Hyperoxia-induced macrophage dysfunction and acute lung injury are attenuated by modulation of α7nAChR via reduced HMGB1 hyperacetylation and release
Prolonged exposure to hyperoxia during mechanical ventilation (MV) can result in acute lung injury (ALI) and is associated with HMGB1 accumulation in the airways. The aim of this study was to determine whether modulation of α7 nicotinic acetylcholine receptor (α7nAChR) with either GTS-21 (partial ag...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Gauthier, Alex [verfasserIn] |
|---|
| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2018transfer abstract |
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| Übergeordnetes Werk: |
Enthalten in: New organic dyes with varied arylamine donors as effective co-sensitizers for ruthenium complex N719 in dye sensitized solar cells - Wu, Zhi-Sheng ELSEVIER, 2020, the official journal of the Oxygen Society, a constituent member of the International Society for Free Radical Research, New York, NY [u.a.] |
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| Übergeordnetes Werk: |
volume:120 ; year:2018 ; day:20 ; month:05 ; pages:88 |
| Links: |
|---|
| DOI / URN: |
10.1016/j.freeradbiomed.2018.04.292 |
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| 520 | |a Prolonged exposure to hyperoxia during mechanical ventilation (MV) can result in acute lung injury (ALI) and is associated with HMGB1 accumulation in the airways. The aim of this study was to determine whether modulation of α7 nicotinic acetylcholine receptor (α7nAChR) with either GTS-21 (partial agonist) or GAT107 (ago-PAM) could inhibit hyperoxia-induced HMGB1 accumulation in the airways and improve innate immunity and clinical outcomes. RAW 264.7 cells, treated with either GTS-21 or GAT107 in the presence of 95% O2 exhibited decreased levels of HMGB1 in culture media and enhanced phagocytic ability. Hyperacetylation of nuclear HMGB1 can lead to its release into the extracellular milieu and is observed in cells exposed to hyperoxia. Activation of α7nAChR is effective in reducing both hyperoxia-induced HMGB1 accumulation and hyperacetylation. To determine whether activation of α7nAChR-mediated macrophage function can be translated into clinical outcomes, mice were exposed to >99% O2 for 3 d with GTS-21 treatment. GTS-21 significantly decreased both the accumulation of airway levels and hyperacetylation of HMGB1, protein content and neutrophil infiltration. Therefore, α7nAChRs represent a possible pharmacological target for the treatment of HALI in patients receiving MV. | ||
| 520 | |a Prolonged exposure to hyperoxia during mechanical ventilation (MV) can result in acute lung injury (ALI) and is associated with HMGB1 accumulation in the airways. The aim of this study was to determine whether modulation of α7 nicotinic acetylcholine receptor (α7nAChR) with either GTS-21 (partial agonist) or GAT107 (ago-PAM) could inhibit hyperoxia-induced HMGB1 accumulation in the airways and improve innate immunity and clinical outcomes. RAW 264.7 cells, treated with either GTS-21 or GAT107 in the presence of 95% O2 exhibited decreased levels of HMGB1 in culture media and enhanced phagocytic ability. Hyperacetylation of nuclear HMGB1 can lead to its release into the extracellular milieu and is observed in cells exposed to hyperoxia. Activation of α7nAChR is effective in reducing both hyperoxia-induced HMGB1 accumulation and hyperacetylation. To determine whether activation of α7nAChR-mediated macrophage function can be translated into clinical outcomes, mice were exposed to >99% O2 for 3 d with GTS-21 treatment. GTS-21 significantly decreased both the accumulation of airway levels and hyperacetylation of HMGB1, protein content and neutrophil infiltration. Therefore, α7nAChRs represent a possible pharmacological target for the treatment of HALI in patients receiving MV. | ||
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| 700 | 1 | |a Thakur, Ganesh S. |4 oth | |
| 700 | 1 | |a Mantell, Lin |4 oth | |
