Role of mitochondrial hydrogen peroxide induced by intermittent hypoxia in airway epithelial wound repair in vitro
The airway epithelium acts as a frontline barrier against various environmental insults and its repair process after airway injury is critical for the lung homeostasis restoration. Recently, the role of intracellular reactive oxygen species (ROS) as transcription-independent damage signaling has bee...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Hamada, Satoshi [verfasserIn] |
|---|
| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2016transfer abstract |
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| Schlagwörter: |
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| Umfang: |
9 |
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| Übergeordnetes Werk: |
Enthalten in: 72 OUTCOMES OF COMBINATION OF HEPATITIS B IMMUNOGLOBULIN AND HEPATITIS B VACCINATION IN HIGH-RISK NEWBORNS BORN TO HBEAG-POSITIVE MOTHERS - 2012, ECR, Orlando, Fla |
|---|---|
| Übergeordnetes Werk: |
volume:344 ; year:2016 ; number:1 ; day:15 ; month:05 ; pages:143-151 ; extent:9 |
| Links: |
|---|
| DOI / URN: |
10.1016/j.yexcr.2016.04.006 |
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| 520 | |a The airway epithelium acts as a frontline barrier against various environmental insults and its repair process after airway injury is critical for the lung homeostasis restoration. Recently, the role of intracellular reactive oxygen species (ROS) as transcription-independent damage signaling has been highlighted in the wound repair process. Both conditions of continuous hypoxia and intermittent hypoxia (IH) induce ROS. Although IH is important in clinical settings, the roles of IH-induced ROS in the airway repair process have not been investigated. In this study, we firstly showed that IH induced mitochondrial hydrogen peroxide (H2O2) production and significantly decreased bronchial epithelial cell migration, prevented by catalase treatment in a wound scratch assay. RhoA activity was higher during repair process in the IH condition compared to in the normoxic condition, resulting in the cellular morphological changes shown by immunofluorescence staining: round cells, reduced central stress fiber numbers, pronounced cortical actin filament distributions, and punctate focal adhesions. These phenotypes were replicated by exogenous H2O2 treatment under the normoxic condition. Our findings confirmed the transcription-independent role of IH-induced intracellular ROS in the bronchial epithelial cell repair process and might have significant implications for impaired bronchial epithelial cell regeneration. | ||
| 520 | |a The airway epithelium acts as a frontline barrier against various environmental insults and its repair process after airway injury is critical for the lung homeostasis restoration. Recently, the role of intracellular reactive oxygen species (ROS) as transcription-independent damage signaling has been highlighted in the wound repair process. Both conditions of continuous hypoxia and intermittent hypoxia (IH) induce ROS. Although IH is important in clinical settings, the roles of IH-induced ROS in the airway repair process have not been investigated. In this study, we firstly showed that IH induced mitochondrial hydrogen peroxide (H2O2) production and significantly decreased bronchial epithelial cell migration, prevented by catalase treatment in a wound scratch assay. RhoA activity was higher during repair process in the IH condition compared to in the normoxic condition, resulting in the cellular morphological changes shown by immunofluorescence staining: round cells, reduced central stress fiber numbers, pronounced cortical actin filament distributions, and punctate focal adhesions. These phenotypes were replicated by exogenous H2O2 treatment under the normoxic condition. Our findings confirmed the transcription-independent role of IH-induced intracellular ROS in the bronchial epithelial cell repair process and might have significant implications for impaired bronchial epithelial cell regeneration. | ||
