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SERPINA3K protects against oxidative stress via modulating ROS generation/degradation and KEAP1-NRF2 pathway in the corneal epithelium.

PURPOSEWe recently reported that SERPINA3K (SA3K), a member of the serine proteinase inhibitor (SERPIN) family, has antiangiogenic and anti-inflammatory activities. Here we investigated the antioxidant effects of SA3K in the corneal epithelium and the mechanism underlying its action. METHODSWe estab... Full description

Journal Title: Investigative ophthalmology & visual science July 27, 2012, Vol.53(8), pp.5033-5043
Main Author: Zhou, Tong
Other Authors: Zong, Rongrong , Zhang, Zhoujing , Zhu, Chengpeng , Pan, Fangyu , Xiao, Xinye , Liu, Zhen , He, Hui , Ma, Jian-Xing , Liu, Zuguo , Zhou, Yueping
Format: Electronic Article Electronic Article
Language: English
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ID: E-ISSN: 1552-5783 ; DOI: 1552-5783 ; DOI: 10.1167/iovs.12-9729
Link: http://search.proquest.com/docview/1030348971/?pq-origsite=primo
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title: SERPINA3K protects against oxidative stress via modulating ROS generation/degradation and KEAP1-NRF2 pathway in the corneal epithelium.
format: Article
creator:
  • Zhou, Tong
  • Zong, Rongrong
  • Zhang, Zhoujing
  • Zhu, Chengpeng
  • Pan, Fangyu
  • Xiao, Xinye
  • Liu, Zhen
  • He, Hui
  • Ma, Jian-Xing
  • Liu, Zuguo
  • Zhou, Yueping
subjects:
  • Animals–Drug Effects
  • Cell Survival–Drug Effects
  • Cells, Cultured–Metabolism
  • Epithelium, Corneal–Metabolism
  • Humans–Metabolism
  • Intracellular Signaling Peptides and Proteins–Drug Effects
  • Nf-E2-Related Factor 2–Metabolism
  • Oxidative Stress–Pharmacology
  • Random Allocation–Pharmacology
  • Rats–Physiology
  • Reactive Oxygen Species–Physiology
  • Serine Proteinase Inhibitors–Physiology
  • Serpins–Physiology
  • Signal Transduction–Physiology
  • Intracellular Signaling Peptides and Proteins
  • Nf-E2-Related Factor 2
  • Reactive Oxygen Species
  • Serine Proteinase Inhibitors
  • Serpina3k Protein, Rat
  • Serpins
ispartof: Investigative ophthalmology & visual science, July 27, 2012, Vol.53(8), pp.5033-5043
description: PURPOSEWe recently reported that SERPINA3K (SA3K), a member of the serine proteinase inhibitor (SERPIN) family, has antiangiogenic and anti-inflammatory activities. Here we investigated the antioxidant effects of SA3K in the corneal epithelium and the mechanism underlying its action. METHODSWe established the oxidative stress models induced by hydrogen peroxide (H₂O₂) in cultured human corneal epithelial (HCE) cells and in rat corneal epithelium in vivo. Cell viability, flow cytometry, and TUNEL analysis were conducted to detect viable cells and cell death; reactive oxygen species (ROS) and 3-Nitrotyrosine fluorescent assay was applied to measure ROS levels. Activity assay, immunostaining, Western blot, and quantitative RT-PCR were performed to analyze the factors of the ROS generation/degradation system and pathway. RESULTSSA3K protected the HCE cells from H₂O₂-induced oxidative stress in a dose- and time-dependent manner. SA3K also significantly reduced the production of ROS. Regarding the mechanism underlying these effects, SA3K downregulated ROS generation by inhibiting NOX4 and upregulated ROS degradation by increasing the activity of superoxide dismutases and catalase. Furthermore, H₂O₂ induced activation of the Kelch-like ECH-associated protein 1 (KEAP1)/NF-E2-related factor-2 (NRF2) pathway, while SA3K inhibited H₂O₂-induced activation of KEAP1 and NRF2 and their downstream factors, including NAD(P)H quinone oxidoreductase and glutathione S-transferase. In the H₂O₂-induced rat corneal epithelium, SA3K alleviated the oxidative stress and downregulated NOX4 and NRF2. CONCLUSIONSCollectively, SA3K protects against oxidative stress by targeting the ROS generation/degradation system and modulating the KEAP1-NRF2 signaling pathway.
