NADPH oxidase 5 promotes proliferation and fibrosis in human hepatic stellate cells
NADPH oxidase (Nox) variants Nox1, Nox2 and Nox4 are implicated in the progression of liver fibrosis. However, the role of Nox5 is not yet known, mainly due to the lack of this enzyme in rat and mouse genomes. Here we describe the expression and functional relevance of Nox5 in the human cell line of...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Andueza, Aitor [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2018transfer abstract |
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| Schlagwörter: |
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| Umfang: |
12 |
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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.] |
|---|---|
| Übergeordnetes Werk: |
volume:126 ; year:2018 ; pages:15-26 ; extent:12 |
| Links: |
|---|
| DOI / URN: |
10.1016/j.freeradbiomed.2018.07.013 |
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ELV044245874 |
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| 520 | |a NADPH oxidase (Nox) variants Nox1, Nox2 and Nox4 are implicated in the progression of liver fibrosis. However, the role of Nox5 is not yet known, mainly due to the lack of this enzyme in rat and mouse genomes. Here we describe the expression and functional relevance of Nox5 in the human cell line of hepatic stellate cells (HSC) LX-2. Under basal conditions, three long (Nox5-L: Nox5α, -β, and -δ) and a short (Nox5-S or Nox5ε) splice variants were detected, which were silenced with specific siRNAs for Nox5. The most abundant isoform was Nox5-S, accounting for more than 90% of Nox5 protein. Overexpression of Nox5β generated reactive oxygen species (ROS) in the presence of calcium, as judged by the production of hydrogen peroxide, L-012 luminescence and cytochrome c reduction. Nox5ε did not generated ROS under these conditions, and a reduced ROS production was observed when co-expressed with Nox5β. In contrast, dihydroethidium oxidation was increased by Nox5β or Nox5ε, suggesting that Nox5ε induced intracellular oxidative stress by an unknown mechanism. Functional studies showed that both Nox5β and Nox5ε stimulated the proliferation of LX-2 cells and the collagen type I levels, while Nox5 siRNAs inhibited these effects. Interestingly, TGF-β and angiotensin II upregulated Nox5 expression, which was reduced in cells pre-incubated with catalase. Further studies silencing Nox5 in TGF-β-treated cells resulted in a reduction of collagen levels via p38 MAPK. Collectively, these results show for the first time that Nox5 can play a relevant role in the proliferation and fibrosis on human HSC. | ||
| 520 | |a NADPH oxidase (Nox) variants Nox1, Nox2 and Nox4 are implicated in the progression of liver fibrosis. However, the role of Nox5 is not yet known, mainly due to the lack of this enzyme in rat and mouse genomes. Here we describe the expression and functional relevance of Nox5 in the human cell line of hepatic stellate cells (HSC) LX-2. Under basal conditions, three long (Nox5-L: Nox5α, -β, and -δ) and a short (Nox5-S or Nox5ε) splice variants were detected, which were silenced with specific siRNAs for Nox5. The most abundant isoform was Nox5-S, accounting for more than 90% of Nox5 protein. Overexpression of Nox5β generated reactive oxygen species (ROS) in the presence of calcium, as judged by the production of hydrogen peroxide, L-012 luminescence and cytochrome c reduction. Nox5ε did not generated ROS under these conditions, and a reduced ROS production was observed when co-expressed with Nox5β. In contrast, dihydroethidium oxidation was increased by Nox5β or Nox5ε, suggesting that Nox5ε induced intracellular oxidative stress by an unknown mechanism. Functional studies showed that both Nox5β and Nox5ε stimulated the proliferation of LX-2 cells and the collagen type I levels, while Nox5 siRNAs inhibited these effects. Interestingly, TGF-β and angiotensin II upregulated Nox5 expression, which was reduced in cells pre-incubated with catalase. Further studies silencing Nox5 in TGF-β-treated cells resulted in a reduction of collagen levels via p38 MAPK. Collectively, these results show for the first time that Nox5 can play a relevant role in the proliferation and fibrosis on human HSC. | ||