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10.1016/j.yexcr.2016.04.006 doi GBVA2016021000016.pica (DE-627)ELV030077567 (ELSEVIER)S0014-4827(16)30075-1 DE-627 ger DE-627 rakwb eng 570 570 DE-600 610 VZ 610 VZ 44.44 bkl Hamada, Satoshi verfasserin aut Role of mitochondrial hydrogen peroxide induced by intermittent hypoxia in airway epithelial wound repair in vitro 2016transfer abstract 9 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The airway epithelium acts as a frontline barrier against various environmental insults and its repair process after airway injury is critical for the lung homeostasis restoration. Recently, the role of intracellular reactive oxygen species (ROS) as transcription-independent damage signaling has been highlighted in the wound repair process. Both conditions of continuous hypoxia and intermittent hypoxia (IH) induce ROS. Although IH is important in clinical settings, the roles of IH-induced ROS in the airway repair process have not been investigated. In this study, we firstly showed that IH induced mitochondrial hydrogen peroxide (H2O2) production and significantly decreased bronchial epithelial cell migration, prevented by catalase treatment in a wound scratch assay. RhoA activity was higher during repair process in the IH condition compared to in the normoxic condition, resulting in the cellular morphological changes shown by immunofluorescence staining: round cells, reduced central stress fiber numbers, pronounced cortical actin filament distributions, and punctate focal adhesions. These phenotypes were replicated by exogenous H2O2 treatment under the normoxic condition. Our findings confirmed the transcription-independent role of IH-induced intracellular ROS in the bronchial epithelial cell repair process and might have significant implications for impaired bronchial epithelial cell regeneration. The airway epithelium acts as a frontline barrier against various environmental insults and its repair process after airway injury is critical for the lung homeostasis restoration. Recently, the role of intracellular reactive oxygen species (ROS) as transcription-independent damage signaling has been highlighted in the wound repair process. Both conditions of continuous hypoxia and intermittent hypoxia (IH) induce ROS. Although IH is important in clinical settings, the roles of IH-induced ROS in the airway repair process have not been investigated. In this study, we firstly showed that IH induced mitochondrial hydrogen peroxide (H2O2) production and significantly decreased bronchial epithelial cell migration, prevented by catalase treatment in a wound scratch assay. RhoA activity was higher during repair process in the IH condition compared to in the normoxic condition, resulting in the cellular morphological changes shown by immunofluorescence staining: round cells, reduced central stress fiber numbers, pronounced cortical actin filament distributions, and punctate focal adhesions. These phenotypes were replicated by exogenous H2O2 treatment under the normoxic condition. Our findings confirmed the transcription-independent role of IH-induced intracellular ROS in the bronchial epithelial cell repair process and might have significant implications for impaired bronchial epithelial cell regeneration. ROCK Elsevier HIF Elsevier HGF Elsevier MitoTEMPO Elsevier O2- Elsevier BEBM Elsevier DMEM Elsevier PEG Elsevier ANOVA Elsevier BEGM Elsevier FBS Elsevier H2O2 Elsevier NOX Elsevier ROS Elsevier DUOX Elsevier H2DCF-DA Elsevier SEM Elsevier DPI Elsevier PHBE Elsevier IH Elsevier Sato, Atsuyasu oth Hara-Chikuma, Mariko oth Satooka, Hiroki oth Hasegawa, Koichi oth Tanimura, Kazuya oth Tanizawa, Kiminobu oth Inouchi, Morito oth Handa, Tomohiro oth Oga, Toru oth Muro, Shigeo oth Mishima, Michiaki oth Chin, Kazuo oth Enthalten in Academic Press 72 OUTCOMES OF COMBINATION OF HEPATITIS B IMMUNOGLOBULIN AND HEPATITIS B VACCINATION IN HIGH-RISK NEWBORNS BORN TO HBEAG-POSITIVE MOTHERS 2012 ECR Orlando, Fla (DE-627)ELV011050691 volume:344 year:2016 number:1 day:15 month:05 pages:143-151 extent:9 https://doi.org/10.1016/j.yexcr.2016.04.006 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_70 44.44 Parasitologie Medizin VZ AR 344 2016 1 15 0515 143-151 9 045F 570 |