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10.1016/j.freeradbiomed.2018.04.292 doi GBV00000000000233A.pica (DE-627)ELV04305689X (ELSEVIER)S0891-5849(18)30457-X DE-627 ger DE-627 rakwb eng 570 610 570 DE-600 610 DE-600 620 VZ 52.57 bkl 53.36 bkl Gauthier, Alex verfasserin aut Hyperoxia-induced macrophage dysfunction and acute lung injury are attenuated by modulation of α7nAChR via reduced HMGB1 hyperacetylation and release 2018transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Prolonged exposure to hyperoxia during mechanical ventilation (MV) can result in acute lung injury (ALI) and is associated with HMGB1 accumulation in the airways. The aim of this study was to determine whether modulation of α7 nicotinic acetylcholine receptor (α7nAChR) with either GTS-21 (partial agonist) or GAT107 (ago-PAM) could inhibit hyperoxia-induced HMGB1 accumulation in the airways and improve innate immunity and clinical outcomes. RAW 264.7 cells, treated with either GTS-21 or GAT107 in the presence of 95% O2 exhibited decreased levels of HMGB1 in culture media and enhanced phagocytic ability. Hyperacetylation of nuclear HMGB1 can lead to its release into the extracellular milieu and is observed in cells exposed to hyperoxia. Activation of α7nAChR is effective in reducing both hyperoxia-induced HMGB1 accumulation and hyperacetylation. To determine whether activation of α7nAChR-mediated macrophage function can be translated into clinical outcomes, mice were exposed to >99% O2 for 3 d with GTS-21 treatment. GTS-21 significantly decreased both the accumulation of airway levels and hyperacetylation of HMGB1, protein content and neutrophil infiltration. Therefore, α7nAChRs represent a possible pharmacological target for the treatment of HALI in patients receiving MV. Prolonged exposure to hyperoxia during mechanical ventilation (MV) can result in acute lung injury (ALI) and is associated with HMGB1 accumulation in the airways. The aim of this study was to determine whether modulation of α7 nicotinic acetylcholine receptor (α7nAChR) with either GTS-21 (partial agonist) or GAT107 (ago-PAM) could inhibit hyperoxia-induced HMGB1 accumulation in the airways and improve innate immunity and clinical outcomes. RAW 264.7 cells, treated with either GTS-21 or GAT107 in the presence of 95% O2 exhibited decreased levels of HMGB1 in culture media and enhanced phagocytic ability. Hyperacetylation of nuclear HMGB1 can lead to its release into the extracellular milieu and is observed in cells exposed to hyperoxia. Activation of α7nAChR is effective in reducing both hyperoxia-induced HMGB1 accumulation and hyperacetylation. To determine whether activation of α7nAChR-mediated macrophage function can be translated into clinical outcomes, mice were exposed to >99% O2 for 3 d with GTS-21 treatment. GTS-21 significantly decreased both the accumulation of airway levels and hyperacetylation of HMGB1, protein content and neutrophil infiltration. Therefore, α7nAChRs represent a possible pharmacological target for the treatment of HALI in patients receiving MV. Sitapara, Ravi oth Thakur, Ganesh S. oth Mantell, Lin oth Enthalten in Elsevier Wu, Zhi-Sheng ELSEVIER New organic dyes with varied arylamine donors as effective co-sensitizers for ruthenium complex N719 in dye sensitized solar cells 2020 the official journal of the Oxygen Society, a constituent member of the International Society for Free Radical Research New York, NY [u.a.] (DE-627)ELV003689417 volume:120 year:2018 day:20 month:05 pages:88 https://doi.org/10.1016/j.freeradbiomed.2018.04.292 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 52.57 Energiespeicherung VZ 53.36 Energiedirektumwandler elektrische Energiespeicher VZ AR 120 2018 20 0520 88 120.2018, S88- 045F 570 |
| spelling |
