our study was aimed at assessing the efficacy of a specific broad-spectrum sunscreen in preventing β-catenin translocation and MMPs enhanced expression in cultured keratinocytes after UVA irradiation. Methods Sunscreen or the vehicle was spread on quartz sheet. Irradiation of HaCaT cells with 6 J/cm2UVA was performed through the sheet, and cells were collected for β-catenin immunostaining then visualization by confocal microscopy, and quantitative real-time polymerase chain reaction analysis of MMP-1, -3 and -9 gene expression. Results As shown by immunostaining and confocal microscopy, the sunscreen abrogated UVA-induced beta-catenin translocation to the nucleus, in comparison with control groups. MMP-1, -3 and -9 mRNA expression was enhanced by 7, 7 and 4 folds (P
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- 2011
8. Epidermal Growth Factor Receptor/β-Catenin/T-Cell Factor 4/Matrix Metalloproteinase 1: A New Pathway for Regulating Keratinocyte Invasiveness after UVA Irradiation
- Author
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Loic Ysebaert, Addolorata-Maria-Luce Coluccia, Eric Delabesse, Guy Laurent, Christine Jean, Hélène Hernandez-Pigeon, Marie-José Haure, Amandine Blanc, Marie Charveron, Nais Prade-Houdellier, and Talal Al Saati
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Keratinocytes ,Cancer Research ,Transcription, Genetic ,Ultraviolet Rays ,Photoaging ,Extracellular matrix component ,chemistry.chemical_compound ,Growth factor receptor ,Cell Adhesion ,medicine ,Humans ,Epidermal growth factor receptor ,Phosphorylation ,beta Catenin ,biology ,Tyrosine phosphorylation ,medicine.disease ,ErbB Receptors ,medicine.anatomical_structure ,Oncology ,chemistry ,Cancer research ,biology.protein ,Matrix Metalloproteinase 1 ,Signal transduction ,TCF Transcription Factors ,Keratinocyte ,Transcription Factor 7-Like 2 Protein ,Signal Transduction - Abstract
Previous studies have established that UV irradiation results in epidermal growth factor receptor (EGFR) activation in keratinocytes. However, the signaling pathways and cellular effects related to this process remain incompletely elucidated. Herein, we describe for the first time that UVA-mediated EGFR activation results in β-catenin tyrosine phosphorylation at the Y654 residue responsible for the dissociation of E-cadherin/α-catenin/β-catenin complexes. Moreover, UVA induces an EGFR-dependent, but Wnt-independent, β-catenin relocalization from the membrane to the nucleus followed by its association with T-cell factor 4 (TCF4). This newly formed β-catenin/TCF4 complex binds to a specific site on matrix metalloproteinase 1 (MMP1) promoter and governs MMP1 gene and protein expression, as well as cell migration in collagen and gelatin. Altogether, these results suggest that UVA stimulates keratinocyte invasiveness through two coordinated EGFR-dependent processes: loss of cell-to-cell contact due to β-catenin/E-cadherin/α-catenin dissociation and increased cell migration through extracellular matrix component degradation due to β-catenin/TCF4–dependent MMP1 regulation. These events may represent an important step in epidermis repair following UVA injury and their abnormal regulation could contribute to photoaging and photocarcinogenesis. [Cancer Res 2009;69(8):3291–9]
- Published
- 2009
9. Mildly oxidized low-density lipoproteins decrease early production of interleukin 2 and nuclear factor κB binding to DNA in activated T-lymphocytes
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Sylvie Caspar-Bauguil, Marie-José Haure, Martine Durand, Julie Alcouffe, Hervé Benoist, Robert Salvayre, Jean Tkaczuk, and Mogens Thomsen
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Interleukin 2 ,medicine.medical_specialty ,P50 ,biology ,Lymphoblast ,CD3 ,Interleukin ,Cell Biology ,Biochemistry ,Molecular biology ,Cytosol ,chemistry.chemical_compound ,Endocrinology ,chemistry ,Internal medicine ,Ionomycin ,medicine ,biology.protein ,lipids (amino acids, peptides, and proteins) ,Molecular Biology ,Phytohaemagglutinin ,medicine.drug - Abstract