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10.1016/j.freeradbiomed.2018.07.013 doi GBV00000000000586.pica (DE-627)ELV044245874 (ELSEVIER)S0891-5849(18)31255-3 DE-627 ger DE-627 rakwb eng 620 VZ 52.57 bkl 53.36 bkl Andueza, Aitor verfasserin aut NADPH oxidase 5 promotes proliferation and fibrosis in human hepatic stellate cells 2018transfer abstract 12 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier NADPH oxidase (Nox) variants Nox1, Nox2 and Nox4 are implicated in the progression of liver fibrosis. However, the role of Nox5 is not yet known, mainly due to the lack of this enzyme in rat and mouse genomes. Here we describe the expression and functional relevance of Nox5 in the human cell line of hepatic stellate cells (HSC) LX-2. Under basal conditions, three long (Nox5-L: Nox5α, -β, and -δ) and a short (Nox5-S or Nox5ε) splice variants were detected, which were silenced with specific siRNAs for Nox5. The most abundant isoform was Nox5-S, accounting for more than 90% of Nox5 protein. Overexpression of Nox5β generated reactive oxygen species (ROS) in the presence of calcium, as judged by the production of hydrogen peroxide, L-012 luminescence and cytochrome c reduction. Nox5ε did not generated ROS under these conditions, and a reduced ROS production was observed when co-expressed with Nox5β. In contrast, dihydroethidium oxidation was increased by Nox5β or Nox5ε, suggesting that Nox5ε induced intracellular oxidative stress by an unknown mechanism. Functional studies showed that both Nox5β and Nox5ε stimulated the proliferation of LX-2 cells and the collagen type I levels, while Nox5 siRNAs inhibited these effects. Interestingly, TGF-β and angiotensin II upregulated Nox5 expression, which was reduced in cells pre-incubated with catalase. Further studies silencing Nox5 in TGF-β-treated cells resulted in a reduction of collagen levels via p38 MAPK. Collectively, these results show for the first time that Nox5 can play a relevant role in the proliferation and fibrosis on human HSC. NADPH oxidase (Nox) variants Nox1, Nox2 and Nox4 are implicated in the progression of liver fibrosis. However, the role of Nox5 is not yet known, mainly due to the lack of this enzyme in rat and mouse genomes. Here we describe the expression and functional relevance of Nox5 in the human cell line of hepatic stellate cells (HSC) LX-2. Under basal conditions, three long (Nox5-L: Nox5α, -β, and -δ) and a short (Nox5-S or Nox5ε) splice variants were detected, which were silenced with specific siRNAs for Nox5. The most abundant isoform was Nox5-S, accounting for more than 90% of Nox5 protein. Overexpression of Nox5β generated reactive oxygen species (ROS) in the presence of calcium, as judged by the production of hydrogen peroxide, L-012 luminescence and cytochrome c reduction. Nox5ε did not generated ROS under these conditions, and a reduced ROS production was observed when co-expressed with Nox5β. In contrast, dihydroethidium oxidation was increased by Nox5β or Nox5ε, suggesting that Nox5ε induced intracellular oxidative stress by an unknown mechanism. Functional studies showed that both Nox5β and Nox5ε stimulated the proliferation of LX-2 cells and the collagen type I levels, while Nox5 siRNAs inhibited these effects. Interestingly, TGF-β and angiotensin II upregulated Nox5 expression, which was reduced in cells pre-incubated with catalase. Further studies silencing Nox5 in TGF-β-treated cells resulted in a reduction of collagen levels via p38 MAPK. Collectively, these results show for the first time that Nox5 can play a relevant role in the proliferation and fibrosis on human HSC. DHE Elsevier Iono Elsevier PMA Elsevier MOI Elsevier HRP Elsevier AdNox5β Elsevier Cyt c Elsevier SOD Elsevier Ang II Elsevier GFP Elsevier Nox5-L Elsevier LX-2 Elsevier Nox Elsevier RACE Elsevier ROS Elsevier HSC Elsevier TGF-β Elsevier HBSS Elsevier Nox5-S or Nox5ε Elsevier siNox5 Elsevier Garde, Naiara oth García-Garzón, Antonia oth Ansorena, Eduardo oth López-Zabalza, María J. oth Iraburu, María J. oth Zalba, Guillermo oth Martínez-Irujo, Juan J. 