Ultraviolet Irradiation

14,000,000 Leading Edge Experts on the ideXlab platform

Scan Science and Technology

Contact Leading Edge Experts & Companies

Scan Science and Technology

Contact Leading Edge Experts & Companies

The Experts below are selected from a list of 32211 Experts worldwide ranked by ideXlab platform

Enrique Nebot - One of the best experts on this subject based on the ideXlab platform.

  • Effect of the length of dark storage following Ultraviolet Irradiation of Tetraselmis suecica and its implications for ballast water management
    Science of The Total Environment, 2019
    Co-Authors: Leonardo Romero-martínez, Ignacio Rivas-zaballos, Javier Moreno-andrés, Ignacio Moreno-garrido, Asunción Acevedo-merino, Enrique Nebot
    Abstract:

    Meeting the recent biological standards established by the Ballast Water Management Convention requires the application of ballast water treatment systems; Ultraviolet Irradiation is a frequently used option. However, organisms can repair the damage caused by Ultraviolet Irradiation primarily with photo-repair mechanisms that are dependent on the availability of light. The objective of this study is to quantify the impact of dark storage following Ultraviolet Irradiation on the viability of the microalgae Tetraselmis suecica. Results showed that one day of dark storage after Ultraviolet Irradiation enhanced the inactivation rate by 50% with respect to the absence of dark storage and increased up to the 84% with five days of dark storage. These results are consistent with photorepair, mostly in the first two days, prevented in the dark. The dose required to inactivate a determined ratio of organisms was correlated with the length of the dark post-treatment according to an inverse proportional function. This correlation may help to optimize the operation of Ultraviolet ballast water treatment systems. Further, the results show that growth assays can detect organisms that are capable of repair after treatment with UV.

Robert J Siverd - One of the best experts on this subject based on the ideXlab platform.

  • A giant planet undergoing extreme-Ultraviolet Irradiation by its hot massive-star host
    Nature, 2017
    Co-Authors: B. Scott Gaudi, Keivan G Stassun, Karen A Collins, Thomas G Beatty, George Zhou, David W Latham, Allyson Bieryla, Jason D Eastman, Robert J Siverd, Justin R. Crepp
    Abstract:

    The giant planet KELT-9b has a dayside temperature of about 4,600 K, which is sufficiently high to dissociate molecules and to evaporate its atmosphere, owing to its hot stellar host. The amount of Ultraviolet Irradiation and ablation experienced by a planet depends strongly on the temperature of its host star. Of the thousands of extrasolar planets now known, only six have been found that transit hot, A-type stars (with temperatures of 7,300–10,000 kelvin), and no planets are known to transit the even hotter B-type stars. For example, WASP-33 is an A-type star with a temperature of about 7,430 kelvin, which hosts the hottest known transiting planet, WASP-33b (ref. 1 ); the planet is itself as hot as a red dwarf star of type M (ref. 2 ). WASP-33b displays a large heat differential between its dayside and nightside^ 2 , and is highly inflated–traits that have been linked to high insolation^ 3 , 4 . However, even at the temperature of its dayside, its atmosphere probably resembles the molecule-dominated atmospheres of other planets and, given the level of Ultraviolet Irradiation it experiences, its atmosphere is unlikely to be substantially ablated over the lifetime of its star. Here we report observations of the bright star HD 195689 (also known as KELT-9), which reveal a close-in (orbital period of about 1.48 days) transiting giant planet, KELT-9b. At approximately 10,170 kelvin, the host star is at the dividing line between stars of type A and B, and we measure the dayside temperature of KELT-9b to be about 4,600 kelvin. This is as hot as stars of stellar type K4 (ref. 5 ). The molecules in K stars are entirely dissociated, and so the primary sources of opacity in the dayside atmosphere of KELT-9b are probably atomic metals. Furthermore, KELT-9b receives 700 times more extreme-Ultraviolet radiation (that is, with wavelengths shorter than 91.2 nanometres) than WASP-33b, leading to a predicted range of mass-loss rates that could leave the planet largely stripped of its envelope during the main-sequence lifetime of the host star^ 6 . Hot Jupiters are exoplanets that are physically similar to Jupiter, but are strongly irradiated by their host stars. Until now, the most extreme example was WASP-33b, but its atmosphere is still cool enough to contain molecules. Scott Gaudi et al . report the discovery of KELT-9b, which has a dayside temperature of about 4,600 kelvin. This is sufficiently high to dissociate molecules, so the primary sources of opacity in the dayside atmosphere of KELT-9b are probably atomic metals. The atmosphere might be evaporated before the host star reaches the end of its life.