10.1016/j.freeradbiomed.2018.04.292 doi GBV00000000000233A.pica (DE-627)ELV04305689X (ELSEVIER)S0891-5849(18)30457-X DE-627 ger DE-627 rakwb eng 570 610 570 DE-600 610 DE-600 620 VZ 52.57 bkl 53.36 bkl Gauthier, Alex verfasserin aut Hyperoxia-induced macrophage dysfunction and acute lung injury are attenuated by modulation of α7nAChR via reduced HMGB1 hyperacetylation and release 2018transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Prolonged exposure to hyperoxia during mechanical ventilation (MV) can result in acute lung injury (ALI) and is associated with HMGB1 accumulation in the airways. The aim of this study was to determine whether modulation of α7 nicotinic acetylcholine receptor (α7nAChR) with either GTS-21 (partial agonist) or GAT107 (ago-PAM) could inhibit hyperoxia-induced HMGB1 accumulation in the airways and improve innate immunity and clinical outcomes. RAW 264.7 cells, treated with either GTS-21 or GAT107 in the presence of 95% O2 exhibited decreased levels of HMGB1 in culture media and enhanced phagocytic ability. Hyperacetylation of nuclear HMGB1 can lead to its release into the extracellular milieu and is observed in cells exposed to hyperoxia. Activation of α7nAChR is effective in reducing both hyperoxia-induced HMGB1 accumulation and hyperacetylation. To determine whether activation of α7nAChR-mediated macrophage function can be translated into clinical outcomes, mice were exposed to >99% O2 for 3 d with GTS-21 treatment. GTS-21 significantly decreased both the accumulation of airway levels and hyperacetylation of HMGB1, protein content and neutrophil infiltration. Therefore, α7nAChRs represent a possible pharmacological target for the treatment of HALI in patients receiving MV. Prolonged exposure to hyperoxia during mechanical ventilation (MV) can result in acute lung injury (ALI) and is associated with HMGB1 accumulation in the airways. The aim of this study was to determine whether modulation of α7 nicotinic acetylcholine receptor (α7nAChR) with either GTS-21 (partial agonist) or GAT107 (ago-PAM) could inhibit hyperoxia-induced HMGB1 accumulation in the airways and improve innate immunity and clinical outcomes. RAW 264.7 cells, treated with either GTS-21 or GAT107 in the presence of 95% O2 exhibited decreased levels of HMGB1 in culture media and enhanced phagocytic ability. Hyperacetylation of nuclear HMGB1 can lead to its release into the extracellular milieu and is observed in cells exposed to hyperoxia. Activation of α7nAChR is effective in reducing both hyperoxia-induced HMGB1 accumulation and hyperacetylation. To determine whether activation of α7nAChR-mediated macrophage function can be translated into clinical outcomes, mice were exposed to >99% O2 for 3 d with GTS-21 treatment. GTS-21 significantly decreased both the accumulation of airway levels and hyperacetylation of HMGB1, protein content and neutrophil infiltration. Therefore, α7nAChRs represent a possible pharmacological target for the treatment of HALI in patients receiving MV. Sitapara, Ravi oth Thakur, Ganesh S. oth Mantell, Lin oth Enthalten in Elsevier Wu, Zhi-Sheng ELSEVIER New organic dyes with varied arylamine donors as effective co-sensitizers for ruthenium complex N719 in dye sensitized solar cells 2020 the official journal of the Oxygen Society, a constituent member of the International Society for Free Radical Research New York, NY [u.a.] (DE-627)ELV003689417 volume:120 year:2018 day:20 month:05 pages:88 https://doi.org/10.1016/j.freeradbiomed.2018.04.292 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 52.57 Energiespeicherung VZ 53.36 Energiedirektumwandler elektrische Energiespeicher VZ AR 120 2018 20 0520 88 120.2018, S88- 045F 570 |
| allfields_unstemmed |