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10.1016/j.yexcr.2016.04.006 doi GBVA2016021000016.pica (DE-627)ELV030077567 (ELSEVIER)S0014-4827(16)30075-1 DE-627 ger DE-627 rakwb eng 570 570 DE-600 610 VZ 610 VZ 44.44 bkl Hamada, Satoshi verfasserin aut Role of mitochondrial hydrogen peroxide induced by intermittent hypoxia in airway epithelial wound repair in vitro 2016transfer abstract 9 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The airway epithelium acts as a frontline barrier against various environmental insults and its repair process after airway injury is critical for the lung homeostasis restoration. Recently, the role of intracellular reactive oxygen species (ROS) as transcription-independent damage signaling has been highlighted in the wound repair process. Both conditions of continuous hypoxia and intermittent hypoxia (IH) induce ROS. Although IH is important in clinical settings, the roles of IH-induced ROS in the airway repair process have not been investigated. In this study, we firstly showed that IH induced mitochondrial hydrogen peroxide (H2O2) production and significantly decreased bronchial epithelial cell migration, prevented by catalase treatment in a wound scratch assay. RhoA activity was higher during repair process in the IH condition compared to in the normoxic condition, resulting in the cellular morphological changes shown by immunofluorescence staining: round cells, reduced central stress fiber numbers, pronounced cortical actin filament distributions, and punctate focal adhesions. These phenotypes were replicated by exogenous H2O2 treatment under the normoxic condition. Our findings confirmed the transcription-independent role of IH-induced intracellular ROS in the bronchial epithelial cell repair process and might have significant implications for impaired bronchial epithelial cell regeneration. The airway epithelium acts as a frontline barrier against various environmental insults and its repair process after airway injury is critical for the lung homeostasis restoration. Recently, the role of intracellular reactive oxygen species (ROS) as transcription-independent damage signaling has been highlighted in the wound repair process. Both conditions of continuous hypoxia and intermittent hypoxia (IH) induce ROS. Although IH is important in clinical settings, the roles of IH-induced ROS in the airway repair process have not been investigated. In this study, we firstly showed that IH induced mitochondrial hydrogen peroxide (H2O2) production and significantly decreased bronchial epithelial cell migration, prevented by catalase treatment in a wound scratch assay. RhoA activity was higher during repair process in the IH condition compared to in the normoxic condition, resulting in the cellular morphological changes shown by immunofluorescence staining: round cells, reduced central stress fiber numbers, pronounced cortical actin filament distributions, and punctate focal adhesions. These phenotypes were replicated by exogenous H2O2 treatment under the normoxic condition. Our findings confirmed the transcription-independent role of IH-induced intracellular ROS in the bronchial epithelial cell repair process and might have significant implications for impaired bronchial epithelial cell regeneration. ROCK Elsevier HIF Elsevier HGF Elsevier MitoTEMPO Elsevier O2- Elsevier BEBM Elsevier DMEM Elsevier PEG Elsevier ANOVA Elsevier BEGM Elsevier FBS Elsevier H2O2 Elsevier NOX Elsevier ROS Elsevier DUOX Elsevier H2DCF-DA Elsevier SEM Elsevier DPI Elsevier PHBE Elsevier IH Elsevier Sato, Atsuyasu oth Hara-Chikuma, Mariko oth Satooka, Hiroki oth Hasegawa, Koichi oth Tanimura, Kazuya oth Tanizawa, Kiminobu oth Inouchi, Morito oth Handa, Tomohiro oth Oga, Toru oth Muro, Shigeo oth Mishima, Michiaki oth Chin, Kazuo oth Enthalten in Academic Press 72 OUTCOMES OF COMBINATION OF HEPATITIS B IMMUNOGLOBULIN AND HEPATITIS B VACCINATION IN HIGH-RISK NEWBORNS BORN TO HBEAG-POSITIVE MOTHERS 2012 ECR Orlando, Fla (DE-627)ELV011050691 volume:344 year:2016 number:1 day:15 month:05 pages:143-151 extent:9 https://doi.org/10.1016/j.yexcr.2016.04.006 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_70 44.44 Parasitologie Medizin VZ AR 344 2016 1 15 0515 143-151 9 045F 570 |
| allfields_unstemmed |