  • a giant planet undergoing extreme Ultraviolet Irradiation by its hot massive star host
    Nature, 2017
    Co-Authors: Scott B Gaudi, Keivan G Stassun, Karen A Collins, Thomas G Beatty, George Zhou, David W Latham, Allyson Bieryla, Jason D Eastman, Robert J Siverd
    Abstract:

    The amount of Ultraviolet Irradiation and ablation experienced by a planet depends strongly on the temperature of its host star. Of the thousands of extrasolar planets now known, only six have been found that transit hot, A-type stars (with temperatures of 7,300–10,000 kelvin), and no planets are known to transit the even hotter B-type stars. For example, WASP-33 is an A-type star with a temperature of about 7,430 kelvin, which hosts the hottest known transiting planet, WASP-33b (ref. 1); the planet is itself as hot as a red dwarf star of type M (ref. 2). WASP-33b displays a large heat differential between its dayside and nightside, and is highly inflated–traits that have been linked to high insolation. However, even at the temperature of its dayside, its atmosphere probably resembles the molecule-dominated atmospheres of other planets and, given the level of Ultraviolet Irradiation it experiences, its atmosphere is unlikely to be substantially ablated over the lifetime of its star. Here we report observations of the bright star HD 195689 (also known as KELT-9), which reveal a close-in (orbital period of about 1.48 days) transiting giant planet, KELT-9b. At approximately 10,170 kelvin, the host star is at the dividing line between stars of type A and B, and we measure the dayside temperature of KELT-9b to be about 4,600 kelvin. This is as hot as stars of stellar type K4 (ref. 5). The molecules in K stars are entirely dissociated, and so the primary sources of opacity in the dayside atmosphere of KELT-9b are probably atomic metals. Furthermore, KELT-9b receives 700 times more extreme-Ultraviolet radiation (that is, with wavelengths shorter than 91.2 nanometres) than WASP-33b, leading to a predicted range of mass-loss rates that could leave the planet largely stripped of its envelope during the main-sequence lifetime of the host star.

John J Voorhees - One of the best experts on this subject based on the ideXlab platform.

  • Ultraviolet Irradiation alters transforming growth factor β/Smad pathway in human skin in vivo
    Journal of Investigative Dermatology, 2002
    Co-Authors: Taihao Quan, Tianyuan He, Sewon Kang, John J Voorhees, Gary J Fisher
    Abstract:

    Solar Ultraviolet Irradiation damages human skin and causes premature skin aging and skin cancer. As transforming growth factor β plays an important role in regulating cell growth and extracellular matrix synthesis, we investigated expression of transforming growth factor β isoforms, transforming growth factor β receptors, and transforming growth factor β regulated Smad transcription factors following Irradiation with an Ultraviolet B source and solar-simulated Ultraviolet Irradiation of human skin in vivo . Full-thickness, sun-protected adult human skin expressed transforming growth factor β1, β2, and β3 transcripts in a ratio of 1:5:3, as determined by quantitative real-time reverse transcription polymerase chain reaction. Northern analysis demonstrated that the Ultraviolet Irradiation (2 minimal erythema dose) caused moderate (2–3-fold) gradual increases of transforming growth factor β1 and β3 mRNA expression during 3 d post exposure. In contrast, expression of transforming growth factor β2 mRNA, the predominant form of transforming growth factor β in human skin, decreased within 4 h after Ultraviolet Irradiation. In situ hybridization revealed transforming growth factor β1, β2, and β3 mRNA expression in cells throughout the epidermis and the dermis in nonirradiated skin. Following Ultraviolet or solar-simulated Ultraviolet Irradiation, transforming growth factor β1 and β3 mRNA were increased and transforming growth factor β2 mRNA was reduced throughout the epidermis and dermis. No significant changes were observed in transforming growth factor β type I receptor mRNA expression after Ultraviolet Irradiation. In contrast, transforming growth factor β type II receptor mRNA expression was reduced 60% within 4 h following Ultraviolet exposure in human skin in vivo . Transforming growth factor β type II receptor mRNA levels remained reduced for 8 h and recovered by 24 h post Ultraviolet. In situ hybridization revealed that Ultraviolet or solar-simulated Ultraviolet Irradiation caused loss of transforming growth factor β type II receptor mRNA in basal and suprabasal cells in the epidermis and dermal cells. In addition, no significant changes were observed in Smad2, Smad3, and Smad4 expression after Ultraviolet Irradiation. In contrast, Ultraviolet and solar-simulated Ultraviolet Irradiation rapidly induced gene expression of Smad7, which antagonizes the actions of the transforming growth factor β/Smad pathway. Smad7 mRNA induction occurred throughout the epidermis and dermal cells as determined by in situ hybridization. Ultraviolet Irradiation also caused reduced DNA binding of Smad3/4 in human skin in vivo . Reduced Smad3/4 DNA binding was observed within 4 h following Irradiation. Taken together, these results demonstrate that Ultraviolet and solar-simulated Ultraviolet Irradiation alter the transforming growth factor β/Smad pathway in human skin in vivo . Ultraviolet induction of Smad7 and reduction of transforming growth factor β2 and transforming growth factor β type II receptor should diminish transforming growth factor β signaling, and probably contribute to the decrease of transforming growth factor β regulated type I and type III procollagen gene expression observed in Ultraviolet and solar-simulated Ultraviolet irradiated human skin in vivo .