10.1016/j.freeradbiomed.2018.04.292 doi GBV00000000000233A.pica (DE-627)ELV04305689X (ELSEVIER)S0891-5849(18)30457-X DE-627 ger DE-627 rakwb eng 570 610 570 DE-600 610 DE-600 620 VZ 52.57 bkl 53.36 bkl Gauthier, Alex verfasserin aut Hyperoxia-induced macrophage dysfunction and acute lung injury are attenuated by modulation of α7nAChR via reduced HMGB1 hyperacetylation and release 2018transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Prolonged exposure to hyperoxia during mechanical ventilation (MV) can result in acute lung injury (ALI) and is associated with HMGB1 accumulation in the airways. The aim of this study was to determine whether modulation of α7 nicotinic acetylcholine receptor (α7nAChR) with either GTS-21 (partial agonist) or GAT107 (ago-PAM) could inhibit hyperoxia-induced HMGB1 accumulation in the airways and improve innate immunity and clinical outcomes. RAW 264.7 cells, treated with either GTS-21 or GAT107 in the presence of 95% O2 exhibited decreased levels of HMGB1 in culture media and enhanced phagocytic ability. Hyperacetylation of nuclear HMGB1 can lead to its release into the extracellular milieu and is observed in cells exposed to hyperoxia. Activation of α7nAChR is effective in reducing both hyperoxia-induced HMGB1 accumulation and hyperacetylation. To determine whether activation of α7nAChR-mediated macrophage function can be translated into clinical outcomes, mice were exposed to >99% O2 for 3 d with GTS-21 treatment. GTS-21 significantly decreased both the accumulation of airway levels and hyperacetylation of HMGB1, protein content and neutrophil infiltration. Therefore, α7nAChRs represent a possible pharmacological target for the treatment of HALI in patients receiving MV. Prolonged exposure to hyperoxia during mechanical ventilation (MV) can result in acute lung injury (ALI) and is associated with HMGB1 accumulation in the airways. The aim of this study was to determine whether modulation of α7 nicotinic acetylcholine receptor (α7nAChR) with either GTS-21 (partial agonist) or GAT107 (ago-PAM) could inhibit hyperoxia-induced HMGB1 accumulation in the airways and improve innate immunity and clinical outcomes. RAW 264.7 cells, treated with either GTS-21 or GAT107 in the presence of 95% O2 exhibited decreased levels of HMGB1 in culture media and enhanced phagocytic ability. Hyperacetylation of nuclear HMGB1 can lead to its release into the extracellular milieu and is observed in cells exposed to hyperoxia. Activation of α7nAChR is effective in reducing both hyperoxia-induced HMGB1 accumulation and hyperacetylation. To determine whether activation of α7nAChR-mediated macrophage function can be translated into clinical outcomes, mice were exposed to >99% O2 for 3 d with GTS-21 treatment. GTS-21 significantly decreased both the accumulation of airway levels and hyperacetylation of HMGB1, protein content and neutrophil infiltration. Therefore, α7nAChRs represent a possible pharmacological target for the treatment of HALI in patients receiving MV. Sitapara, Ravi oth Thakur, Ganesh S. oth Mantell, Lin oth Enthalten in Elsevier Wu, Zhi-Sheng ELSEVIER New organic dyes with varied arylamine donors as effective co-sensitizers for ruthenium complex N719 in dye sensitized solar cells 2020 the official journal of the Oxygen Society, a constituent member of the International Society for Free Radical Research New York, NY [u.a.] (DE-627)ELV003689417 volume:120 year:2018 day:20 month:05 pages:88 https://doi.org/10.1016/j.freeradbiomed.2018.04.292 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 52.57 Energiespeicherung VZ 53.36 Energiedirektumwandler elektrische Energiespeicher VZ AR 120 2018 20 0520 88 120.2018, S88- 045F 570 |
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10.1016/j.freeradbiomed.2018.04.292 doi GBV00000000000233A.pica (DE-627)ELV04305689X (ELSEVIER)S0891-5849(18)30457-X DE-627 ger DE-627 rakwb eng 570 610 570 DE-600 610 DE-600 620 VZ 52.57 bkl 53.36 bkl Gauthier, Alex verfasserin aut Hyperoxia-induced macrophage dysfunction and acute lung injury are attenuated by modulation of α7nAChR via reduced HMGB1 hyperacetylation and release 2018transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Prolonged exposure to hyperoxia during mechanical ventilation (MV) can result in acute lung injury (ALI) and is associated with HMGB1 accumulation in the airways. The aim of this study was to determine whether modulation of α7 nicotinic acetylcholine receptor (α7nAChR) with either GTS-21 (partial agonist) or GAT107 (ago-PAM) could