Role of protein kinase C and oxidative stress in interleukin-1β-induced human proximal tubule cell injury and fibrogenesis
Background: Interleukin (IL)-1β, a pro-inflammatory macrophage-derived cytokine, is implicated as a key mediator of interstitial fibrosis and tubular loss or injury in progressive renal insufficiency. This study investigates some of the mechanisms of action of IL-1β on the proximal tubule.Methods: ...
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| Autor*in: |
VESEY, DAVID A [verfasserIn] CHEUNG, CATHERINE [verfasserIn] ENDRE, ZOLTAN [verfasserIn] |
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E-Artikel |
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| Erschienen: |
Melbourne, Australia: Blackwell Science Pty ; 2005 |
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Online-Ressource |
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| Reproduktion: |
2005 ; Blackwell Publishing Journal Backfiles 1879-2005 |
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| Übergeordnetes Werk: |
In: Nephrology - Oxford [u.a.] : Wiley-Blackwell, 1995, 10(2005), 1, Seite 0 |
| Übergeordnetes Werk: |
volume:10 ; year:2005 ; number:1 ; pages:0 |
| Links: |
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| DOI / URN: |
10.1111/j.1440-1797.2005.00363.x |
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NLEJ243521332 |
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| 520 | |a Background: Interleukin (IL)-1β, a pro-inflammatory macrophage-derived cytokine, is implicated as a key mediator of interstitial fibrosis and tubular loss or injury in progressive renal insufficiency. This study investigates some of the mechanisms of action of IL-1β on the proximal tubule.Methods: Confluent cultures of primary human proximal tubule cells (PTC) were incubated in serum-free media supplemented with either IL-1β (0–4 ng/mL), phorbol-12-myristate 13-acetate (PMA, protein kinase C activator) (6.25–100 nmol/L), or vehicle (control), together with a non-specific protein kinase C inhibitor (H7), a specific protein kinase C inhibitor (BIM-1), an anti-oxidant (NAC) or a NADPH oxidase inhibitor (AEBSF).Results: Interleukin-1β-treated PTC exhibited time-dependent increases in fibronectin secretion (ELISA), cell injury (LDH release) and reactive nitrogen species (RNS) release (Griess assay). Proximal tubule cell DNA synthesis (thymidine incorporation) was also significantly suppressed. The effects of IL-1β, which were reproduced by incubation of PTC with PMA (6.25–100 nmol/L), were blocked by H7 but not by BIM-1. The anti-oxidant (4 mmol/L) partially blocked IL-1β-induced fibronectin secretion by PTC, but did not affect IL-1β-induced LDH release, RNS release or growth inhibition. The NADPH oxidase inhibitor (AEBSF) significantly attenuated all observed deleterious effects of IL-1β on PTC.Conclusion: Interleukin-1β directly induces proximal tubule injury, extracellular matrix production and impaired growth. The anti-oxidant, NAC, appears to ameliorate part of the fibrogenic effect of IL-1β on PTC through mechanisms that do not significantly involve protein kinase C activation or nitric oxide release. | ||
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10.1111/j.1440-1797.2005.00363.x doi (DE-627)NLEJ243521332 DE-627 ger DE-627 rakwb VESEY, DAVID A verfasserin aut Role of protein kinase C and oxidative stress in interleukin-1β-induced human proximal tubule cell injury and fibrogenesis Melbourne, Australia Blackwell Science Pty 2005 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Background: Interleukin (IL)-1β, a pro-inflammatory macrophage-derived cytokine, is implicated as a key mediator of interstitial fibrosis and tubular loss or injury in progressive renal insufficiency. This study investigates some of the mechanisms of