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:126 year:2018 pages:15-26 extent:12 https://doi.org/10.1016/j.freeradbiomed.2018.07.013 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 52.57 Energiespeicherung VZ 53.36 Energiedirektumwandler elektrische Energiespeicher VZ AR 126 2018 15-26 12 |
| spelling |
10.1016/j.freeradbiomed.2018.07.013 doi GBV00000000000586.pica (DE-627)ELV044245874 (ELSEVIER)S0891-5849(18)31255-3 DE-627 ger DE-627 rakwb eng 620 VZ 52.57 bkl 53.36 bkl Andueza, Aitor verfasserin aut NADPH oxidase 5 promotes proliferation and fibrosis in human hepatic stellate cells 2018transfer abstract 12 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier NADPH oxidase (Nox) variants Nox1, Nox2 and Nox4 are implicated in the progression of liver fibrosis. However, the role of Nox5 is not yet known, mainly due to the lack of this enzyme in rat and mouse genomes. Here we describe the expression and functional relevance of Nox5 in the human cell line of hepatic stellate cells (HSC) LX-2. Under basal conditions, three long (Nox5-L: Nox5α, -β, and -δ) and a short (Nox5-S or Nox5ε) splice variants were detected, which were silenced with specific siRNAs for Nox5. The most abundant isoform was Nox5-S, accounting for more than 90% of Nox5 protein. Overexpression of Nox5β generated reactive oxygen species (ROS) in the presence of calcium, as judged by the production of hydrogen peroxide, L-012 luminescence and cytochrome c reduction. Nox5ε did not generated ROS under these conditions, and a reduced ROS production was observed when co-expressed with Nox5β. In contrast, dihydroethidium oxidation was increased by Nox5β or Nox5ε, suggesting that Nox5ε induced intracellular oxidative stress by an unknown mechanism. Functional studies showed that both Nox5β and Nox5ε stimulated the proliferation of LX-2 cells and the collagen type I levels, while Nox5 siRNAs inhibited these effects. Interestingly, TGF-β and angiotensin II upregulated Nox5 expression, which was reduced in cells pre-incubated with catalase. Further studies silencing Nox5 in TGF-β-treated cells resulted in a reduction of collagen levels via p38 MAPK. Collectively, these results show for the first time that Nox5 can play a relevant role in the proliferation and fibrosis on human HSC. NADPH oxidase (Nox) variants Nox1, Nox2 and Nox4 are implicated in the progression of liver fibrosis. However, the role of Nox5 is not yet known, mainly due to the lack of this enzyme in rat and mouse genomes. Here we describe the expression and functional relevance of Nox5 in the human cell line of hepatic stellate cells (HSC) LX-2. Under basal conditions, three long (Nox5-L: Nox5α, -β, and -δ) and a short (Nox5-S or Nox5ε) splice variants were detected, which were silenced with specific siRNAs for Nox5. The most abundant isoform was Nox5-S, accounting for more than 90% of Nox5 protein. Overexpression of Nox5β generated reactive oxygen species (ROS) in the presence of calcium, as judged by the production of hydrogen peroxide, L-012 luminescence and cytochrome c reduction. Nox5ε did not generated ROS under these conditions, and a reduced ROS production was observed when co-expressed with Nox5β. In contrast, dihydroethidium oxidation was increased by Nox5β or Nox5ε, suggesting that Nox5ε induced intracellular oxidative stress by an unknown mechanism. Functional studies showed that both Nox5β and Nox5ε stimulated the proliferation of LX-2 cells and the collagen type I levels, while Nox5 