The Experts below are selected from a list of 724719 Experts worldwide ranked by ideXlab platform
Siwanon Jirawatnotai - One of the best experts on this subject based on the ideXlab platform.
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ultraviolet radiation induced skin aging the role of DNA damage and oxidative stress in epidermal stem Cell damage mediated skin aging
Stem Cells International, 2016Co-Authors: Uraiwan Panich, Gunya Sittithumcharee, Natwarath Rathviboon, Siwanon JirawatnotaiAbstract:Skin is the largest human organ. Skin continually reconstructs itself to ensure its viability, integrity, and ability to provide protection for the body. Some areas of skin are continuously exposed to a variety of environmental stressors that can inflict direct and indirect damage to skin Cell DNA. Skin homeostasis is maintained by mesenchymal stem Cells in inner layer dermis and epidermal stem Cells (ESCs) in the outer layer epidermis. Reduction of skin stem Cell number and function has been linked to impaired skin homeostasis (e.g., skin premature aging and skin cancers). Skin stem Cells, with self-renewal capability and multipotency, are frequently affected by environment. Ultraviolet radiation (UVR), a major cause of stem Cell DNA damage, can contribute to depletion of stem Cells (ESCs and mesenchymal stem Cells) and damage of stem Cell niche, eventually leading to photoinduced skin aging. In this review, we discuss the role of UV-induced DNA damage and oxidative stress in the skin stem Cell aging in order to gain insights into the pathogenesis and develop a way to reduce photoaging of skin Cells.
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ultraviolet radiation induced skin aging the role of DNA damage and oxidative stress in epidermal stem Cell damage mediated skin aging
Stem Cells International, 2016Co-Authors: Uraiwan Panich, Gunya Sittithumcharee, Natwarath Rathviboon, Siwanon JirawatnotaiAbstract:Skin is the largest human organ. Skin continually reconstructs itself to ensure its viability, integrity, and ability to provide protection for the body. Some areas of skin are continuously exposed to a variety of environmental stressors that can inflict direct and indirect damage to skin Cell DNA. Skin homeostasis is maintained by mesenchymal stem Cells in inner layer dermis and epidermal stem Cells (ESCs) in the outer layer epidermis. Reduction of skin stem Cell number and function has been linked to impaired skin homeostasis (e.g., skin premature aging and skin cancers). Skin stem Cells, with self-renewal capability and multipotency, are frequently affected by environment. Ultraviolet radiation (UVR), a major cause of stem Cell DNA damage, can contribute to depletion of stem Cells (ESCs and mesenchymal stem Cells) and damage of stem Cell niche, eventually leading to photoinduced skin aging. In this review, we discuss the role of UV-induced DNA damage and oxidative stress in the skin stem Cell aging in order to gain insights into the pathogenesis and develop a way to reduce photoaging of skin Cells.
James E. Klaunig - One of the best experts on this subject based on the ideXlab platform.
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Kupffer Cells participate in 2-butoxyethanol-induced liver hemangiosarcomas.
Toxicology, 2010Co-Authors: Lisa M. Kamendulis, Stacy M Corthals, James E. KlaunigAbstract:2-Butoxyethanol increases hemangiosarcomas selectively in male mouse liver after chronic inhalation through mechanisms that have not fully been elucidated. Hemolysis, a primary toxic effect associated with 2-butoxyethanol exposure in rodents, increased hemosiderin (iron) deposition in Kupffer Cells in the liver. These findings, along with the induction of hepatic neoplastic lesions, led to our hypothesis that the induction hemangiosarcomas by 2-butoxyethanol is due to the activation of Kupffer Cells, subsequent to hemolysis, that results in the induction of DNA synthesis in target Cells (endothelial Cells); allowing for the selective proliferation of preneoplastic target Cells and/or the promotion of new initiated Cells. The present studies were conducted to determine whether Kupffer Cells contributed to 2-butoxyethanol-induced endothelial DNA synthesis in the liver, thereby determining whether a linkage exists between these events. Male B6C3F1 mice were treated with 450 and 900 mg/kg 2-butoxyethanol (via daily gavage; 5x/week) for 7 days in the presence or absence of Kupffer Cell depletion (via clodronate-encapsulated liposomes). 2-Butoxyethanol (450 and 900 mg/kg/day) increased the number of F4/80 stained Cells (Kupffer Cells) compared to controls (approximately 1.3- and approximately 1.6-fold over control, respectively). Clodronate liposome treatment reduced the number of Kupffer Cells by >90%, as assessed by F4/80 immunohistochemistry. Increased hemolysis, measured by increases in relative spleen weights and decreased hematocrit was confirmed in 2-butoxyethanol treated mice. The percentage of iron-stained endothelial Cells increased by approximately 11-fold over control, and endothelial Cell DNA synthesis increased approximately 1.7-fold over control in 2-butoxyethanol exposed mice. Importantly, Kupffer Cell depletion reduced 2-butoxyethanol-induced iron staining and hepatic endothelial Cell DNA synthesis. These studies provide evidence supporting the hypothesis that the Kupffer Cell modulates 2-butoxyethanol-induced endothelial Cell DNA synthesis, and therefore may contribute to hemangiosarcoma induction by 2-butoxyethanol.