action of IL-1β on the proximal tubule.Methods: Confluent cultures of primary human proximal tubule cells (PTC) were incubated in serum-free media supplemented with either IL-1β (0–4 ng/mL), phorbol-12-myristate 13-acetate (PMA, protein kinase C activator) (6.25–100 nmol/L), or vehicle (control), together with a non-specific protein kinase C inhibitor (H7), a specific protein kinase C inhibitor (BIM-1), an anti-oxidant (NAC) or a NADPH oxidase inhibitor (AEBSF).Results: Interleukin-1β-treated PTC exhibited time-dependent increases in fibronectin secretion (ELISA), cell injury (LDH release) and reactive nitrogen species (RNS) release (Griess assay). Proximal tubule cell DNA synthesis (thymidine incorporation) was also significantly suppressed. The effects of IL-1β, which were reproduced by incubation of PTC with PMA (6.25–100 nmol/L), were blocked by H7 but not by BIM-1. The anti-oxidant (4 mmol/L) partially blocked IL-1β-induced fibronectin secretion by PTC, but did not affect IL-1β-induced LDH release, RNS release or growth inhibition. The NADPH oxidase inhibitor (AEBSF) significantly attenuated all observed deleterious effects of IL-1β on PTC.Conclusion: Interleukin-1β directly induces proximal tubule injury, extracellular matrix production and impaired growth. The anti-oxidant, NAC, appears to ameliorate part of the fibrogenic effect of IL-1β on PTC through mechanisms that do not significantly involve protein kinase C activation or nitric oxide release. 2005 Blackwell Publishing Journal Backfiles 1879-2005 |2005|||||||||| interleukin-1β CHEUNG, CATHERINE verfasserin aut ENDRE, ZOLTAN verfasserin aut GOBÉ, GLENDA oth JOHNSON, DAVID W oth In Nephrology Oxford [u.a.] : Wiley-Blackwell, 1995 10(2005), 1, Seite 0 Online-Ressource (DE-627)NLEJ243925859 (DE-600)2008235-6 1440-1797 nnns volume:10 year:2005 number:1 pages:0 http://dx.doi.org/10.1111/j.1440-1797.2005.00363.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 10 2005 1 0 |
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10.1111/j.1440-1797.2005.00363.x doi (DE-627)NLEJ243521332 DE-627 ger DE-627 rakwb VESEY, DAVID A verfasserin aut Role of protein kinase C and oxidative stress in interleukin-1β-induced human proximal tubule cell injury and fibrogenesis Melbourne, Australia Blackwell Science Pty 2005 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Background: Interleukin (IL)-1β, a pro-inflammatory macrophage-derived cytokine, is implicated as a key mediator of interstitial fibrosis and tubular loss or injury in progressive renal insufficiency. This study investigates some of the mechanisms of action of IL-1β on the proximal tubule.Methods: Confluent cultures of primary human proximal tubule cells (PTC) were incubated in serum-free media supplemented with either IL-1β (0–4 ng/mL), phorbol-12-myristate 13-acetate (PMA, protein kinase C activator) (6.25–100 nmol/L), or vehicle (control), together with a non-specific protein kinase C inhibitor (H7), a specific protein kinase C inhibitor (BIM-1), an anti-oxidant (NAC) or a NADPH oxidase inhibitor (AEBSF).Results: Interleukin-1β-treated PTC exhibited time-dependent increases in fibronectin secretion (ELISA), cell injury (LDH release) and reactive nitrogen species (RNS) release (Griess assay). Proximal tubule cell DNA synthesis (thymidine incorporation) was also significantly suppressed. The effects of IL-1β, which were reproduced by incubation of PTC with PMA (6.25–100 nmol/L), were blocked by H7 but not by BIM-1. The anti-oxidant (4 mmol/L) partially blocked IL-1β-induced fibronectin secretion by PTC, but did not affect IL-1β-induced LDH release, RNS release or growth inhibition. The NADPH oxidase inhibitor (AEBSF) significantly attenuated all observed deleterious effects of IL-1β on PTC.Conclusion: Interleukin-1β directly induces proximal tubule injury, extracellular matrix production and impaired growth. The anti-oxidant, NAC, appears to ameliorate part of the fibrogenic effect of IL-1β on PTC through mechanisms that do not significantly involve protein kinase C activation or nitric oxide release. 