10.1016/j.yexcr.2016.04.006 doi GBVA2016021000016.pica (DE-627)ELV030077567 (ELSEVIER)S0014-4827(16)30075-1 DE-627 ger DE-627 rakwb eng 570 570 DE-600 610 VZ 610 VZ 44.44 bkl Hamada, Satoshi verfasserin aut Role of mitochondrial hydrogen peroxide induced by intermittent hypoxia in airway epithelial wound repair in vitro 2016transfer abstract 9 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The airway epithelium acts as a frontline barrier against various environmental insults and its repair process after airway injury is critical for the lung homeostasis restoration. Recently, the role of intracellular reactive oxygen species (ROS) as transcription-independent damage signaling has been highlighted in the wound repair process. Both conditions of continuous hypoxia and intermittent hypoxia (IH) induce ROS. Although IH is important in clinical settings, the roles of IH-induced ROS in the airway repair process have not been investigated. In this study, we firstly showed that IH induced mitochondrial hydrogen peroxide (H2O2) production and significantly decreased bronchial epithelial cell migration, prevented by catalase treatment in a wound scratch assay. RhoA activity was higher during repair process in the IH condition compared to in the normoxic condition, resulting in the cellular morphological changes shown by immunofluorescence staining: round cells, reduced central stress fiber numbers, pronounced cortical actin filament distributions, and punctate focal adhesions. These phenotypes were replicated by exogenous H2O2 treatment under the normoxic condition. Our findings confirmed the transcription-independent role of IH-induced intracellular ROS in the bronchial epithelial cell repair process and might have significant implications for impaired bronchial epithelial cell regeneration. The airway epithelium acts as a frontline barrier against various environmental insults and its repair process after airway injury is critical for the lung homeostasis restoration. Recently, the role of intracellular reactive oxygen species (ROS) as transcription-independent damage signaling has been highlighted in the wound repair process. Both conditions of continuous hypoxia and intermittent hypoxia (IH) induce ROS. Although IH is important in clinical settings, the roles of IH-induced ROS in the airway repair process have not been investigated. In this study, we firstly showed that IH induced mitochondrial hydrogen peroxide (H2O2) production and significantly decreased bronchial epithelial cell migration, prevented by catalase treatment in a wound scratch assay. RhoA activity was higher during repair process in the IH condition compared to in the normoxic condition, resulting in the cellular morphological changes shown by immunofluorescence staining: round cells, reduced central stress fiber numbers, pronounced cortical actin filament distributions, and punctate focal adhesions. These phenotypes were replicated by exogenous H2O2 treatment under the normoxic condition. Our findings confirmed the transcription-independent role of IH-induced intracellular ROS in the bronchial epithelial cell repair process and might have significant implications for impaired bronchial epithelial cell regeneration. ROCK Elsevier HIF Elsevier HGF Elsevier MitoTEMPO Elsevier O2- Elsevier BEBM Elsevier DMEM Elsevier PEG Elsevier ANOVA Elsevier BEGM Elsevier FBS Elsevier H2O2 Elsevier NOX Elsevier ROS Elsevier DUOX Elsevier H2DCF-DA Elsevier SEM Elsevier DPI Elsevier PHBE Elsevier IH Elsevier Sato, Atsuyasu oth Hara-Chikuma, Mariko oth Satooka, Hiroki oth Hasegawa, Koichi oth Tanimura, Kazuya oth Tanizawa, Kiminobu oth Inouchi, Morito oth Handa, Tomohiro oth Oga, Toru oth Muro, Shigeo oth Mishima, Michiaki oth Chin, Kazuo oth Enthalten in Academic Press 72 OUTCOMES OF COMBINATION OF HEPATITIS B IMMUNOGLOBULIN AND HEPATITIS B VACCINATION IN HIGH-RISK NEWBORNS BORN TO HBEAG-POSITIVE MOTHERS 2012 ECR Orlando, Fla (DE-627)ELV011050691 volume:344 year:2016 number:1 day:15 month:05 pages:143-151 extent:9 https://doi.org/10.1016/j.yexcr.2016.04.006 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_70 44.44 Parasitologie Medizin VZ AR 344 2016 1 15 0515 143-151 9 045F 570 |
| allfieldsGer |
10.1016/j.yexcr.2016.04.006 doi GBVA2016021000016.pica (DE-627)ELV030077567 (ELSEVIER)S0014-4827(16)30075-1 DE-627 ger DE-627 rakwb eng 570 570 DE-600 610 VZ 610 VZ 44.44 bkl Hamada, Satoshi verfasserin aut Role of mitochondrial hydrogen peroxide induced by intermittent hypoxia in airway epithelial wound repair in vitro 2016transfer abstract 9 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The airway epithelium acts as a frontline barrier against various environmental insults and its repair process after airway injury is critical for the lung homeostasis restoration. Recently, the role of intracellular reactive oxygen species (ROS) as transcription-independent damage signaling has been highlighted in the wound repair process. Both conditions of continuous hypoxia and intermittent hypoxia (IH) induce ROS. Although IH is important in clinical settings, the roles of IH-induced ROS in the airway repair process have not been investigated. In this study, we firstly showed that IH induced mitochondrial hydrogen peroxide (H2O2) production and significantly decreased bronchial epithelial cell migration, prevented by catalase treatment in a wound scratch assay. RhoA activity was higher during repair process in the IH condition compared to in the normoxic condition, resulting in the cellular morphological changes shown by immunofluorescence staining: round cells, reduced central stress fiber numbers, pronounced cortical actin filament distributions, and punctate focal adhesions. These phenotypes were replicated by exogenous H2O2 treatment under the normoxic condition. Our findings confirmed the transcription-independent role of IH-induced intracellular ROS in the bronchial epithelial cell repair process and might have significant implications for impaired bronchial epithelial cell regeneration. The airway epithelium acts as a frontline barrier against various environmental insults and its repair process after airway injury is critical for the lung homeostasis restoration. Recently, the role of intracellular reactive oxygen species (ROS) as transcription-independent damage signaling has been highlighted in the wound repair process. Both conditions of continuous hypoxia and intermittent hypoxia (IH) induce ROS. Although IH is important in clinical settings, the roles of IH-induced ROS in the airway repair process have not been investigated. In this study, we firstly showed that IH induced mitochondrial hydrogen peroxide (H2O2) production and significantly decreased bronchial epithelial cell migration, prevented by catalase treatment in a wound scratch assay. RhoA activity was higher during repair process in the IH condition compared to in the normoxic condition, resulting in the cellular morphological changes shown by immunofluorescence staining: round cells, reduced central stress fiber numbers, pronounced cortical actin filament distributions, and punctate focal adhesions. These phenotypes were replicated by exogenous H2O2 treatment under the normoxic condition. Our findings confirmed the transcription-independent role of IH-induced intracellular ROS in the bronchial epithelial cell repair process and might have significant implications for impaired bronchial epithelial cell regeneration. ROCK Elsevier HIF Elsevier HGF Elsevier MitoTEMPO Elsevier O2- Elsevier BEBM Elsevier DMEM Elsevier PEG Elsevier ANOVA Elsevier BEGM Elsevier FBS Elsevier H2O2 Elsevier NOX Elsevier ROS Elsevier DUOX Elsevier H2DCF-DA Elsevier SEM Elsevier DPI Elsevier PHBE Elsevier IH Elsevier Sato, Atsuyasu oth Hara-Chikuma, Mariko oth Satooka, Hiroki oth Hasegawa, Koichi oth Tanimura, Kazuya oth Tanizawa, Kiminobu oth Inouchi, Morito oth Handa, Tomohiro oth Oga, Toru oth Muro, Shigeo oth Mishima, Michiaki oth Chin, Kazuo oth Enthalten in Academic Press 72 OUTCOMES OF COMBINATION OF HEPATITIS B IMMUNOGLOBULIN AND HEPATITIS B VACCINATION IN HIGH-RISK NEWBORNS BORN TO HBEAG-POSITIVE MOTHERS 2012 ECR Orlando, Fla (DE-627)ELV011050691 volume:344 year:2016 number:1 day:15 month:05 pages:143-151 extent:9 https://doi.org/10.1016/j.yexcr.2016.04.006 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_70 44.44 Parasitologie Medizin VZ AR 344 2016 1 15 0515 143-151 9 045F 570 |
| allfieldsSound |
10.1016/j.yexcr.2016.04.006 doi GBVA2016021000016.pica (DE-627)ELV030077567 (ELSEVIER)S0014-4827(16)30075-1 DE-627 ger DE-627 rakwb eng 570 570 DE-600 610 VZ 610 VZ 44.44 bkl Hamada, Satoshi verfasserin aut Role of mitochondrial hydrogen peroxide induced by intermittent hypoxia in airway epithelial wound repair in vitro 2016transfer abstract 9 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The airway epithelium acts as a frontline barrier against various environmental insults and its repair process after airway injury is critical for the lung homeostasis restoration. Recently, the role of intracellular reactive oxygen species (ROS) as transcription-independent damage signaling has been highlighted in the wound repair process. Both conditions of continuous hypoxia and intermittent hypoxia (IH) induce ROS. Although IH is important in clinical settings, the roles of IH-induced ROS in the airway repair process have not been investigated. In this study, we firstly showed that IH induced