Activated T-lymphocytes are found early in atherosclerosis lesions, but little is known about their role. Oxidized low-density lipoproteins (oxLDLs) are considered to be involved in the pathogenesis of the lesions, and we have previously demonstrated that oxLDLs inhibit not only interleukin (IL)-2-receptor expression on the surface of in vitro-activated T-lymphocytes but also their proliferation. We have now investigated the effect of oxLDLs on blast differentiation, on IL-2 synthesis and on the activation of the nuclear factor kappaB (NF-kappaB) system in activated lymphocytes. Mildly oxLDLs (50 and 100 microgram/ml) decreased the number of lymphoblasts and the level of IL-2 concentration in the culture supernatants after activation of lymphocytes by phytohaemagglutinin and PMA+ionomycin. The inhibition of IL-2 production was observed in the CD3(+) T-lymphocyte cytoplasm as early as 4 h after activation by PMA+ionomycin. The study of NF-kappaB showed that oxLDLs led to a decrease of activation-induced p65/p50 NF-kappaB heterodimer binding to DNA, whereas the presence of the constitutive nuclear form of p50 dimer was unchanged. This was correlated with an unchanged level of the active form of the cytosolic inhibitor protein IkappaB-alpha. Taken together, these observations suggest that the immunosuppressive effect of oxLDLs might operate via a dysregulation of the T-lymphocyte activation mechanisms.
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- 1999
10. UVA-activated synthesis of metalloproteinases 1, 3 and 9 is prevented by a broad-spectrum sunscreen
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Christine, Jean, Patrick, Bogdanowicz, Marie-José, Haure, Nathalie, Castex-Rizzi, Jean-Jacques, Fournié, and Guy, Laurent
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Cell Nucleus ,Keratinocytes ,Matrix Metalloproteinase 9 ,Ultraviolet Rays ,Active Transport, Cell Nucleus ,Humans ,Matrix Metalloproteinase 3 ,Fibroblasts ,Matrix Metalloproteinase 1 ,Sunscreening Agents ,Gene Expression Regulation, Enzymologic ,beta Catenin ,Cell Line - Abstract
Specific sunscreens against ultraviolet (UV) A and B radiations are essential to prevent matrix degradation and the activation of intracellular signaling pathways involved in photoaging and photocarcinogenesis. Matrix degradation results from UVA-induced production of matrix metalloproteinases (MMP) and activation of intracellular pathways in fibroblasts and keratinocytes. In particular, in keratinocytes, UVA radiation induces β-catenin nuclear translocation and stimulates MMP gene transcription. Our study was aimed at assessing the efficacy of a specific broad-spectrum sunscreen in preventing β-catenin translocation and MMPs enhanced expression in cultured keratinocytes after UVA irradiation.Sunscreen or the vehicle was spread on quartz sheet. Irradiation of HaCaT cells with 6 J/cm(2) UVA was performed through the sheet, and cells were collected for β-catenin immunostaining then visualization by confocal microscopy, and quantitative real-time polymerase chain reaction analysis of MMP-1, -3 and -9 gene expression.As shown by immunostaining and confocal microscopy, the sunscreen abrogated UVA-induced beta-catenin translocation to the nucleus, in comparison with control groups. MMP-1, -3 and -9 mRNA expression was enhanced by 7, 7 and 4 folds (P0.0001, P0.001 and P0.01, respectively) in unprotected UVA-irradiated cells compared to the non-irradiated control. Sunscreen protection of the cells significantly reduced UVA-induced expression of MMP-1, -3 and -9 by 83% (P0.01), 80% (P0.01) and 65% (P0.05), respectively.This study demonstrated the efficacy of this broad-spectrum sunscreen in preventing UVA-induced effects on the markers of photoaging and photocarcinogenesis in vitro. It was able to protect HaCaT keratinocytes from UVA-induced β-catenin translocation to the nucleus and MMPs expression.