siRNAs inhibited these effects. Interestingly, TGF-β and angiotensin II upregulated Nox5 expression, which was reduced in cells pre-incubated with catalase. Further studies silencing Nox5 in TGF-β-treated cells resulted in a reduction of collagen levels via p38 MAPK. Collectively, these results show for the first time that Nox5 can play a relevant role in the proliferation and fibrosis on human HSC. DHE Elsevier Iono Elsevier PMA Elsevier MOI Elsevier HRP Elsevier AdNox5β Elsevier Cyt c Elsevier SOD Elsevier Ang II Elsevier GFP Elsevier Nox5-L Elsevier LX-2 Elsevier Nox Elsevier RACE Elsevier ROS Elsevier HSC Elsevier TGF-β Elsevier HBSS Elsevier Nox5-S or Nox5ε Elsevier siNox5 Elsevier Garde, Naiara oth García-Garzón, Antonia oth Ansorena, Eduardo oth López-Zabalza, María J. oth Iraburu, María J. oth Zalba, Guillermo oth Martínez-Irujo, Juan J. 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:126 year:2018 pages:15-26 extent:12 https://doi.org/10.1016/j.freeradbiomed.2018.07.013 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 52.57 Energiespeicherung VZ 53.36 Energiedirektumwandler elektrische Energiespeicher VZ AR 126 2018 15-26 12 |
| allfields_unstemmed |
10.1016/j.freeradbiomed.2018.07.013 doi GBV00000000000586.pica (DE-627)ELV044245874 (ELSEVIER)S0891-5849(18)31255-3 DE-627 ger DE-627 rakwb eng 620 VZ 52.57 bkl 53.36 bkl Andueza, Aitor verfasserin aut NADPH oxidase 5 promotes proliferation and fibrosis in human hepatic stellate cells 2018transfer abstract 12 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier NADPH oxidase (Nox) variants Nox1, Nox2 and Nox4 are implicated in the progression of liver fibrosis. However, the role of Nox5 is not yet known, mainly due to the lack of this enzyme in rat and mouse genomes. Here we describe the expression and functional relevance of Nox5 in the human cell line of hepatic stellate cells (HSC) LX-2. Under basal conditions, three long (Nox5-L: Nox5α, -β, and -δ) and a short (Nox5-S or Nox5ε) splice variants were detected, which were silenced with specific siRNAs for Nox5. The most abundant isoform was Nox5-S, accounting for more than 90% of Nox5 protein. Overexpression of Nox5β generated reactive oxygen species (ROS) in the presence of calcium, as judged by the production of hydrogen peroxide, L-012 luminescence and cytochrome c reduction. Nox5ε did not generated ROS under these conditions, and a reduced ROS production was observed when co-expressed with Nox5β. In contrast, dihydroethidium oxidation was increased by Nox5β or Nox5ε, suggesting that Nox5ε induced intracellular oxidative stress by an unknown mechanism. Functional studies showed that both Nox5β and Nox5ε stimulated the proliferation of LX-2 cells and the collagen type I levels, while Nox5 siRNAs inhibited these effects. Interestingly, TGF-β and angiotensin II upregulated Nox5 expression, which was reduced in cells pre-incubated with catalase. Further studies silencing Nox5 in TGF-β-treated cells resulted in a reduction of collagen levels via p38 MAPK. Collectively, these results show for the first time that Nox5 can play a relevant role in the proliferation and fibrosis on human HSC. NADPH oxidase (Nox) variants Nox1, Nox2 and Nox4 are implicated in the progression of liver fibrosis. However, the role of Nox5 is not yet known, mainly due to the lack of this enzyme in rat and mouse genomes. Here we describe the expression and functional relevance of Nox5 in the human cell line of hepatic stellate cells (HSC) LX-2. Under basal conditions, three long (Nox5-L: Nox5α, -β, and -δ) and a short (Nox5-S or Nox5ε) splice variants were detected, which were silenced with specific siRNAs for Nox5. The most abundant isoform was Nox5-S, accounting for more than 90% of Nox5 protein. Overexpression of Nox5β generated reactive oxygen species (ROS) in the presence of calcium, as judged by the production of hydrogen peroxide, L-012 luminescence and cytochrome c reduction. Nox5ε did not