mitochondrial hydrogen peroxide (H2O2) production and significantly decreased bronchial epithelial cell migration, prevented by catalase treatment in a wound scratch assay. RhoA activity was higher during repair process in the IH condition compared to in the normoxic condition, resulting in the cellular morphological changes shown by immunofluorescence staining: round cells, reduced central stress fiber numbers, pronounced cortical actin filament distributions, and punctate focal adhesions. These phenotypes were replicated by exogenous H2O2 treatment under the normoxic condition. Our findings confirmed the transcription-independent role of IH-induced intracellular ROS in the bronchial epithelial cell repair process and might have significant implications for impaired bronchial epithelial cell regeneration. The airway epithelium acts as a frontline barrier against various environmental insults and its repair process after airway injury is critical for the lung homeostasis restoration. Recently, the role of intracellular reactive oxygen species (ROS) as transcription-independent damage signaling has been highlighted in the wound repair process. Both conditions of continuous hypoxia and intermittent hypoxia (IH) induce ROS. Although IH is important in clinical settings, the roles of IH-induced ROS in the airway repair process have not been investigated. In this study, we firstly showed that IH induced mitochondrial hydrogen peroxide (H2O2) production and significantly decreased bronchial epithelial cell migration, prevented by catalase treatment in a wound scratch assay. RhoA activity was higher during repair process in the IH condition compared to in the normoxic condition, resulting in the cellular morphological changes shown by immunofluorescence staining: round cells, reduced central stress fiber numbers, pronounced cortical actin filament distributions, and punctate focal adhesions. These phenotypes were replicated by exogenous H2O2 treatment under the normoxic condition. Our findings confirmed the transcription-independent role of IH-induced intracellular ROS in the bronchial epithelial cell repair process and might have significant implications for impaired bronchial epithelial cell regeneration. ROCK Elsevier HIF Elsevier HGF Elsevier MitoTEMPO Elsevier O2- Elsevier BEBM Elsevier DMEM Elsevier PEG Elsevier ANOVA Elsevier BEGM Elsevier FBS Elsevier H2O2 Elsevier NOX Elsevier ROS Elsevier DUOX Elsevier H2DCF-DA Elsevier SEM Elsevier DPI Elsevier PHBE Elsevier IH Elsevier Sato, Atsuyasu oth Hara-Chikuma, Mariko oth Satooka, Hiroki oth Hasegawa, Koichi oth Tanimura, Kazuya oth Tanizawa, Kiminobu oth Inouchi, Morito oth Handa, Tomohiro oth Oga, Toru oth Muro, Shigeo oth Mishima, Michiaki oth Chin, Kazuo oth Enthalten in Academic Press 72 OUTCOMES OF COMBINATION OF HEPATITIS B IMMUNOGLOBULIN AND HEPATITIS B VACCINATION IN HIGH-RISK NEWBORNS BORN TO HBEAG-POSITIVE MOTHERS 2012 ECR Orlando, Fla (DE-627)ELV011050691 volume:344 year:2016 number:1 day:15 month:05 pages:143-151 extent:9 https://doi.org/10.1016/j.yexcr.2016.04.006 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_70 44.44 Parasitologie Medizin VZ AR 344 2016 1 15 0515 143-151 9 045F 570 |
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Enthalten in 72 OUTCOMES OF COMBINATION OF HEPATITIS B IMMUNOGLOBULIN AND HEPATITIS B VACCINATION IN HIGH-RISK NEWBORNS BORN TO HBEAG-POSITIVE MOTHERS Orlando, Fla volume:344 year:2016 number:1 day:15 month:05 pages:143-151 extent:9 |
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Role of mitochondrial hydrogen peroxide induced by intermittent hypoxia in airway epithelial wound repair in vitro |
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The airway epithelium acts as a frontline barrier against various environmental insults and its repair process after airway injury is critical for the lung homeostasis restoration. Recently, the role of intracellular reactive oxygen species (ROS) as transcription-independent damage signaling has been highlighted in the wound repair process. Both conditions of continuous hypoxia and intermittent hypoxia (IH) induce ROS. Although IH is important in clinical settings, the roles of IH-induced ROS in the airway repair process have not been investigated. In this study, we firstly showed that IH induced mitochondrial hydrogen peroxide (H2O2) production and significantly decreased bronchial epithelial