language: eng
source:
identifier: E-ISSN: 1552-5783 ; DOI: 1552-5783 ; DOI: 10.1167/iovs.12-9729
fulltext: fulltext
issn:
  • 15525783
  • 1552-5783
url: Link


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titleSERPINA3K protects against oxidative stress via modulating ROS generation/degradation and KEAP1-NRF2 pathway in the corneal epithelium.
creatorZhou, Tong ; Zong, Rongrong ; Zhang, Zhoujing ; Zhu, Chengpeng ; Pan, Fangyu ; Xiao, Xinye ; Liu, Zhen ; He, Hui ; Ma, Jian-Xing ; Liu, Zuguo ; Zhou, Yueping
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ispartofInvestigative ophthalmology & visual science, July 27, 2012, Vol.53(8), pp.5033-5043
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subjectAnimals–Drug Effects ; Cell Survival–Drug Effects ; Cells, Cultured–Metabolism ; Epithelium, Corneal–Metabolism ; Humans–Metabolism ; Intracellular Signaling Peptides and Proteins–Drug Effects ; Nf-E2-Related Factor 2–Metabolism ; Oxidative Stress–Pharmacology ; Random Allocation–Pharmacology ; Rats–Physiology ; Reactive Oxygen Species–Physiology ; Serine Proteinase Inhibitors–Physiology ; Serpins–Physiology ; Signal Transduction–Physiology ; Intracellular Signaling Peptides and Proteins ; Nf-E2-Related Factor 2 ; Reactive Oxygen Species ; Serine Proteinase Inhibitors ; Serpina3k Protein, Rat ; Serpins
descriptionPURPOSEWe recently reported that SERPINA3K (SA3K), a member of the serine proteinase inhibitor (SERPIN) family, has antiangiogenic and anti-inflammatory activities. Here we investigated the antioxidant effects of SA3K in the corneal epithelium and the mechanism underlying its action. METHODSWe established the oxidative stress models induced by hydrogen peroxide (H₂O₂) in cultured human corneal epithelial (HCE) cells and in rat corneal epithelium in vivo. Cell viability, flow cytometry, and TUNEL analysis were conducted to detect viable cells and cell death; reactive oxygen species (ROS) and 3-Nitrotyrosine fluorescent assay was applied to measure ROS levels. Activity assay, immunostaining, Western blot, and quantitative RT-PCR were performed to analyze the factors of the ROS generation/degradation system and pathway. RESULTSSA3K protected the HCE cells from H₂O₂-induced oxidative stress in a dose- and time-dependent manner. SA3K also significantly reduced the production of ROS. Regarding the mechanism underlying these effects, SA3K downregulated ROS generation by inhibiting NOX4 and upregulated ROS degradation by increasing the activity of superoxide dismutases and catalase. Furthermore, H₂O₂ induced activation of the Kelch-like ECH-associated protein 1 (KEAP1)/NF-E2-related factor-2 (NRF2) pathway, while SA3K inhibited H₂O₂-induced activation of KEAP1 and NRF2 and their downstream factors, including NAD(P)H quinone oxidoreductase and glutathione S-transferase. In the H₂O₂-induced rat corneal epithelium, SA3K alleviated the oxidative stress and downregulated NOX4 and NRF2. CONCLUSIONSCollectively, SA3K protects against oxidative stress by targeting the ROS generation/degradation system and modulating the KEAP1-NRF2 signaling pathway.