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Mechanisms of 2-butoxyethanol-induced hemangiosarcomas.
Toxicological Sciences, 2006Co-Authors: Stacy M Corthals, Lisa M. Kamendulis, James E. KlaunigAbstract:Chronic exposure to 2-butoxyethanol increased liver hemangiosarcomas in male mice. The mechanism for the selective induction of hemangiosarcomas by 2-butoxyethanol is unknown but has been suggested to occur through non–DNA-reactive mechanisms. The occurrence of liver hemangiosarcomas in male mice has been linked to oxidative damage subsequent to RBC hemolysis and iron deposition and activation of macrophages (Kupffer Cells) in the liver, events that exhibit a threshold in both animals and humans. 2-Butoxyethanol is metabolized to 2-butoxyacetaldehyde and 2butoxyacetic acid, and although the aldehyde metabolite is short lived, the potential exists for this metabolite to cause DNA damage. The present study examined whether 2-butoxyethanol and its metabolites, 2-butoxyacetaldehyde and 2-butoxyacetic acid, damaged mouse endothelial Cell DNA using the comet assay. No increase in DNA damage was observed following 2-butoxyethanol (1–10mM), 2-butoxyacetaldehyde (0.1–1.0mM), or 2-butoxyacetic acid (1–10mM) in endothelial Cells after 2, 4, or 24 h of exposure. Additional studies examined the involvement of hemolysis and macrophage activation in 2-butoxyethanol carcinogenesis. DNA damage was produced by hemolyzed RBCs (10 3 10 6 , 4 h), ferrous sulfate (0.1–1.0mM; 2–24 h), and hydrogen peroxide (50–100mM; 1–4 h) in endothelial Cells. Hemolyzed RBCs also activated macrophages, as evidenced by increased tumor necrosis factor (TNF) a, while neither 2-butoxyethanol nor butoxyacetic acid increased TNF-a from macrophages. The effect of activated macrophages on endothelial Cell DNA damage and DNA synthesis was also studied. Coculture of endothelial Cells with activated macrophages increased endothelial Cell DNA damage after 4 or 24 h and increased endothelial Cell DNA synthesis after 24 h. These data demonstrate that 2-butoxyethanol and related metabolites do not directly cause DNA damage. Supportive evidence also demonstrated that damaged RBCs, iron, and/or products from macrophage activation (possibly reactive oxygen species) produce DNA damage in endothelial Cells and that activated macrophages stimulate endothelial Cell proliferation. These events coupled together provide the events necessary for the induction of hemangiosarco
Uraiwan Panich - One of the best experts on this subject based on the ideXlab platform.
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ultraviolet radiation induced skin aging the role of DNA damage and oxidative stress in epidermal stem Cell damage mediated skin aging
Stem Cells International, 2016Co-Authors: Uraiwan Panich, Gunya Sittithumcharee, Natwarath Rathviboon, Siwanon JirawatnotaiAbstract:Skin is the largest human organ. Skin continually reconstructs itself to ensure its viability, integrity, and ability to provide protection for the body. Some areas of skin are continuously exposed to a variety of environmental stressors that can inflict direct and indirect damage to skin Cell DNA. Skin homeostasis is maintained by mesenchymal stem Cells in inner layer dermis and epidermal stem Cells (ESCs) in the outer layer epidermis. Reduction of skin stem Cell number and function has been linked to impaired skin homeostasis (e.g., skin premature aging and skin cancers). Skin stem Cells, with self-renewal capability and multipotency, are frequently affected by environment. Ultraviolet radiation (UVR), a major cause of stem Cell DNA damage, can contribute to depletion of stem Cells (ESCs and mesenchymal stem Cells) and damage of stem Cell niche, eventually leading to photoinduced skin aging. In this review, we discuss the role of UV-induced DNA damage and oxidative stress in the skin stem Cell aging in order to gain insights into the pathogenesis and develop a way to reduce photoaging of skin Cells.