generated ROS under these conditions, and a reduced ROS production was observed when co-expressed with Nox5β. In contrast, dihydroethidium oxidation was increased by Nox5β or Nox5ε, suggesting that Nox5ε induced intracellular oxidative stress by an unknown mechanism. Functional studies showed that both Nox5β and Nox5ε stimulated the proliferation of LX-2 cells and the collagen type I levels, while Nox5 siRNAs inhibited these effects. Interestingly, TGF-β and angiotensin II upregulated Nox5 expression, which was reduced in cells pre-incubated with catalase. Further studies silencing Nox5 in TGF-β-treated cells resulted in a reduction of collagen levels via p38 MAPK. Collectively, these results show for the first time that Nox5 can play a relevant role in the proliferation and fibrosis on human HSC. DHE Elsevier Iono Elsevier PMA Elsevier MOI Elsevier HRP Elsevier AdNox5β Elsevier Cyt c Elsevier SOD Elsevier Ang II Elsevier GFP Elsevier Nox5-L Elsevier LX-2 Elsevier Nox Elsevier RACE Elsevier ROS Elsevier HSC Elsevier TGF-β Elsevier HBSS Elsevier Nox5-S or Nox5ε Elsevier siNox5 Elsevier Garde, Naiara oth García-Garzón, Antonia oth Ansorena, Eduardo oth López-Zabalza, María J. oth Iraburu, María J. oth Zalba, Guillermo oth Martínez-Irujo, Juan J. 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:126 year:2018 pages:15-26 extent:12 https://doi.org/10.1016/j.freeradbiomed.2018.07.013 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 52.57 Energiespeicherung VZ 53.36 Energiedirektumwandler elektrische Energiespeicher VZ AR 126 2018 15-26 12 |
| allfieldsGer |
10.1016/j.freeradbiomed.2018.07.013 doi GBV00000000000586.pica (DE-627)ELV044245874 (ELSEVIER)S0891-5849(18)31255-3 DE-627 ger DE-627 rakwb eng 620 VZ 52.57 bkl 53.36 bkl Andueza, Aitor verfasserin aut NADPH oxidase 5 promotes proliferation and fibrosis in human hepatic stellate cells 2018transfer abstract 12 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier NADPH oxidase (Nox) variants Nox1, Nox2 and Nox4 are implicated in the progression of liver fibrosis. However, the role of Nox5 is not yet known, mainly due to the lack of this enzyme in rat and mouse genomes. Here we describe the expression and functional relevance of Nox5 in the human cell line of hepatic stellate cells (HSC) LX-2. Under basal conditions, three long (Nox5-L: Nox5α, -β, and -δ) and a short (Nox5-S or Nox5ε) splice variants were detected, which were silenced with specific siRNAs for Nox5. The most abundant isoform was Nox5-S, accounting for more than 90% of Nox5 protein. Overexpression of Nox5β generated reactive oxygen species (ROS) in the presence of calcium, as judged by the production of hydrogen peroxide, L-012 luminescence and cytochrome c reduction. Nox5ε did not generated ROS under these conditions, and a reduced ROS production was observed when co-expressed with Nox5β. In contrast, dihydroethidium oxidation was increased by Nox5β or Nox5ε, suggesting that Nox5ε induced intracellular oxidative stress by an unknown mechanism. Functional studies showed that both Nox5β and Nox5ε stimulated the proliferation of LX-2 cells and the collagen type I levels, while Nox5 siRNAs inhibited these effects. Interestingly, TGF-β and angiotensin II upregulated Nox5 expression, which was reduced in cells pre-incubated with catalase. Further studies silencing Nox5 in TGF-β-treated cells resulted in a reduction of collagen levels via p38 MAPK. Collectively, these results show for the first time that Nox5 can play a relevant role in the proliferation and fibrosis on human HSC. NADPH oxidase (Nox) variants Nox1, Nox2 and Nox4 are implicated in the progression of liver fibrosis. However, the role of Nox5 is not yet known, mainly due to the lack of this enzyme in rat and mouse genomes. Here we describe the expression and functional relevance of Nox5 in the human cell line of hepatic stellate cells (HSC) LX-2. Under basal conditions, three long (Nox5-L: Nox5α, -β, and -δ) and