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Résumés en français (p. 1) et en anglais (p. 2)

VASCULAR ENDOTHELIAL GROWTH FACTOR --- IMMUNOLOGY --- VASCULAR ENDOTHELIAL GROWTH FACTOR --- IMMUNOLOGY

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Mammary glands are exocrine glands able to secrete milk during lactations. The expression of the sodium iodine supporter (NIS) ensures the necessary iodine supply to the infant. Like the thyroid, mammary glands are sensitive to iodine deficiency (ID). Indeed, structural and function alterations were observed in mammary glands following ID. Similarly, epidemiological studies suggest a protective role for iodine against pathologies such as mammary fibrosis or breast cancer because the prevalence of these pathologies is low in various areas with high iodine intake. From a molecular point of view, ID induces the overexpression of the Vascular Endothelial Growth Factor (CEGF), which is responsible of vascular activation in NIS-expressing organs such as the thyroid, salivary glands and stomach. Furthermore, radiation increases VEGF level expression in mammary glands and exposure to ionizing radiation (RA) can also increase the risk of breast cancer. The purpose of this work, is, on the one hand, to determine whether in vitro ID and RA have an additive or synergistic effect on the expression of VEGF in MCF7 (cancerous) and MCF12A (non-cancerous) breast cells, and, on the other hand, to investigate the molecular pathway activated by these factors. IN MCF12A, the combination of ID-RA increases VEGF mRNA expression more than what is observed in separate treatments. Regarding the MCF7 cells, it was observed that ID tends to increase the VEGF mRNA whereas the RA tends to decrease it. However, the CI-RA combination induces an increase in VEGF. The study of ROS production under different treatments led to similar observations in MCF12A, with higher ROS production in cells exposed to ID combined with radiation. However, the 3 treatments induce a similar increase in ROS in MCF7 cells. In addition, by using 2 ROS inhibitors, Mitotempo and DPI, the involvement of flavoenzymes in the overexpression of VEGF mRNA was demonstrated in both cell lines; however, mitochondrial ROS are only involved in the effects of RA combined of not with ID in MCF12A cells. A non-significant increase in mTOR activity was involved in the effects of RA combined or not with ID in MCF12A cells. A non-significant increase in mTOR activity was induced by all 3 treatments in both cell lines, and mTOR inhibition prevented the overexpression if VEGF mRNA in MCF12A cells, suggesting a role of mTOR in the activated pathway, at least in MCF12A cells. Thus, the radiation-induced response is different in the two cell lines, but this response is modulated by ID. An additive effect of ID and radiation is observed on the regulation of the expression of VEGF mRNA only in non-cancerous cells. However, because VEGF overexpression is liked to poor prognosis in breast cancer, the iodized status of persons exposed to radiation for medical or other reasons should not be ignored Les glandes mammaires sont responsables de la sécrétion du lait Durant la lactation et le symporteur sodium/iode (NIS) assure l’apport en iode nécessaire au nourrisson. Ces glandes sont sensibles à la carence en iode (CI). En effet, il a été montré que les glandes mammaires présentaient des altérations structurelles et fonctionnelles suit à la CI. De même, les études épidémiologiques suggèrent un rôle protecteur de l’iode contre des pathologies telles que la fibrose mammaire ou le cancer du sein car la prévalence de ces pathologies est faible dans diverses zones à fort apport alimentaire en iode. D’un point de vue moléculaire, la CI dans les organes exprimant NIS tels que la thyroïde, les glandes salivaires et l’estomac, surexpriment le facteur angiogénique Vascular Endothelial Growth Factor (VEGF). Par ailleurs, les radiations ionisantes augmentent également l’expression du VEGF dans les glandes mammaires et augmenterait aussi le risque de cancer du sein. Le but de ce travail est d’une part de déterminer si, in vitro, la CI et les RA ont un effet additif voir synergique sur l’expression du VEGF dans des cellules de sein MCF7 (cancéreuses) et MCF12A (non cancéreuses) et d’autres part, d’étudier la voie moléculaire activée par ces deux facteurs. Dans les MCF12A, la combinaison CI-RA induit une augmentation de l’ARNm du VEGF plus importante que celle observée lors des traitements séparés. Concernant les MCF7, la CI tend à augmenter l’ARNm du VEGF alors que les RA tendent à la diminuer. Cependant, la combinaison CI-RA induit une augmentation du VEGF. L’étude des ROS lors des différents traitements a mené à des observations similaires dans les MCF12A, avec une production de ROS plus importante dans les cellules exposées à la CI combinée aux radiations. Par contre, les 3 traitements induisent une augmentation des ROS similaires dans les MCF7. De plus, l’utilisation de deux inhibiteurs de ROS, le Mitotempo et le DPI, a permis de montrer l’implication des flavoenzymes dans l’augmentation du VEGF induite par tous les traitements dans les deux lignées ; les ROS mitochondriales par contre ne semblent avoir un rôle que dans l’augmentation du VEGF induite par les radiations combinées ou non à la CI, et ce dans les MCF12A. Une augmentation non significative de l’activité de mTOR a été observée lors des 3 traitements dans les deux lignées, et l’inhibition de ce dernier empêche l’augmentation de l’ARNm du VEGF induite par la CI combinée aux radiations dans les MCF12A, suggérant un rôle de mTOR dans la voie activée, du mois pour les MCF12A. Ainsi, la réponse induite par les radiations est différente dans les deux lignées cellulaires, mais cette réponse est modulée par la CI. Un effet additif de la CI et des radiations est observée sur la régulation de l’expression de l’ARNm du VEGH uniquement dans les cellules non cancéreuse. Toutefois, la surexpression du VEGF étant liée à un mauvais pronostic dans le cancer du sein, le statut iodé des personnes exposées à des radiations pour des raisons médicales ou autres ne devrait pas être ignoré