2005 Blackwell Publishing Journal Backfiles 1879-2005 |2005|||||||||| interleukin-1β CHEUNG, CATHERINE verfasserin aut ENDRE, ZOLTAN verfasserin aut GOBÉ, GLENDA oth JOHNSON, DAVID W oth In Nephrology Oxford [u.a.] : Wiley-Blackwell, 1995 10(2005), 1, Seite 0 Online-Ressource (DE-627)NLEJ243925859 (DE-600)2008235-6 1440-1797 nnns volume:10 year:2005 number:1 pages:0 http://dx.doi.org/10.1111/j.1440-1797.2005.00363.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 10 2005 1 0 |
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10.1111/j.1440-1797.2005.00363.x doi (DE-627)NLEJ243521332 DE-627 ger DE-627 rakwb VESEY, DAVID A verfasserin aut Role of protein kinase C and oxidative stress in interleukin-1β-induced human proximal tubule cell injury and fibrogenesis Melbourne, Australia Blackwell Science Pty 2005 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Background: Interleukin (IL)-1β, a pro-inflammatory macrophage-derived cytokine, is implicated as a key mediator of interstitial fibrosis and tubular loss or injury in progressive renal insufficiency. This study investigates some of the mechanisms of action of IL-1β on the proximal tubule.Methods: Confluent cultures of primary human proximal tubule cells (PTC) were incubated in serum-free media supplemented with either IL-1β (0–4 ng/mL), phorbol-12-myristate 13-acetate (PMA, protein kinase C activator) (6.25–100 nmol/L), or vehicle (control), together with a non-specific protein kinase C inhibitor (H7), a specific protein kinase C inhibitor (BIM-1), an anti-oxidant (NAC) or a NADPH oxidase inhibitor (AEBSF).Results: Interleukin-1β-treated PTC exhibited time-dependent increases in fibronectin secretion (ELISA), cell injury (LDH release) and reactive nitrogen species (RNS) release (Griess assay). Proximal tubule cell DNA synthesis (thymidine incorporation) was also significantly suppressed. The effects of IL-1β, which were reproduced by incubation of PTC with PMA (6.25–100 nmol/L), were blocked by H7 but not by BIM-1. The anti-oxidant (4 mmol/L) partially blocked IL-1β-induced fibronectin secretion by PTC, but did not affect IL-1β-induced LDH release, RNS release or growth inhibition. The NADPH oxidase inhibitor (AEBSF) significantly attenuated all observed deleterious effects of IL-1β on PTC.Conclusion: Interleukin-1β directly induces proximal tubule injury, extracellular matrix production and impaired growth. The anti-oxidant, NAC, appears to ameliorate part of the fibrogenic effect of IL-1β on PTC through mechanisms that do not significantly involve protein kinase C activation or nitric oxide release. 2005 Blackwell Publishing Journal Backfiles 1879-2005 |2005|||||||||| interleukin-1β CHEUNG, CATHERINE verfasserin aut ENDRE, ZOLTAN verfasserin aut GOBÉ, GLENDA oth JOHNSON, DAVID W oth In Nephrology Oxford [u.a.] : Wiley-Blackwell, 1995 10(2005), 1, Seite 0 Online-Ressource (DE-627)NLEJ243925859 (DE-600)2008235-6 1440-1797 nnns volume:10 year:2005 number:1 pages:0 http://dx.doi.org/10.1111/j.1440-1797.2005.00363.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 10 2005 1 0 |