inhibit hyperoxia-induced HMGB1 accumulation in the airways and improve innate immunity and clinical outcomes. RAW 264.7 cells, treated with either GTS-21 or GAT107 in the presence of 95% O2 exhibited decreased levels of HMGB1 in culture media and enhanced phagocytic ability. Hyperacetylation of nuclear HMGB1 can lead to its release into the extracellular milieu and is observed in cells exposed to hyperoxia. Activation of α7nAChR is effective in reducing both hyperoxia-induced HMGB1 accumulation and hyperacetylation. To determine whether activation of α7nAChR-mediated macrophage function can be translated into clinical outcomes, mice were exposed to >99% O2 for 3 d with GTS-21 treatment. GTS-21 significantly decreased both the accumulation of airway levels and hyperacetylation of HMGB1, protein content and neutrophil infiltration. Therefore, α7nAChRs represent a possible pharmacological target for the treatment of HALI in patients receiving MV. Prolonged exposure to hyperoxia during mechanical ventilation (MV) can result in acute lung injury (ALI) and is associated with HMGB1 accumulation in the airways. The aim of this study was to determine whether modulation of α7 nicotinic acetylcholine receptor (α7nAChR) with either GTS-21 (partial agonist) or GAT107 (ago-PAM) could inhibit hyperoxia-induced HMGB1 accumulation in the airways and improve innate immunity and clinical outcomes. RAW 264.7 cells, treated with either GTS-21 or GAT107 in the presence of 95% O2 exhibited decreased levels of HMGB1 in culture media and enhanced phagocytic ability. Hyperacetylation of nuclear HMGB1 can lead to its release into the extracellular milieu and is observed in cells exposed to hyperoxia. Activation of α7nAChR is effective in reducing both hyperoxia-induced HMGB1 accumulation and hyperacetylation. To determine whether activation of α7nAChR-mediated macrophage function can be translated into clinical outcomes, mice were exposed to >99% O2 for 3 d with GTS-21 treatment. GTS-21 significantly decreased both the accumulation of airway levels and hyperacetylation of HMGB1, protein content and neutrophil infiltration. Therefore, α7nAChRs represent a possible pharmacological target for the treatment of HALI in patients receiving MV. Sitapara, Ravi oth Thakur, Ganesh S. oth Mantell, Lin oth Enthalten in Elsevier Wu, Zhi-Sheng ELSEVIER New organic dyes with varied arylamine donors as effective co-sensitizers for ruthenium complex N719 in dye sensitized solar cells 2020 the official journal of the Oxygen Society, a constituent member of the International Society for Free Radical Research New York, NY [u.a.] (DE-627)ELV003689417 volume:120 year:2018 day:20 month:05 pages:88 https://doi.org/10.1016/j.freeradbiomed.2018.04.292 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 52.57 Energiespeicherung VZ 53.36 Energiedirektumwandler elektrische Energiespeicher VZ AR 120 2018 20 0520 88 120.2018, S88- 045F 570 |
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10.1016/j.freeradbiomed.2018.04.292 doi GBV00000000000233A.pica (DE-627)ELV04305689X (ELSEVIER)S0891-5849(18)30457-X DE-627 ger DE-627 rakwb eng 570 610 570 DE-600 610 DE-600 620 VZ 52.57 bkl 53.36 bkl Gauthier, Alex verfasserin aut Hyperoxia-induced macrophage dysfunction and acute lung injury are attenuated by modulation of α7nAChR via reduced HMGB1 hyperacetylation and release 2018transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Prolonged exposure to hyperoxia during mechanical ventilation (MV) can result in acute lung injury (ALI) and is associated with HMGB1 accumulation in the airways. The aim of this study was to determine whether modulation of α7 nicotinic acetylcholine receptor (α7nAChR) with either GTS-21 (partial agonist) or GAT107 (ago-PAM) could inhibit hyperoxia-induced HMGB1 accumulation in the airways and improve innate immunity and clinical outcomes. RAW 264.7 cells, treated with either GTS-21 or GAT107 in the presence of 95% O2 exhibited decreased levels of HMGB1 in culture media and