Iodine --- Radiation --- Mammary Glands, Human --- Vascular Endothelial Growth Factor A

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CD40 Ligand --- Antigens, CD40 --- Graft Rejection --- Inflammation --- Transplantation, Homologous --- Vascular Endothelial Growth Factor A --- physiology. --- immunology. --- etiology. --- Theses --- CD40 Antigens --- physiology --- immunology --- etiology --- Allogeneic Grafting --- Allogeneic Transplantation --- Allografting --- Homografting --- Homologous Transplantation --- Transplantation, Allogeneic --- Grafting, Allogeneic --- Allogeneic Cells --- Allografts --- transplantation

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In this reprint, we hope to review the basics and highlight the latest developments in AMD. This demonstrates the benefits of the international scientific community working on this disease, to limit its negative impacts, the most vital of which is the loss of visual function, leading to a loss of autonomy and a decrease in patients’ quality of life.

Medicine --- aflibercept monotherapy --- polypoidal choroidal vasculopathy --- neovascular age-related macular degeneration --- good baseline visual acuity --- ForeseeHome AMD Monitoring System® --- AREDS2-HOME study --- age-related macular degeneration --- exudation --- optical coherence tomography angiography --- anti-vascular endothelial growth factor --- brolucizumab --- epithelial tear --- optical coherence tomography --- Sorsby's fundus dystrophy --- Sorsby --- hereditary retinal dystrophy --- choroidal neovascularisation --- macular neovascularization --- anti-VEGF treatment --- long-term FU --- treatment outcome --- emerging treatment --- neovascular age-related macular degeneration (nAMD) --- Vascular Endothelial Growth Factor (VEGF) --- cataract surgery --- clinical trials --- real-world evidence --- AMD --- oct-angiography --- fellow eye --- choriocapillaris --- quiescent macular neovascularization --- ranibizumab --- aflibercept --- anti-VEGF --- visual acuity --- reading acuity --- disease activity --- treatment change --- treat and extend --- switch therapy --- retina --- choroidal neovascularization --- angiogenesis --- meteorin --- therapeutic innovation --- prevention --- nutrients --- lifestyle --- treatment-naive --- anti-vascular endothelial growth factor --- cardiovascular risk factors --- arterial hypertension --- macula-off rhegmatogenous detachment --- superficial perifoveal capillary plexus --- retinal deep perifoveal capillary plexus --- identification --- risk --- Delphi --- STARS® --- food supplement --- bevacizumab --- meta-analysis --- meta-regression --- age-related macular degeneration (AMD) --- comparative therapies --- effectiveness --- intravitreal anti-vascular endothelial growth factor --- treat-and-extend --- pro re nata regimen --- aflibercept monotherapy --- polypoidal choroidal vasculopathy --- neovascular age-related macular degeneration --- good baseline visual acuity --- ForeseeHome AMD Monitoring System® --- AREDS2-HOME study --- age-related macular degeneration --- exudation --- optical coherence tomography angiography --- anti-vascular endothelial growth factor --- brolucizumab --- epithelial tear --- optical coherence tomography --- Sorsby's fundus dystrophy --- Sorsby --- hereditary retinal dystrophy --- choroidal neovascularisation --- macular neovascularization --- anti-VEGF treatment --- long-term FU --- treatment outcome --- emerging treatment --- neovascular age-related macular degeneration (nAMD) --- Vascular Endothelial Growth Factor (VEGF) --- cataract surgery --- clinical trials --- real-world evidence --- AMD --- oct-angiography --- fellow eye --- choriocapillaris --- quiescent macular neovascularization --- ranibizumab --- aflibercept --- anti-VEGF --- visual acuity --- reading acuity --- disease activity --- treatment change --- treat and extend --- switch therapy --- retina --- choroidal neovascularization --- angiogenesis --- meteorin --- therapeutic innovation --- prevention --- nutrients --- lifestyle --- treatment-naive --- anti-vascular endothelial growth factor --- cardiovascular risk factors --- arterial hypertension --- macula-off rhegmatogenous detachment --- superficial perifoveal capillary plexus --- retinal deep perifoveal capillary plexus --- identification --- risk --- Delphi --- STARS® --- food supplement --- bevacizumab --- meta-analysis --- meta-regression --- age-related macular degeneration (AMD) --- comparative therapies --- effectiveness --- intravitreal anti-vascular endothelial growth factor --- treat-and-extend --- pro re nata regimen

Choose an application

• Reference Manager
• EndNote
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In this reprint, we hope to review the basics and highlight the latest developments in AMD. This demonstrates the benefits of the international scientific community working on this disease, to limit its negative impacts, the most vital of which is the loss of visual function, leading to a loss of autonomy and a decrease in patients’ quality of life.

aflibercept monotherapy --- polypoidal choroidal vasculopathy --- neovascular age-related macular degeneration --- good baseline visual acuity --- ForeseeHome AMD Monitoring System® --- AREDS2-HOME study --- age-related macular degeneration --- exudation --- optical coherence tomography angiography --- anti-vascular endothelial growth factor --- brolucizumab --- epithelial tear --- optical coherence tomography --- Sorsby’s fundus dystrophy --- Sorsby --- hereditary retinal dystrophy --- choroidal neovascularisation --- macular neovascularization --- anti-VEGF treatment --- long-term FU --- treatment outcome --- emerging treatment --- neovascular age-related macular degeneration (nAMD) --- Vascular Endothelial Growth Factor (VEGF) --- cataract surgery --- clinical trials --- real-world evidence --- AMD --- oct-angiography --- fellow eye --- choriocapillaris --- quiescent macular neovascularization --- ranibizumab --- aflibercept --- anti-VEGF --- visual acuity --- reading acuity --- disease activity --- treatment change --- treat and extend --- switch therapy --- retina --- choroidal neovascularization --- angiogenesis --- meteorin --- therapeutic innovation --- prevention --- nutrients --- lifestyle --- treatment-naive --- anti–vascular endothelial growth factor --- cardiovascular risk factors --- arterial hypertension --- macula-off rhegmatogenous detachment --- superficial perifoveal capillary plexus --- retinal deep perifoveal capillary plexus --- identification --- risk --- Delphi --- STARS® --- food supplement --- bevacizumab --- meta-analysis --- meta-regression --- n/a --- age-related macular degeneration (AMD) --- comparative therapies --- effectiveness --- intravitreal anti-vascular endothelial growth factor --- treat-and-extend --- pro re nata regimen --- Sorsby's fundus dystrophy