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10.1111/j.1440-1797.2005.00363.x doi (DE-627)NLEJ243521332 DE-627 ger DE-627 rakwb VESEY, DAVID A verfasserin aut Role of protein kinase C and oxidative stress in interleukin-1β-induced human proximal tubule cell injury and fibrogenesis Melbourne, Australia Blackwell Science Pty 2005 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Background: Interleukin (IL)-1β, a pro-inflammatory macrophage-derived cytokine, is implicated as a key mediator of interstitial fibrosis and tubular loss or injury in progressive renal insufficiency. This study investigates some of the mechanisms of action of IL-1β on the proximal tubule.Methods: Confluent cultures of primary human proximal tubule cells (PTC) were incubated in serum-free media supplemented with either IL-1β (0–4 ng/mL), phorbol-12-myristate 13-acetate (PMA, protein kinase C activator) (6.25–100 nmol/L), or vehicle (control), together with a non-specific protein kinase C inhibitor (H7), a specific protein kinase C inhibitor (BIM-1), an anti-oxidant (NAC) or a NADPH oxidase inhibitor (AEBSF).Results: Interleukin-1β-treated PTC exhibited time-dependent increases in fibronectin secretion (ELISA), cell injury (LDH release) and reactive nitrogen species (RNS) release (Griess assay). Proximal tubule cell DNA synthesis (thymidine incorporation) was also significantly suppressed. The effects of IL-1β, which were reproduced by incubation of PTC with PMA (6.25–100 nmol/L), were blocked by H7 but not by BIM-1. The anti-oxidant (4 mmol/L) partially blocked IL-1β-induced fibronectin secretion by PTC, but did not affect IL-1β-induced LDH release, RNS release or growth inhibition. The NADPH oxidase inhibitor (AEBSF) significantly attenuated all observed deleterious effects of IL-1β on PTC.Conclusion: Interleukin-1β directly induces proximal tubule injury, extracellular matrix production and impaired growth. The anti-oxidant, NAC, appears to ameliorate part of the fibrogenic effect of IL-1β on PTC through mechanisms that do not significantly involve protein kinase C activation or nitric oxide release. 2005 Blackwell Publishing Journal Backfiles 1879-2005 |2005|||||||||| interleukin-1β CHEUNG, CATHERINE verfasserin aut ENDRE, ZOLTAN verfasserin aut GOBÉ, GLENDA oth JOHNSON, DAVID W oth In Nephrology Oxford [u.a.] : Wiley-Blackwell, 1995 10(2005), 1, Seite 0 Online-Ressource (DE-627)NLEJ243925859 (DE-600)2008235-6 1440-1797 nnns volume:10 year:2005 number:1 pages:0 http://dx.doi.org/10.1111/j.1440-1797.2005.00363.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 10 2005 1 0 |
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10.1111/j.1440-1797.2005.00363.x doi (DE-627)NLEJ243521332 DE-627 ger DE-627 rakwb VESEY, DAVID A verfasserin aut Role of protein kinase C and oxidative stress in interleukin-1β-induced human proximal tubule cell injury and fibrogenesis Melbourne, Australia Blackwell Science Pty 2005 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Background: Interleukin (IL)-1β, a pro-inflammatory macrophage-derived cytokine, is implicated as a key mediator of interstitial fibrosis and tubular loss or injury in progressive renal insufficiency. This study investigates some of the mechanisms of action of IL-1β on the proximal tubule.Methods: Confluent cultures of primary human proximal tubule cells (PTC) were incubated in serum-free media supplemented with either IL-1β (0–4 ng/mL), phorbol-12-myristate 13-acetate (PMA, protein kinase C activator) (6.25–100 nmol/L), or vehicle (control), together with a non-specific protein kinase C inhibitor (H7), a specific protein kinase C inhibitor (BIM-1), an anti-oxidant (NAC) or a NADPH oxidase inhibitor (AEBSF).Results: Interleukin-1β-treated PTC exhibited time-dependent increases in fibronectin secretion (ELISA), cell injury (LDH release) and reactive nitrogen species (RNS) release (Griess assay). Proximal tubule cell DNA synthesis (thymidine incorporation) was also significantly suppressed. The effects of IL-1β, which were reproduced by incubation of PTC with PMA (6.25–100 nmol/L), were blocked by H7 but not by BIM-1. The anti-oxidant (4 mmol/L) partially blocked IL-1β-induced fibronectin secretion by PTC, but did not affect IL-1β-induced LDH release, RNS release or growth inhibition. The NADPH oxidase inhibitor (AEBSF) significantly attenuated all observed deleterious effects of IL-1β on PTC.Conclusion: Interleukin-1β directly induces proximal tubule injury, extracellular matrix production and impaired growth. The anti-oxidant, NAC, appears to ameliorate part of the fibrogenic effect of IL-1β on PTC through mechanisms that do not significantly involve protein kinase C activation or nitric oxide release. 