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- 2011
11. Assessment of the Photoprotection Properties of Sunscreens by Chromatographic Measurement of DNA Damage in Skin Explants
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Marie-José Haure, Alain Favier, Patrick Bogdanowicz, Jean Cadet, Thierry Douki, Stéphane Mouret, Nathalie Castex-Rizzi, Laboratoire Lésions des Acides Nucléiques (LAN), Service de Chimie Inorganique et Biologique (SCIB - UMR E3), Institut Nanosciences et Cryogénie (INAC), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Université Grenoble Alpes [2016-2019] (UGA [2016-2019])-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Université Grenoble Alpes [2016-2019] (UGA [2016-2019])-Centre National de la Recherche Scientifique (CNRS)-Institut Nanosciences et Cryogénie (INAC), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Université Grenoble Alpes [2016-2019] (UGA [2016-2019])-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Université Grenoble Alpes [2016-2019] (UGA [2016-2019])-Centre National de la Recherche Scientifique (CNRS), Chimie Interface Biologie pour l’Environnement, la Santé et la Toxicologie (CIBEST ), SYstèmes Moléculaires et nanoMatériaux pour l’Energie et la Santé (SYMMES), Institut de Chimie du CNRS (INC)-Université Grenoble Alpes [2016-2019] (UGA [2016-2019])-Institut de Recherche Interdisciplinaire de Grenoble (IRIG), Direction de Recherche Fondamentale (CEA) (DRF (CEA)), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Direction de Recherche Fondamentale (CEA) (DRF (CEA)), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Centre National de la Recherche Scientifique (CNRS)-Institut de Chimie du CNRS (INC)-Université Grenoble Alpes [2016-2019] (UGA [2016-2019])-Institut de Recherche Interdisciplinaire de Grenoble (IRIG), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Centre National de la Recherche Scientifique (CNRS), Institut de Chimie du CNRS (INC)-Centre National de la Recherche Scientifique (CNRS)-Université Grenoble Alpes [2016-2019] (UGA [2016-2019])-Institut de Recherche Interdisciplinaire de Grenoble (IRIG), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Institut de Chimie du CNRS (INC)-Centre National de la Recherche Scientifique (CNRS)-Université Grenoble Alpes [2016-2019] (UGA [2016-2019])-Institut de Recherche Interdisciplinaire de Grenoble (IRIG), and Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)
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Erythema ,DNA damage ,Human skin ,In Vitro Techniques ,Biology ,Photochemistry ,Biochemistry ,030207 dermatology & venereal diseases ,03 medical and health sciences ,chemistry.chemical_compound ,0302 clinical medicine ,Tandem Mass Spectrometry ,[CHIM.ANAL]Chemical Sciences/Analytical chemistry ,medicine ,Humans ,Physical and Theoretical Chemistry ,Chromatography, High Pressure Liquid ,Skin ,030304 developmental biology ,0303 health sciences ,integumentary system ,General Medicine ,medicine.disease ,Molecular biology ,3. Good health ,chemistry ,Photoprotection ,[SDV.TOX]Life Sciences [q-bio]/Toxicology ,Skin cancer ,medicine.symptom ,Sunscreening Agents ,Ex vivo ,DNA ,DNA Damage ,Explant culture - Abstract
Evaluation of the photoprotection provided by sunscreens is performed either through the induction of erythema and expressed as the sun protection factor (SPF), or by the UVA-mediated persistent pigment darkening (PPD). None of these two endpoints has a link with skin cancer, the most deleterious consequence of excess exposure to solar UV radiation. We thus set up a complementary approach to evaluate the protection provided by sunscreens to the genome of human skin. This is based on the quantification of the thymine cyclobutane dimer (TT-CPD), the main DNA lesion induced by both UVB and UVA radiations. Irradiations were performed ex vivo on human skin explants and the level of TT-CPD in DNA was determined by HPLC associated with tandem mass spectrometry. The technique was first optimized and validated with three standard sunscreens. The study was then extended to the evaluation of a commercial high SPF sunscreen exhibiting efficient UVA photoprotection. The DNA protecting factor was found to reflect the ratio between UVB and UVA photoprotection, although the absolute values of the genomic protection were, as a general trend, lower than either SPF or PPD. These data show the usefulness of the proposed approach for the evaluation of the genoprotection afforded by sunscreens.