a short (Nox5-S or Nox5ε) splice variants were detected, which were silenced with specific siRNAs for Nox5. The most abundant isoform was Nox5-S, accounting for more than 90% of Nox5 protein. Overexpression of Nox5β generated reactive oxygen species (ROS) in the presence of calcium, as judged by the production of hydrogen peroxide, L-012 luminescence and cytochrome c reduction. Nox5ε did not generated ROS under these conditions, and a reduced ROS production was observed when co-expressed with Nox5β. In contrast, dihydroethidium oxidation was increased by Nox5β or Nox5ε, suggesting that Nox5ε induced intracellular oxidative stress by an unknown mechanism. Functional studies showed that both Nox5β and Nox5ε stimulated the proliferation of LX-2 cells and the collagen type I levels, while Nox5 siRNAs inhibited these effects. Interestingly, TGF-β and angiotensin II upregulated Nox5 expression, which was reduced in cells pre-incubated with catalase. Further studies silencing Nox5 in TGF-β-treated cells resulted in a reduction of collagen levels via p38 MAPK. Collectively, these results show for the first time that Nox5 can play a relevant role in the proliferation and fibrosis on human HSC. DHE Elsevier Iono Elsevier PMA Elsevier MOI Elsevier HRP Elsevier AdNox5β Elsevier Cyt c Elsevier SOD Elsevier Ang II Elsevier GFP Elsevier Nox5-L Elsevier LX-2 Elsevier Nox Elsevier RACE Elsevier ROS Elsevier HSC Elsevier TGF-β Elsevier HBSS Elsevier Nox5-S or Nox5ε Elsevier siNox5 Elsevier Garde, Naiara oth García-Garzón, Antonia oth Ansorena, Eduardo oth López-Zabalza, María J. oth Iraburu, María J. oth Zalba, Guillermo oth Martínez-Irujo, Juan J. 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:126 year:2018 pages:15-26 extent:12 https://doi.org/10.1016/j.freeradbiomed.2018.07.013 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 52.57 Energiespeicherung VZ 53.36 Energiedirektumwandler elektrische Energiespeicher VZ AR 126 2018 15-26 12 |
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nadph oxidase 5 promotes proliferation and fibrosis in human hepatic stellate cells |
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NADPH oxidase 5 promotes proliferation and fibrosis in human hepatic stellate cells |
| abstract |
NADPH oxidase (Nox) variants Nox1, Nox2 and Nox4 are implicated in the progression of liver fibrosis. However, the role of Nox5 is not yet known, mainly due to the lack of this enzyme in rat and mouse genomes. Here we describe the expression and functional relevance of Nox5 in the human cell line of hepatic stellate cells (HSC) LX-2. Under basal conditions, three long (Nox5-L: Nox5α, -β, and -δ) and a short (Nox5-S or Nox5ε) splice variants were detected, which were silenced with specific siRNAs for Nox5. The most abundant isoform was Nox5-S, accounting for more than 90% of Nox5 protein. Overexpression of Nox5β generated reactive oxygen species (ROS) in the presence of calcium, as judged by the production of hydrogen peroxide, L-012 luminescence and cytochrome c reduction. Nox5ε did not generated ROS under these conditions, and a reduced ROS production was observed when co-expressed with Nox5β. In contrast, dihydroethidium oxidation was increased by Nox5β or Nox5ε, suggesting that Nox5ε induced intracellular oxidative stress by an unknown mechanism. Functional studies showed that both Nox5β and Nox5ε stimulated the proliferation of LX-2 cells and the collagen type I levels, while Nox5 siRNAs inhibited these effects. Interestingly, TGF-β and angiotensin II upregulated Nox5 expression, which was reduced in cells pre-incubated with catalase. Further studies silencing Nox5 in TGF-β-treated cells resulted in a reduction of collagen levels via p38 MAPK. Collectively, these results show for the first time that Nox5 can play a relevant role in the proliferation and fibrosis on human HSC. |
| abstractGer |