2005 Blackwell Publishing Journal Backfiles 1879-2005 |2005|||||||||| interleukin-1β CHEUNG, CATHERINE verfasserin aut ENDRE, ZOLTAN verfasserin aut GOBÉ, GLENDA oth JOHNSON, DAVID W oth In Nephrology Oxford [u.a.] : Wiley-Blackwell, 1995 10(2005), 1, Seite 0 Online-Ressource (DE-627)NLEJ243925859 (DE-600)2008235-6 1440-1797 nnns volume:10 year:2005 number:1 pages:0 http://dx.doi.org/10.1111/j.1440-1797.2005.00363.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 10 2005 1 0 |
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Role of protein kinase C and oxidative stress in interleukin-1β-induced human proximal tubule cell injury and fibrogenesis interleukin-1β |
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Role of protein kinase C and oxidative stress in interleukin-1β-induced human proximal tubule cell injury and fibrogenesis |
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Role of protein kinase C and oxidative stress in interleukin-1β-induced human proximal tubule cell injury and fibrogenesis |
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VESEY, DAVID A |
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VESEY, DAVID A CHEUNG, CATHERINE ENDRE, ZOLTAN |
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VESEY, DAVID A |
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10.1111/j.1440-1797.2005.00363.x |
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role of protein kinase c and oxidative stress in interleukin-1β-induced human proximal tubule cell injury and fibrogenesis |
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Role of protein kinase C and oxidative stress in interleukin-1β-induced human proximal tubule cell injury and fibrogenesis |
| abstract |
Background: Interleukin (IL)-1β, a pro-inflammatory macrophage-derived cytokine, is implicated as a key mediator of interstitial fibrosis and tubular loss or injury in progressive renal insufficiency. This study investigates some of the mechanisms of action of IL-1β on the proximal tubule.Methods: Confluent cultures of primary human proximal tubule cells (PTC) were incubated in serum-free media supplemented with either IL-1β (0–4 ng/mL), phorbol-12-myristate 13-acetate (PMA, protein kinase C activator) (6.25–100 nmol/L), or vehicle (control), together with a non-specific protein kinase C inhibitor (H7), a specific protein kinase C inhibitor (BIM-1), an anti-oxidant (NAC) or a NADPH oxidase inhibitor (AEBSF).Results: Interleukin-1β-treated PTC exhibited time-dependent increases in fibronectin secretion (ELISA), cell injury (LDH release) and reactive nitrogen species (RNS) release (Griess assay). Proximal tubule cell DNA synthesis (thymidine incorporation) was also significantly suppressed. The effects of IL-1β, which were reproduced by incubation of PTC with PMA (6.25–100 nmol/L), were blocked by H7 but not by BIM-1. The anti-oxidant (4 mmol/L) partially blocked IL-1β-induced fibronectin secretion by PTC, but did not affect IL-1β-induced LDH release, RNS release or growth inhibition. The NADPH oxidase inhibitor (AEBSF) significantly attenuated all observed deleterious effects of IL-1β on PTC.Conclusion: Interleukin-1β directly induces proximal tubule injury, extracellular matrix production and impaired growth. The anti-oxidant, NAC, appears to ameliorate part of the fibrogenic effect of IL-1β on PTC through mechanisms that do not significantly involve protein kinase C activation or nitric oxide release. |