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ultraviolet radiation induced skin aging the role of DNA damage and oxidative stress in epidermal stem Cell damage mediated skin aging
Stem Cells International, 2016Co-Authors: Uraiwan Panich, Gunya Sittithumcharee, Natwarath Rathviboon, Siwanon JirawatnotaiAbstract:Skin is the largest human organ. Skin continually reconstructs itself to ensure its viability, integrity, and ability to provide protection for the body. Some areas of skin are continuously exposed to a variety of environmental stressors that can inflict direct and indirect damage to skin Cell DNA. Skin homeostasis is maintained by mesenchymal stem Cells in inner layer dermis and epidermal stem Cells (ESCs) in the outer layer epidermis. Reduction of skin stem Cell number and function has been linked to impaired skin homeostasis (e.g., skin premature aging and skin cancers). Skin stem Cells, with self-renewal capability and multipotency, are frequently affected by environment. Ultraviolet radiation (UVR), a major cause of stem Cell DNA damage, can contribute to depletion of stem Cells (ESCs and mesenchymal stem Cells) and damage of stem Cell niche, eventually leading to photoinduced skin aging. In this review, we discuss the role of UV-induced DNA damage and oxidative stress in the skin stem Cell aging in order to gain insights into the pathogenesis and develop a way to reduce photoaging of skin Cells.
Gryte Satas - One of the best experts on this subject based on the ideXlab platform.
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single Cell tumor phylogeny inference with copy number constrained mutation losses
Research in Computational Molecular Biology, 2020Co-Authors: Gryte Satas, Simone Zaccaria, Geoffrey Mon, Benjamin J RaphaelAbstract:Motivation: Single-Cell DNA sequencing enables the measurement of somatic mutations in individual tumor Cells, and provides data to reconstruct the evolutionary history of the tumor.
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scarlet single Cell tumor phylogeny inference with copy number constrained mutation losses
Cell systems, 2020Co-Authors: Gryte Satas, Simone Zaccaria, Geoffrey Mon, Benjamin J RaphaelAbstract:Motivation: Single-Cell DNA sequencing enables the measurement of somatic mutations in individual tumor Cells, and provides data to reconstruct the evolutionary history of the tumor.
Gunya Sittithumcharee - One of the best experts on this subject based on the ideXlab platform.
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ultraviolet radiation induced skin aging the role of DNA damage and oxidative stress in epidermal stem Cell damage mediated skin aging
Stem Cells International, 2016Co-Authors: Uraiwan Panich, Gunya Sittithumcharee, Natwarath Rathviboon, Siwanon JirawatnotaiAbstract:Skin is the largest human organ. Skin continually reconstructs itself to ensure its viability, integrity, and ability to provide protection for the body. Some areas of skin are continuously exposed to a variety of environmental stressors that can inflict direct and indirect damage to skin Cell DNA. Skin homeostasis is maintained by mesenchymal stem Cells in inner layer dermis and epidermal stem Cells (ESCs) in the outer layer epidermis. Reduction of skin stem Cell number and function has been linked to impaired skin homeostasis (e.g., skin premature aging and skin cancers). Skin stem Cells, with self-renewal capability and multipotency, are frequently affected by environment. Ultraviolet radiation (UVR), a major cause of stem Cell DNA damage, can contribute to depletion of stem Cells (ESCs and mesenchymal stem Cells) and damage of stem Cell niche, eventually leading to photoinduced skin aging. In this review, we discuss the role of UV-induced DNA damage and oxidative stress in the skin stem Cell aging in order to gain insights into the pathogenesis and develop a way to reduce photoaging of skin Cells.
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ultraviolet radiation induced skin aging the role of DNA damage and oxidative stress in epidermal stem Cell damage mediated skin aging
Stem Cells International, 2016Co-Authors: Uraiwan Panich, Gunya Sittithumcharee, Natwarath Rathviboon, Siwanon JirawatnotaiAbstract:Skin is the largest human organ. Skin continually reconstructs itself to ensure its viability, integrity, and ability to provide protection for the body. Some areas of skin are continuously exposed to a variety of environmental stressors that can inflict direct and indirect damage to skin Cell DNA. Skin homeostasis is maintained by mesenchymal stem Cells in inner layer dermis and epidermal stem Cells (ESCs) in the outer layer epidermis. Reduction of skin stem Cell number and function has been linked to impaired skin homeostasis (e.g., skin premature aging and skin cancers). Skin stem Cells, with self-renewal capability and multipotency, are frequently affected by environment. Ultraviolet radiation (UVR), a major cause of stem Cell DNA damage, can contribute to depletion of stem Cells (ESCs and mesenchymal stem Cells) and damage of stem Cell niche, eventually leading to photoinduced skin aging. In this review, we discuss the role of UV-induced DNA damage and oxidative stress in the skin stem Cell aging in order to gain insights into the pathogenesis and develop a way to reduce photoaging of skin Cells.