  • Ultraviolet Irradiation increases matrix metalloproteinase 8 protein in human skin in vivo
    Journal of Investigative Dermatology, 2001
    Co-Authors: Gary J Fisher, Sewon Kang, H C Choi, Zsuzsanna Batacsorgo, Yuan Shao, Subhash C Datta, Zengquan Wang, John J Voorhees
    Abstract:

    Humans express three distinct collagenases, MMP-1, MMP-8, and MMP-13, that initiate degradation of fibrillar type I collagen. We have previously reported that Ultraviolet Irradiation causes increased expression of MMP-1, but not MMP-13, in keratinocytes and fibroblasts in human skin in vivo. We report here that Ultraviolet Irradiation increases expression of MMP-8 in human skin in vivo. Western analysis revealed that levels of the full-length, 85 kDa proenzyme form of MMP-8 increased significantly within 8 h post Ultraviolet Irradiation (2 minimal erythema doses). Increased full-length MMP-8 protein was associated with infiltration into the skin of neutrophils, which are the major cell type that expresses MMP-8. Immunofluorescence revealed coexpression of MMP-8 and neutrophil elastase, a marker for neutrophils. Immunohistology demonstrated MMP-8 expression in neutrophils in the papillary dermis between 4 and 8 h post Ultraviolet Irradiation, and in the epidermis at 24 h post radiation. MMP-8 mRNA expression was not detected in nonirradiated or Ultraviolet-irradiated human skin, indicating that increased MMP-8 following Ultraviolet Irradiation resulted from preexisting MMP-8 protein in infiltrating neutrophils. Pretreatment of skin with the glucocorticoid clobetasol, but not all-trans retinoic acid, significantly blocked Ultraviolet-induced increases in MMP-8 protein levels, and neutrophil infiltration. In contrast, all-trans retinoic acid and clobetasol were equally effective in blocking Ultraviolet induction of MMP-1 and degradation of collagen in human skin in vivo. Taken together, these data demonstrate that Ultraviolet Irradiation increases MMP-8 protein, which exists predominantly in a latent form within neutrophils, in human skin in vivo. Although Ultraviolet Irradiation induces both MMP-1 and MMP-8, Ultraviolet-induced collagen degradation is initiated primarily by MMP-1, with little, if any, contribution by MMP-8.

  • molecular mechanisms of photoaging and its prevention by retinoic acid Ultraviolet Irradiation induces map kinase signal transduction cascades that induce ap 1 regulated matrix metalloproteinases that degrade human skin in vivo
    Journal of Investigative Dermatology Symposium Proceedings, 1998
    Co-Authors: Gary J Fisher, John J Voorhees
    Abstract:

    Ultraviolet radiation from the sun damages human skin, resulting in an old and wrinkled appearance. A substantial amount of circumstantial evidence indicates that photoaging results in part from alterations in the composition, organization, and structure of the colla-genous extracellular matrix in the dermis. This paper reviews the authors' investigations into the molecular mechanisms by which Ultraviolet Irradiation damages the dermal extracellular matrix and provides evidence for prevention of this damage by all-trans retinoic acid in human skin in vivo . Based on experimental evidence a working model is proposed whereby Ultraviolet Irradiation activates growth factor and cytokine receptors on keratinocytes and dermal cells, resulting in downstream signal transduction through activation of MAP kinase pathways. These signaling pathways converge in the nucleus of cells to induce c-Jun, which hetero-dimerizes with constitutively expressed c-Fos to form activated complexes of the transcription factor AP-1. In the dermis and epidermis, AP-1 induces expression of matrix metalloproteinases collagenase, 92kDa gelatinase, and stromelysin, which degrade collagen and other proteins that comprise the dermal extracellular matrix. It is hypothesized that dermal breakdown is followed by repair that, like all wound repair, is imperfect. Imperfect repair yields a deficit in the structural integrity of the dermis, a solar scar. Dermal degradation followed by imperfect repair is repeated with each intermittent exposure to Ultraviolet Irradiation, leading to accumulation of solar scarring, and ultimately visible photoaging. All-trans retinoic acid acts to inhibit induction of c-Jun protein by Ultraviolet Irradiation, thereby preventing increased matrix metalloproteinases and ensuing dermal damage. Journal of Investigative Dermatology Symposium Proceedings 3:61-68, 1998

Keivan G Stassun - One of the best experts on this subject based on the ideXlab platform.

  • A giant planet undergoing extreme-Ultraviolet Irradiation by its hot massive-star host
    Nature, 2017
    Co-Authors: B. Scott Gaudi, Keivan G Stassun, Karen A Collins, Thomas G Beatty, George Zhou, David W Latham, Allyson Bieryla, Jason D Eastman, Robert J Siverd, Justin R. Crepp
    Abstract:

    The giant planet KELT-9b has a dayside temperature of about 4,600 K, which is sufficiently high to dissociate molecules and to evaporate its atmosphere, owing to its hot stellar host. The amount of Ultraviolet Irradiation and ablation experienced by a planet depends strongly on the temperature of its host star. Of the thousands of extrasolar planets now known, only six have been found that transit hot, A-type stars (with temperatures of 7,300–10,000 kelvin), and no planets are known to transit the even hotter B-type stars. For example, WASP-33 is an A-type star with a temperature of about 7,430 kelvin, which hosts the hottest known transiting planet, WASP-33b (ref. 1 ); the planet is itself as hot as a red dwarf star of type M (ref. 2 ). WASP-33b displays a large heat differential between its dayside and nightside^ 2 , and is highly inflated–traits that have been linked to high insolation^ 3 , 4 . However, even at the temperature of its dayside, its atmosphere probably resembles the molecule-dominated atmospheres of other planets and, given the level of Ultraviolet Irradiation it experiences, its atmosphere is unlikely to be substantially ablated over the lifetime of its star. Here we report observations of the bright star HD 195689 (also known as KELT-9), which reveal a close-in (orbital period of about 1.48 days) transiting giant planet, KELT-9b. At approximately 10,170 kelvin, the host star is at the dividing line between stars of type A and B, and we measure the dayside temperature of KELT-9b to be about 4,600 kelvin. This is as hot as stars of stellar type K4 (ref. 5 ). The molecules in K stars are entirely dissociated, and so the primary sources of opacity in the dayside atmosphere of KELT-9b are probably atomic metals. Furthermore, KELT-9b receives 700 times more extreme-Ultraviolet radiation (that is, with wavelengths shorter than 91.2 nanometres) than WASP-33b, leading to a predicted range of mass-loss rates that could leave the planet largely stripped of its envelope during the main-sequence lifetime of the host star^ 6 . Hot Jupiters are exoplanets that are physically similar to Jupiter, but are strongly irradiated by their host stars. Until now, the most extreme example was WASP-33b, but its atmosphere is still cool enough to contain molecules. Scott Gaudi et al . report the discovery of KELT-9b, which has a dayside temperature of about 4,600 kelvin. This is sufficiently high to dissociate molecules, so the primary sources of opacity in the dayside atmosphere of KELT-9b are probably atomic metals. The atmosphere might be evaporated before the host star reaches the end of its life.

  • a giant planet undergoing extreme Ultraviolet Irradiation by its hot massive star host
    Nature, 2017
    Co-Authors: Scott B Gaudi, Keivan G Stassun, Karen A Collins, Thomas G Beatty, George Zhou, David W Latham, Allyson Bieryla, Jason D Eastman, Robert J Siverd
    Abstract:

    The amount of Ultraviolet Irradiation and ablation experienced by a planet depends strongly on the temperature of its host star. Of the thousands of extrasolar planets now known, only six have been found that transit hot, A-type stars (with temperatures of 7,300–10,000 kelvin), and no planets are known to transit the even hotter B-type stars. For example, WASP-33 is an A-type star with a temperature of about 7,430 kelvin, which hosts the hottest known transiting planet, WASP-33b (ref. 1); the planet is itself as hot as a red dwarf star of type M (ref. 2). WASP-33b displays a large heat differential between its dayside and nightside, and is highly inflated–traits that have been linked to high insolation. However, even at the temperature of its dayside, its atmosphere probably resembles the molecule-dominated atmospheres of other planets and, given the level of Ultraviolet Irradiation it experiences, its atmosphere is unlikely to be substantially ablated over the lifetime of its star. Here we report observations of the bright star HD 195689 (also known as KELT-9), which reveal a close-in (orbital period of about 1.48 days) transiting giant planet, KELT-9b. At approximately 10,170 kelvin, the host star is at the dividing line between stars of type A and B, and we measure the dayside temperature of KELT-9b to be about 4,600 kelvin. This is as hot as stars of stellar type K4 (ref. 5). The molecules in K stars are entirely dissociated, and so the primary sources of opacity in the dayside atmosphere of KELT-9b are probably atomic metals. Furthermore, KELT-9b receives 700 times more extreme-Ultraviolet radiation (that is, with wavelengths shorter than 91.2 nanometres) than WASP-33b, leading to a predicted range of mass-loss rates that could leave the planet largely stripped of its envelope during the main-sequence lifetime of the host star.

Gary J Fisher - One of the best experts on this subject based on the ideXlab platform.

  • Ultraviolet Irradiation alters transforming growth factor β/Smad pathway in human skin in vivo
    Journal of Investigative Dermatology, 2002
    Co-Authors: Taihao Quan, Tianyuan He, Sewon Kang, John J Voorhees, Gary J Fisher
    Abstract:

    Solar Ultraviolet Irradiation damages human skin and causes premature skin aging and skin cancer. As transforming growth factor β plays an important role in regulating cell growth and extracellular matrix synthesis, we investigated expression of transforming growth factor β isoforms, transforming growth factor β receptors, and transforming growth factor β regulated Smad transcription factors following Irradiation with an Ultraviolet B source and solar-simulated Ultraviolet Irradiation of human skin in vivo . Full-thickness, sun-protected adult human skin expressed transforming growth factor β1, β2, and β3 transcripts in a ratio of 1:5:3, as determined by quantitative real-time reverse transcription polymerase chain reaction. Northern analysis demonstrated that the Ultraviolet Irradiation (2 minimal erythema dose) caused moderate (2–3-fold) gradual increases of transforming growth factor β1 and β3 mRNA expression during 3 d post exposure. In contrast, expression of transforming growth factor β2 mRNA, the predominant form of transforming growth factor β in human skin, decreased within 4 h after Ultraviolet Irradiation. In situ hybridization revealed transforming growth factor β1, β2, and β3 mRNA expression in cells throughout the epidermis and the dermis in nonirradiated skin. Following Ultraviolet or solar-simulated Ultraviolet Irradiation, transforming growth factor β1 and β3 mRNA were increased and transforming growth factor β2 mRNA was reduced throughout the epidermis and dermis. No significant changes were observed in transforming growth factor β type I receptor mRNA expression after Ultraviolet Irradiation. In contrast, transforming growth factor β type II receptor mRNA expression was reduced 60% within 4 h following Ultraviolet exposure in human skin in vivo . Transforming growth factor β type II receptor mRNA levels remained reduced for 8 h and recovered by 24 h post Ultraviolet. In situ hybridization revealed that Ultraviolet or solar-simulated Ultraviolet Irradiation caused loss of transforming growth factor β type II receptor mRNA in basal and suprabasal cells in the epidermis and dermal cells. In addition, no significant changes were observed in Smad2, Smad3, and Smad4 expression after Ultraviolet Irradiation. In contrast, Ultraviolet and solar-simulated Ultraviolet Irradiation rapidly induced gene expression of Smad7, which antagonizes the actions of the transforming growth factor β/Smad pathway. Smad7 mRNA induction occurred throughout the epidermis and dermal cells as determined by in situ hybridization. Ultraviolet Irradiation also caused reduced DNA binding of Smad3/4 in human skin in vivo . Reduced Smad3/4 DNA binding was observed within 4 h following Irradiation. Taken together, these results demonstrate that Ultraviolet and solar-simulated Ultraviolet Irradiation alter the transforming growth factor β/Smad pathway in human skin in vivo . Ultraviolet induction of Smad7 and reduction of transforming growth factor β2 and transforming growth factor β type II receptor should diminish transforming growth factor β signaling, and probably contribute to the decrease of transforming growth factor β regulated type I and type III procollagen gene expression observed in Ultraviolet and solar-simulated Ultraviolet irradiated human skin in vivo .