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- 2011
12. UVA Induces Granzyme B in Human Keratinocytes through MIF
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Caroline Baudouin, Christine Jean, Marie Charveron, Anne Quillet-Mary, Alexandra Charruyer, Marie-José Haure, Hélène Hernandez-Pigeon, Guy Laurent, Centre de Physiopathologie de Toulouse-Purpan (INSERM U563 - CNRS UMR1037), Centre National de la Recherche Scientifique (CNRS)-Centre de lutte contre le cancer (CLCC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Hôpital Purpan [Toulouse], CHU Toulouse [Toulouse]-CHU Toulouse [Toulouse]-Institut Claudius Regaud, Laboratoires Expanscience, Laboratoires Expanscience, R&D, Laboratoire de Biologie Cellulaire Cutanée, Institut de Recherche Pierre Fabre, CHU Toulouse [Toulouse]-Institut Claudius Regaud-Hôpital Purpan [Toulouse], CHU Toulouse [Toulouse]-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre de lutte contre le cancer (CLCC)-Centre National de la Recherche Scientifique (CNRS), Centre de Recherche Pierre Fabre (Centre de R&D Pierre Fabre), and PIERRE FABRE-PIERRE FABRE
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Photoaging ,Context (language use) ,[SDV.CAN]Life Sciences [q-bio]/Cancer ,Biology ,Biochemistry ,Extracellular matrix ,03 medical and health sciences ,0302 clinical medicine ,medicine ,Molecular Biology ,ComputingMilieux_MISCELLANEOUS ,030304 developmental biology ,0303 health sciences ,Cell migration ,Cell Biology ,medicine.disease ,Cell biology ,Fibronectin ,Granzyme B ,medicine.anatomical_structure ,030220 oncology & carcinogenesis ,biology.protein ,[SDV.IMM]Life Sciences [q-bio]/Immunology ,Vitronectin ,Keratinocyte ,hormones, hormone substitutes, and hormone antagonists - Abstract
In a previous study, we have described that UVB induces granzyme B (GrB) in human keratinocyte cells, and that confers potent cellular cytotoxicity against various cellular models, including immune cells (Hernandez-Pigeon, H., Jean, C., Charruyer, A., Haure, M. J., Titeux, M., Tonasso, L., Quillet-Mary, A., Baudouin, C., Charveron, M., and Laurent, G. (2006) J. Biol. Chem. 281, 13525-13532). Herein, we have found that, in contrast to UVB, UVA failed to enhance keratinocyte cellular cytotoxicity but was still able to trigger GrB production. We show that GrB is accumulated through a p38 MAPK-dependent transcriptional mechanism stimulated by redox-dependent migration inhibitory factor release. Moreover, GrB purified from UVA-treated cellular extracts was found to degrade fibronectin in vitro. Treatment with antisense oligonucleotide directed against GrB resulted in the inhibition of UVA-induced cell detachment and cell death and facilitated cell migration through fibronectin and vitronectin matrix upon UVA exposure. Altogether, these results suggest another function for GrB in the context of the UV response. Indeed, combined with our previous study, it appears that, whereas this enzyme mediates keratinocyte cellular cytotoxicity following UVB irradiation, GrB supports the capacity of keratinocyte to degrade extracellular matrix components following UVA irradiation. UV-mediated GrB production may thus have important consequences in photoaging and photocarcinogenesis.