enhanced phagocytic ability. Hyperacetylation of nuclear HMGB1 can lead to its release into the extracellular milieu and is observed in cells exposed to hyperoxia. Activation of α7nAChR is effective in reducing both hyperoxia-induced HMGB1 accumulation and hyperacetylation. To determine whether activation of α7nAChR-mediated macrophage function can be translated into clinical outcomes, mice were exposed to >99% O2 for 3 d with GTS-21 treatment. GTS-21 significantly decreased both the accumulation of airway levels and hyperacetylation of HMGB1, protein content and neutrophil infiltration. Therefore, α7nAChRs represent a possible pharmacological target for the treatment of HALI in patients receiving MV. Prolonged exposure to hyperoxia during mechanical ventilation (MV) can result in acute lung injury (ALI) and is associated with HMGB1 accumulation in the airways. The aim of this study was to determine whether modulation of α7 nicotinic acetylcholine receptor (α7nAChR) with either GTS-21 (partial agonist) or GAT107 (ago-PAM) could inhibit hyperoxia-induced HMGB1 accumulation in the airways and improve innate immunity and clinical outcomes. RAW 264.7 cells, treated with either GTS-21 or GAT107 in the presence of 95% O2 exhibited decreased levels of HMGB1 in culture media and enhanced phagocytic ability. Hyperacetylation of nuclear HMGB1 can lead to its release into the extracellular milieu and is observed in cells exposed to hyperoxia. Activation of α7nAChR is effective in reducing both hyperoxia-induced HMGB1 accumulation and hyperacetylation. To determine whether activation of α7nAChR-mediated macrophage function can be translated into clinical outcomes, mice were exposed to >99% O2 for 3 d with GTS-21 treatment. GTS-21 significantly decreased both the accumulation of airway levels and hyperacetylation of HMGB1, protein content and neutrophil infiltration. Therefore, α7nAChRs represent a possible pharmacological target for the treatment of HALI in patients receiving MV. Sitapara, Ravi oth Thakur, Ganesh S. oth Mantell, Lin oth Enthalten in Elsevier Wu, Zhi-Sheng ELSEVIER New organic dyes with varied arylamine donors as effective co-sensitizers for ruthenium complex N719 in dye sensitized solar cells 2020 the official journal of the Oxygen Society, a constituent member of the International Society for Free Radical Research New York, NY [u.a.] (DE-627)ELV003689417 volume:120 year:2018 day:20 month:05 pages:88 https://doi.org/10.1016/j.freeradbiomed.2018.04.292 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 52.57 Energiespeicherung VZ 53.36 Energiedirektumwandler elektrische Energiespeicher VZ AR 120 2018 20 0520 88 120.2018, S88- 045F 570 |
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Enthalten in New organic dyes with varied arylamine donors as effective co-sensitizers for ruthenium complex N719 in dye sensitized solar cells New York, NY [u.a.] volume:120 year:2018 day:20 month:05 pages:88 |
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Enthalten in New organic dyes with varied arylamine donors as effective co-sensitizers for ruthenium complex N719 in dye sensitized solar cells New York, NY [u.a.] volume:120 year:2018 day:20 month:05 pages:88 |
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New organic dyes with varied arylamine donors as effective co-sensitizers for ruthenium complex N719 in dye sensitized solar cells |
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hyperoxia-induced macrophage dysfunction and acute lung injury are attenuated by modulation of α7nachr via reduced hmgb1 hyperacetylation and release |
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Hyperoxia-induced macrophage dysfunction and acute lung injury are attenuated by modulation of α7nAChR via reduced HMGB1 hyperacetylation and release |
| abstract |