| abstractGer |
Background: Interleukin (IL)-1β, a pro-inflammatory macrophage-derived cytokine, is implicated as a key mediator of interstitial fibrosis and tubular loss or injury in progressive renal insufficiency. This study investigates some of the mechanisms of action of IL-1β on the proximal tubule.Methods: Confluent cultures of primary human proximal tubule cells (PTC) were incubated in serum-free media supplemented with either IL-1β (0–4 ng/mL), phorbol-12-myristate 13-acetate (PMA, protein kinase C activator) (6.25–100 nmol/L), or vehicle (control), together with a non-specific protein kinase C inhibitor (H7), a specific protein kinase C inhibitor (BIM-1), an anti-oxidant (NAC) or a NADPH oxidase inhibitor (AEBSF).Results: Interleukin-1β-treated PTC exhibited time-dependent increases in fibronectin secretion (ELISA), cell injury (LDH release) and reactive nitrogen species (RNS) release (Griess assay). Proximal tubule cell DNA synthesis (thymidine incorporation) was also significantly suppressed. The effects of IL-1β, which were reproduced by incubation of PTC with PMA (6.25–100 nmol/L), were blocked by H7 but not by BIM-1. The anti-oxidant (4 mmol/L) partially blocked IL-1β-induced fibronectin secretion by PTC, but did not affect IL-1β-induced LDH release, RNS release or growth inhibition. The NADPH oxidase inhibitor (AEBSF) significantly attenuated all observed deleterious effects of IL-1β on PTC.Conclusion: Interleukin-1β directly induces proximal tubule injury, extracellular matrix production and impaired growth. The anti-oxidant, NAC, appears to ameliorate part of the fibrogenic effect of IL-1β on PTC through mechanisms that do not significantly involve protein kinase C activation or nitric oxide release. |
| abstract_unstemmed |
Background: Interleukin (IL)-1β, a pro-inflammatory macrophage-derived cytokine, is implicated as a key mediator of interstitial fibrosis and tubular loss or injury in progressive renal insufficiency. This study investigates some of the mechanisms of action of IL-1β on the proximal tubule.Methods: Confluent cultures of primary human proximal tubule cells (PTC) were incubated in serum-free media supplemented with either IL-1β (0–4 ng/mL), phorbol-12-myristate 13-acetate (PMA, protein kinase C activator) (6.25–100 nmol/L), or vehicle (control), together with a non-specific protein kinase C inhibitor (H7), a specific protein kinase C inhibitor (BIM-1), an anti-oxidant (NAC) or a NADPH oxidase inhibitor (AEBSF).Results: Interleukin-1β-treated PTC exhibited time-dependent increases in fibronectin secretion (ELISA), cell injury (LDH release) and reactive nitrogen species (RNS) release (Griess assay). Proximal tubule cell DNA synthesis (thymidine incorporation) was also significantly suppressed. The effects of IL-1β, which were reproduced by incubation of PTC with PMA (6.25–100 nmol/L), were blocked by H7 but not by BIM-1. The anti-oxidant (4 mmol/L) partially blocked IL-1β-induced fibronectin secretion by PTC, but did not affect IL-1β-induced LDH release, RNS release or growth inhibition. The NADPH oxidase inhibitor (AEBSF) significantly attenuated all observed deleterious effects of IL-1β on PTC.Conclusion: Interleukin-1β directly induces proximal tubule injury, extracellular matrix production and impaired growth. The anti-oxidant, NAC, appears to ameliorate part of the fibrogenic effect of IL-1β on PTC through mechanisms that do not significantly involve protein kinase C activation or nitric oxide release. |
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Role of protein kinase C and oxidative stress in interleukin-1β-induced human proximal tubule cell injury and fibrogenesis |
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