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- 2007
13. UVA induces granzyme B in human keratinocytes through MIF: implication in extracellular matrix remodeling
- Author
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Hélène, Hernandez-Pigeon, Christine, Jean, Alexandra, Charruyer, Marie-José, Haure, Caroline, Baudouin, Marie, Charveron, Anne, Quillet-Mary, and Guy, Laurent
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Keratinocytes ,Reverse Transcriptase Polymerase Chain Reaction ,Ultraviolet Rays ,Oligonucleotides, Antisense ,p38 Mitogen-Activated Protein Kinases ,Granzymes ,Extracellular Matrix ,Fibronectins ,Intramolecular Oxidoreductases ,Cell Movement ,Humans ,Immunoprecipitation ,Enzyme Inhibitors ,Macrophage Migration-Inhibitory Factors - Abstract
In a previous study, we have described that UVB induces granzyme B (GrB) in human keratinocyte cells, and that confers potent cellular cytotoxicity against various cellular models, including immune cells (Hernandez-Pigeon, H., Jean, C., Charruyer, A., Haure, M. J., Titeux, M., Tonasso, L., Quillet-Mary, A., Baudouin, C., Charveron, M., and Laurent, G. (2006) J. Biol. Chem. 281, 13525-13532). Herein, we have found that, in contrast to UVB, UVA failed to enhance keratinocyte cellular cytotoxicity but was still able to trigger GrB production. We show that GrB is accumulated through a p38 MAPK-dependent transcriptional mechanism stimulated by redox-dependent migration inhibitory factor release. Moreover, GrB purified from UVA-treated cellular extracts was found to degrade fibronectin in vitro. Treatment with antisense oligonucleotide directed against GrB resulted in the inhibition of UVA-induced cell detachment and cell death and facilitated cell migration through fibronectin and vitronectin matrix upon UVA exposure. Altogether, these results suggest another function for GrB in the context of the UV response. Indeed, combined with our previous study, it appears that, whereas this enzyme mediates keratinocyte cellular cytotoxicity following UVB irradiation, GrB supports the capacity of keratinocyte to degrade extracellular matrix components following UVA irradiation. UV-mediated GrB production may thus have important consequences in photoaging and photocarcinogenesis.
- Published
- 2007
14. Human Keratinocytes Acquire Cellular Cytotoxicity under UV-B Irradiation
- Author
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Christine Jean, Caroline Baudouin, Guy Laurent, Marie-José Haure, Matthias Titeux, Anne Quillet-Mary, Alexandra Charruyer, Hélène Hernandez-Pigeon, Marie Charveron, Laure Tonasso, Centre de Physiopathologie de Toulouse-Purpan (INSERM U563 - CNRS UMR1037), CHU Toulouse [Toulouse]-Institut Claudius Regaud-Hôpital Purpan [Toulouse], CHU Toulouse [Toulouse]-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre de lutte contre le cancer (CLCC)-Centre National de la Recherche Scientifique (CNRS), Laboratoires Expanscience, Laboratoires Expanscience, R&D, Laboratoire de Biologie Cellulaire Cutanée, Centre de Recherche Pierre Fabre (Centre de R&D Pierre Fabre), PIERRE FABRE-PIERRE FABRE, Centre National de la Recherche Scientifique (CNRS)-Centre de lutte contre le cancer (CLCC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Hôpital Purpan [Toulouse], CHU Toulouse [Toulouse]-CHU Toulouse [Toulouse]-Institut Claudius Regaud, and Institut de Recherche Pierre Fabre
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Photoaging ,Human skin ,Biochemistry ,03 medical and health sciences ,0302 clinical medicine ,medicine ,Cytotoxic T cell ,Epidermal growth factor receptor ,Cytotoxicity ,Molecular Biology ,ComputingMilieux_MISCELLANEOUS ,030304 developmental biology ,0303 health sciences ,integumentary system ,biology ,Cell Biology ,medicine.disease ,3. Good health ,Cell biology ,Granzyme B ,medicine.anatomical_structure ,Perforin ,030220 oncology & carcinogenesis ,Immunology ,biology.protein ,[SDV.IMM]Life Sciences [q-bio]/Immunology ,Keratinocyte ,hormones, hormone substitutes, and hormone antagonists - Abstract