  • Ultraviolet Irradiation increases matrix metalloproteinase 8 protein in human skin in vivo
    Journal of Investigative Dermatology, 2001
    Co-Authors: Gary J Fisher, Sewon Kang, H C Choi, Zsuzsanna Batacsorgo, Yuan Shao, Subhash C Datta, Zengquan Wang, John J Voorhees
    Abstract:

    Humans express three distinct collagenases, MMP-1, MMP-8, and MMP-13, that initiate degradation of fibrillar type I collagen. We have previously reported that Ultraviolet Irradiation causes increased expression of MMP-1, but not MMP-13, in keratinocytes and fibroblasts in human skin in vivo. We report here that Ultraviolet Irradiation increases expression of MMP-8 in human skin in vivo. Western analysis revealed that levels of the full-length, 85 kDa proenzyme form of MMP-8 increased significantly within 8 h post Ultraviolet Irradiation (2 minimal erythema doses). Increased full-length MMP-8 protein was associated with infiltration into the skin of neutrophils, which are the major cell type that expresses MMP-8. Immunofluorescence revealed coexpression of MMP-8 and neutrophil elastase, a marker for neutrophils. Immunohistology demonstrated MMP-8 expression in neutrophils in the papillary dermis between 4 and 8 h post Ultraviolet Irradiation, and in the epidermis at 24 h post radiation. MMP-8 mRNA expression was not detected in nonirradiated or Ultraviolet-irradiated human skin, indicating that increased MMP-8 following Ultraviolet Irradiation resulted from preexisting MMP-8 protein in infiltrating neutrophils. Pretreatment of skin with the glucocorticoid clobetasol, but not all-trans retinoic acid, significantly blocked Ultraviolet-induced increases in MMP-8 protein levels, and neutrophil infiltration. In contrast, all-trans retinoic acid and clobetasol were equally effective in blocking Ultraviolet induction of MMP-1 and degradation of collagen in human skin in vivo. Taken together, these data demonstrate that Ultraviolet Irradiation increases MMP-8 protein, which exists predominantly in a latent form within neutrophils, in human skin in vivo. Although Ultraviolet Irradiation induces both MMP-1 and MMP-8, Ultraviolet-induced collagen degradation is initiated primarily by MMP-1, with little, if any, contribution by MMP-8.

  • molecular mechanisms of photoaging and its prevention by retinoic acid Ultraviolet Irradiation induces map kinase signal transduction cascades that induce ap 1 regulated matrix metalloproteinases that degrade human skin in vivo
    Journal of Investigative Dermatology Symposium Proceedings, 1998
    Co-Authors: Gary J Fisher, John J Voorhees
    Abstract:

    Ultraviolet radiation from the sun damages human skin, resulting in an old and wrinkled appearance. A substantial amount of circumstantial evidence indicates that photoaging results in part from alterations in the composition, organization, and structure of the colla-genous extracellular matrix in the dermis. This paper reviews the authors' investigations into the molecular mechanisms by which Ultraviolet Irradiation damages the dermal extracellular matrix and provides evidence for prevention of this damage by all-trans retinoic acid in human skin in vivo . Based on experimental evidence a working model is proposed whereby Ultraviolet Irradiation activates growth factor and cytokine receptors on keratinocytes and dermal cells, resulting in downstream signal transduction through activation of MAP kinase pathways. These signaling pathways converge in the nucleus of cells to induce c-Jun, which hetero-dimerizes with constitutively expressed c-Fos to form activated complexes of the transcription factor AP-1. In the dermis and epidermis, AP-1 induces expression of matrix metalloproteinases collagenase, 92kDa gelatinase, and stromelysin, which degrade collagen and other proteins that comprise the dermal extracellular matrix. It is hypothesized that dermal breakdown is followed by repair that, like all wound repair, is imperfect. Imperfect repair yields a deficit in the structural integrity of the dermis, a solar scar. Dermal degradation followed by imperfect repair is repeated with each intermittent exposure to Ultraviolet Irradiation, leading to accumulation of solar scarring, and ultimately visible photoaging. All-trans retinoic acid acts to inhibit induction of c-Jun protein by Ultraviolet Irradiation, thereby preventing increased matrix metalloproteinases and ensuing dermal damage. Journal of Investigative Dermatology Symposium Proceedings 3:61-68, 1998