NADPH oxidase (Nox) variants Nox1, Nox2 and Nox4 are implicated in the progression of liver fibrosis. However, the role of Nox5 is not yet known, mainly due to the lack of this enzyme in rat and mouse genomes. Here we describe the expression and functional relevance of Nox5 in the human cell line of hepatic stellate cells (HSC) LX-2. Under basal conditions, three long (Nox5-L: Nox5α, -β, and -δ) and a short (Nox5-S or Nox5ε) splice variants were detected, which were silenced with specific siRNAs for Nox5. The most abundant isoform was Nox5-S, accounting for more than 90% of Nox5 protein. Overexpression of Nox5β generated reactive oxygen species (ROS) in the presence of calcium, as judged by the production of hydrogen peroxide, L-012 luminescence and cytochrome c reduction. Nox5ε did not generated ROS under these conditions, and a reduced ROS production was observed when co-expressed with Nox5β. In contrast, dihydroethidium oxidation was increased by Nox5β or Nox5ε, suggesting that Nox5ε induced intracellular oxidative stress by an unknown mechanism. Functional studies showed that both Nox5β and Nox5ε stimulated the proliferation of LX-2 cells and the collagen type I levels, while Nox5 siRNAs inhibited these effects. Interestingly, TGF-β and angiotensin II upregulated Nox5 expression, which was reduced in cells pre-incubated with catalase. Further studies silencing Nox5 in TGF-β-treated cells resulted in a reduction of collagen levels via p38 MAPK. Collectively, these results show for the first time that Nox5 can play a relevant role in the proliferation and fibrosis on human HSC. |
| abstract_unstemmed |
NADPH oxidase (Nox) variants Nox1, Nox2 and Nox4 are implicated in the progression of liver fibrosis. However, the role of Nox5 is not yet known, mainly due to the lack of this enzyme in rat and mouse genomes. Here we describe the expression and functional relevance of Nox5 in the human cell line of hepatic stellate cells (HSC) LX-2. Under basal conditions, three long (Nox5-L: Nox5α, -β, and -δ) and a short (Nox5-S or Nox5ε) splice variants were detected, which were silenced with specific siRNAs for Nox5. The most abundant isoform was Nox5-S, accounting for more than 90% of Nox5 protein. Overexpression of Nox5β generated reactive oxygen species (ROS) in the presence of calcium, as judged by the production of hydrogen peroxide, L-012 luminescence and cytochrome c reduction. Nox5ε did not generated ROS under these conditions, and a reduced ROS production was observed when co-expressed with Nox5β. In contrast, dihydroethidium oxidation was increased by Nox5β or Nox5ε, suggesting that Nox5ε induced intracellular oxidative stress by an unknown mechanism. Functional studies showed that both Nox5β and Nox5ε stimulated the proliferation of LX-2 cells and the collagen type I levels, while Nox5 siRNAs inhibited these effects. Interestingly, TGF-β and angiotensin II upregulated Nox5 expression, which was reduced in cells pre-incubated with catalase. Further studies silencing Nox5 in TGF-β-treated cells resulted in a reduction of collagen levels via p38 MAPK. Collectively, these results show for the first time that Nox5 can play a relevant role in the proliferation and fibrosis on human HSC. |
| collection_details |
GBV_USEFLAG_U GBV_ELV SYSFLAG_U |
| title_short |
NADPH oxidase 5 promotes proliferation and fibrosis in human hepatic stellate cells |
| url |
https://doi.org/10.1016/j.freeradbiomed.2018.07.013 |
| remote_bool |
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| author2 |
Garde, Naiara García-Garzón, Antonia Ansorena, Eduardo López-Zabalza, María J. Iraburu, María J. Zalba, Guillermo Martínez-Irujo, Juan J. |
| author2Str |
Garde, Naiara García-Garzón, Antonia Ansorena, Eduardo López-Zabalza, María J. Iraburu, María J. Zalba, Guillermo Martínez-Irujo, Juan J. |
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| doi_str |
10.1016/j.freeradbiomed.2018.07.013 |
| up_date |
2024-07-06T20:58:30.677Z |
| _version_ |
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