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titleSERPINA3K protects against oxidative stress via modulating ROS generation/degradation and KEAP1-NRF2 pathway in the corneal epithelium.
descriptionPURPOSEWe recently reported that SERPINA3K (SA3K), a member of the serine proteinase inhibitor (SERPIN) family, has antiangiogenic and anti-inflammatory activities. Here we investigated the antioxidant effects of SA3K in the corneal epithelium and the mechanism underlying its action. METHODSWe established the oxidative stress models induced by hydrogen peroxide (H₂O₂) in cultured human corneal epithelial (HCE) cells and in rat corneal epithelium in vivo. Cell viability, flow cytometry, and TUNEL analysis were conducted to detect viable cells and cell death; reactive oxygen species (ROS) and 3-Nitrotyrosine fluorescent assay was applied to measure ROS levels. Activity assay, immunostaining, Western blot, and quantitative RT-PCR were performed to analyze the factors of the ROS generation/degradation system and pathway. RESULTSSA3K protected the HCE cells from H₂O₂-induced oxidative stress in a dose- and time-dependent manner. SA3K also significantly reduced the production of ROS. Regarding the mechanism underlying these effects, SA3K downregulated ROS generation by inhibiting NOX4 and upregulated ROS degradation by increasing the activity of superoxide dismutases and catalase. Furthermore, H₂O₂ induced activation of the Kelch-like ECH-associated protein 1 (KEAP1)/NF-E2-related factor-2 (NRF2) pathway, while SA3K inhibited H₂O₂-induced activation of KEAP1 and NRF2 and their downstream factors, including NAD(P)H quinone oxidoreductase and glutathione S-transferase. In the H₂O₂-induced rat corneal epithelium, SA3K alleviated the oxidative stress and downregulated NOX4 and NRF2. CONCLUSIONSCollectively, SA3K protects against oxidative stress by targeting the ROS generation/degradation system and modulating the KEAP1-NRF2 signaling pathway.
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titleSERPINA3K protects against oxidative stress via modulating ROS generation/degradation and KEAP1-NRF2 pathway in the corneal epithelium.
authorZhou, Tong ; Zong, Rongrong ; Zhang, Zhoujing ; Zhu, Chengpeng ; Pan, Fangyu ; Xiao, Xinye ; Liu, Zhen ; He, Hui ; Ma, Jian-Xing ; Liu, Zuguo ; Zhou, Yueping
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abstractPURPOSEWe recently reported that SERPINA3K (SA3K), a member of the serine proteinase inhibitor (SERPIN) family, has antiangiogenic and anti-inflammatory activities. Here we investigated the antioxidant effects of SA3K in the corneal epithelium and the mechanism underlying its action. METHODSWe established the oxidative stress models induced by hydrogen peroxide (H₂O₂) in cultured human corneal epithelial (HCE) cells and in rat corneal epithelium in vivo. Cell viability, flow cytometry, and TUNEL analysis were conducted to detect viable cells and cell death; reactive oxygen species (ROS) and 3-Nitrotyrosine fluorescent assay was applied to measure ROS levels. Activity assay, immunostaining, Western blot, and quantitative RT-PCR were performed to analyze the factors of the ROS generation/degradation system and pathway. RESULTSSA3K protected the HCE cells from H₂O₂-induced oxidative stress in a dose- and time-dependent manner. SA3K also significantly reduced the production of ROS. Regarding the mechanism underlying these effects, SA3K downregulated ROS generation by inhibiting NOX4 and upregulated ROS degradation by increasing the activity of superoxide dismutases and catalase. Furthermore, H₂O₂ induced activation of the Kelch-like ECH-associated protein 1 (KEAP1)/NF-E2-related factor-2 (NRF2) pathway, while SA3K inhibited H₂O₂-induced activation of KEAP1 and NRF2 and their downstream factors, including NAD(P)H quinone oxidoreductase and glutathione S-transferase. In the H₂O₂-induced rat corneal epithelium, SA3K alleviated the oxidative stress and downregulated NOX4 and NRF2. CONCLUSIONSCollectively, SA3K protects against oxidative stress by targeting the ROS generation/degradation system and modulating the KEAP1-NRF2 signaling pathway.
doi10.1167/iovs.12-9729
urlhttp://search.proquest.com/docview/1030348971/
date2012-07-27