Ultraviolet (UV) radiation from the sun is widely considered as a major cause of human skin photoaging and skin cancer. Granzyme B (GrB) and perforin (PFN) are two proteins contained in granules and implicated in one of the mechanisms by which cytotoxic lymphocytes and natural killer cells exert their cytotoxicity against virus-infected, alloreactive, or transformed cells. The distribution of GrB and PFN in the skin has received little attention. However, Berthou and co-workers (Berthou, C., Michel, L., Soulie, A., Jean-Louis, F., Flageul, B., Dubertret, L., Sigaux, F., Zhang, Y., and Sasportes, M. (1997) J. Immunol. 159, 5293-5300) described that, whereas freshly isolated epidermal cells did not express GrB or PFN, keratinocyte growth to confluence was associated with GrB and PFN mRNA and protein synthesis. In this work, we have investigated the possible role of UV-B on GrB and PFN expression in keratinocytes. We found that UV-B induces GrB and PFN expression in these cells through redox-, epidermal growth factor receptor-, and mitogen-activated protein kinase-dependent signaling. Furthermore, under UV irradiation, keratinocytes acquire a significant cytotoxicity, which is GrB and PFN dependent, toward a variety of cellular targets including transformed T-lymphocytes, melanocytes, and keratinocytes. This phenomenon may have important functional consequences in the regulation of skin inflammatory response and in the emergence of cancer skin.
- Published
- 2006
15. Human keratinocytes acquire cellular cytotoxicity under UV-B irradiation. Implication of granzyme B and perforin
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Hélène, Hernandez-Pigeon, Christine, Jean, Alexandra, Charruyer, Marie-José, Haure, Matthias, Titeux, Laure, Tonasso, Anne, Quillet-Mary, Caroline, Baudouin, Marie, Charveron, and Guy, Laurent
- Subjects
Keratinocytes ,Pore Forming Cytotoxic Proteins ,Membrane Glycoproteins ,MAP Kinase Signaling System ,Perforin ,Ultraviolet Rays ,T-Lymphocytes ,Serine Endopeptidases ,Granzymes ,Cell Line ,ErbB Receptors ,Gene Expression Regulation ,Humans ,Melanocytes ,RNA, Messenger - Abstract
Ultraviolet (UV) radiation from the sun is widely considered as a major cause of human skin photoaging and skin cancer. Granzyme B (GrB) and perforin (PFN) are two proteins contained in granules and implicated in one of the mechanisms by which cytotoxic lymphocytes and natural killer cells exert their cytotoxicity against virus-infected, alloreactive, or transformed cells. The distribution of GrB and PFN in the skin has received little attention. However, Berthou and co-workers (Berthou, C., Michel, L., Soulie, A., Jean-Louis, F., Flageul, B., Dubertret, L., Sigaux, F., Zhang, Y., and Sasportes, M. (1997) J. Immunol. 159, 5293-5300) described that, whereas freshly isolated epidermal cells did not express GrB or PFN, keratinocyte growth to confluence was associated with GrB and PFN mRNA and protein synthesis. In this work, we have investigated the possible role of UV-B on GrB and PFN expression in keratinocytes. We found that UV-B induces GrB and PFN expression in these cells through redox-, epidermal growth factor receptor-, and mitogen-activated protein kinase-dependent signaling. Furthermore, under UV irradiation, keratinocytes acquire a significant cytotoxicity, which is GrB and PFN dependent, toward a variety of cellular targets including transformed T-lymphocytes, melanocytes, and keratinocytes. This phenomenon may have important functional consequences in the regulation of skin inflammatory response and in the emergence of cancer skin.
- Published
- 2006
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