Prolonged exposure to hyperoxia during mechanical ventilation (MV) can result in acute lung injury (ALI) and is associated with HMGB1 accumulation in the airways. The aim of this study was to determine whether modulation of α7 nicotinic acetylcholine receptor (α7nAChR) with either GTS-21 (partial agonist) or GAT107 (ago-PAM) could inhibit hyperoxia-induced HMGB1 accumulation in the airways and improve innate immunity and clinical outcomes. RAW 264.7 cells, treated with either GTS-21 or GAT107 in the presence of 95% O2 exhibited decreased levels of HMGB1 in culture media and enhanced phagocytic ability. Hyperacetylation of nuclear HMGB1 can lead to its release into the extracellular milieu and is observed in cells exposed to hyperoxia. Activation of α7nAChR is effective in reducing both hyperoxia-induced HMGB1 accumulation and hyperacetylation. To determine whether activation of α7nAChR-mediated macrophage function can be translated into clinical outcomes, mice were exposed to >99% O2 for 3 d with GTS-21 treatment. GTS-21 significantly decreased both the accumulation of airway levels and hyperacetylation of HMGB1, protein content and neutrophil infiltration. Therefore, α7nAChRs represent a possible pharmacological target for the treatment of HALI in patients receiving MV. |
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Prolonged exposure to hyperoxia during mechanical ventilation (MV) can result in acute lung injury (ALI) and is associated with HMGB1 accumulation in the airways. The aim of this study was to determine whether modulation of α7 nicotinic acetylcholine receptor (α7nAChR) with either GTS-21 (partial agonist) or GAT107 (ago-PAM) could inhibit hyperoxia-induced HMGB1 accumulation in the airways and improve innate immunity and clinical outcomes. RAW 264.7 cells, treated with either GTS-21 or GAT107 in the presence of 95% O2 exhibited decreased levels of HMGB1 in culture media and enhanced phagocytic ability. Hyperacetylation of nuclear HMGB1 can lead to its release into the extracellular milieu and is observed in cells exposed to hyperoxia. Activation of α7nAChR is effective in reducing both hyperoxia-induced HMGB1 accumulation and hyperacetylation. To determine whether activation of α7nAChR-mediated macrophage function can be translated into clinical outcomes, mice were exposed to >99% O2 for 3 d with GTS-21 treatment. GTS-21 significantly decreased both the accumulation of airway levels and hyperacetylation of HMGB1, protein content and neutrophil infiltration. Therefore, α7nAChRs represent a possible pharmacological target for the treatment of HALI in patients receiving MV. |
| abstract_unstemmed |
Prolonged exposure to hyperoxia during mechanical ventilation (MV) can result in acute lung injury (ALI) and is associated with HMGB1 accumulation in the airways. The aim of this study was to determine whether modulation of α7 nicotinic acetylcholine receptor (α7nAChR) with either GTS-21 (partial agonist) or GAT107 (ago-PAM) could inhibit hyperoxia-induced HMGB1 accumulation in the airways and improve innate immunity and clinical outcomes. RAW 264.7 cells, treated with either GTS-21 or GAT107 in the presence of 95% O2 exhibited decreased levels of HMGB1 in culture media and enhanced phagocytic ability. Hyperacetylation of nuclear HMGB1 can lead to its release into the extracellular milieu and is observed in cells exposed to hyperoxia. Activation of α7nAChR is effective in reducing both hyperoxia-induced HMGB1 accumulation and hyperacetylation. To determine whether activation of α7nAChR-mediated macrophage function can be translated into clinical outcomes, mice were exposed to >99% O2 for 3 d with GTS-21 treatment. GTS-21 significantly decreased both the accumulation of airway levels and hyperacetylation of HMGB1, protein content and neutrophil infiltration. Therefore, α7nAChRs represent a possible pharmacological target for the treatment of HALI in patients receiving MV. |
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Hyperoxia-induced macrophage dysfunction and acute lung injury are attenuated by modulation of α7nAChR via reduced HMGB1 hyperacetylation and release |
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