cell migration, prevented by catalase treatment in a wound scratch assay. RhoA activity was higher during repair process in the IH condition compared to in the normoxic condition, resulting in the cellular morphological changes shown by immunofluorescence staining: round cells, reduced central stress fiber numbers, pronounced cortical actin filament distributions, and punctate focal adhesions. These phenotypes were replicated by exogenous H2O2 treatment under the normoxic condition. Our findings confirmed the transcription-independent role of IH-induced intracellular ROS in the bronchial epithelial cell repair process and might have significant implications for impaired bronchial epithelial cell regeneration. |
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The airway epithelium acts as a frontline barrier against various environmental insults and its repair process after airway injury is critical for the lung homeostasis restoration. Recently, the role of intracellular reactive oxygen species (ROS) as transcription-independent damage signaling has been highlighted in the wound repair process. Both conditions of continuous hypoxia and intermittent hypoxia (IH) induce ROS. Although IH is important in clinical settings, the roles of IH-induced ROS in the airway repair process have not been investigated. In this study, we firstly showed that IH induced mitochondrial hydrogen peroxide (H2O2) production and significantly decreased bronchial epithelial cell migration, prevented by catalase treatment in a wound scratch assay. RhoA activity was higher during repair process in the IH condition compared to in the normoxic condition, resulting in the cellular morphological changes shown by immunofluorescence staining: round cells, reduced central stress fiber numbers, pronounced cortical actin filament distributions, and punctate focal adhesions. These phenotypes were replicated by exogenous H2O2 treatment under the normoxic condition. Our findings confirmed the transcription-independent role of IH-induced intracellular ROS in the bronchial epithelial cell repair process and might have significant implications for impaired bronchial epithelial cell regeneration. |
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The airway epithelium acts as a frontline barrier against various environmental insults and its repair process after airway injury is critical for the lung homeostasis restoration. Recently, the role of intracellular reactive oxygen species (ROS) as transcription-independent damage signaling has been highlighted in the wound repair process. Both conditions of continuous hypoxia and intermittent hypoxia (IH) induce ROS. Although IH is important in clinical settings, the roles of IH-induced ROS in the airway repair process have not been investigated. In this study, we firstly showed that IH induced mitochondrial hydrogen peroxide (H2O2) production and significantly decreased bronchial epithelial cell migration, prevented by catalase treatment in a wound scratch assay. RhoA activity was higher during repair process in the IH condition compared to in the normoxic condition, resulting in the cellular morphological changes shown by immunofluorescence staining: round cells, reduced central stress fiber numbers, pronounced cortical actin filament distributions, and punctate focal adhesions. These phenotypes were replicated by exogenous H2O2 treatment under the normoxic condition. Our findings confirmed the transcription-independent role of IH-induced intracellular ROS in the bronchial epithelial cell repair process and might have significant implications for impaired bronchial epithelial cell regeneration. |
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In this study, we firstly showed that IH induced mitochondrial hydrogen peroxide (H2O2) production and significantly decreased bronchial epithelial cell migration, prevented by catalase treatment in a wound scratch assay. RhoA activity was higher during repair process in the IH condition compared to in the normoxic condition, resulting in the cellular morphological changes shown by immunofluorescence staining: round cells, reduced central stress fiber numbers, pronounced cortical actin filament distributions, and punctate focal adhesions. These phenotypes were replicated by exogenous H2O2 treatment under the normoxic condition. 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