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Effects of chlorogenic acid on thermal stress tolerance in C. elegans via HIF- 1, HSF-1 and autophagy

Colaborador(es): Valle Carranza, Andrea del. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas. Departamento de Bioquímica Clínica (CIBICI). Argentina | Saragusti, Alejandra. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas. Departamento de Bioquímica Clínica (CIBICI). Argentina | Chiabrando, Gustavo Alberto. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas. Departamento de Bioquímica Clínica (CIBICI). Argentina | Carrari, Fernando. Universidad de Buenos Aires. Instituto de Fisiología Biología Molecular y Neurociencias (IFIBYNE-CONICET-UBA). Buenos Aires, Argentina. CONICET - Universidad de Buenos Aires. Instituto de Fisiología Biología Molecular y Neurociencias (IFIBYNE-CONICET-UBA). Buenos Aires, Argentina. Universidad de Buenos Aires. Facultad de Agronomía. Buenos Aires, Argentina | Asís, Ramón. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas. Departamento de Bioquímica Clínica (CIBICI). Argentina.
ISSN: 0944-7113.Tipo de material: Artículos y capítulos. Recurso electrónico.Tema(s): | AUTOPHAGY | C. ELEGANS | CHLOROGENIC ACID | HIF-1 | HSF-1 | THERMAL STRESS | Recursos en línea: Haga clic para acceso en línea | LINK AL EDITOR En: Phytomedicine Vol.66 (2020), art.153132, 10 p.,grafs.Resumen: Background: Chlorogenic acid (CGA) is a polyphenol widely distributed in plants and plant-derived food with antioxidant and protective activities against cell stress. Caenorhabditis elegans is a model organism particularly useful for understanding the molecular and biochemical mechanisms associated with aging and stress in mammals. In C. elegans, CGA was shown to improve resistance to thermal, while the underlying mechanisms that lead to this effect require further understanding. Purpose: The present study was conducted to investigate the underlying molecular mechanisms behind CGA response conferring thermotolerance to C. elegans. Methods and results: Signaling pathways that could be involved in the CGA-induced thermotolerance were evaluated in C. elegans strains with loss-of-function mutation. CGA-induced thermotolerance required hypoxiainducible factor HIF-1 but no insulin pathway. CGA exposition (1.4 μM CGA for 18 h) before thermal stress treatment increased HIF-1 levels and activity. HIF-1 activation could be partly attributed to an increase in radical oxygen species and a decrease in superoxide dismutase activity. In addition, CGA exposition before thermal stress also increased autophagy just as hormetic heat condition (HHC), worms incubated at 36 °C for 1 h. RNAi experiments evidenced that autophagy was increased by CGA via HIF-1, heat-shock transcription factor HSF-1 and heat-shock protein HSP-16 and HSP-70. In contrast, autophagy induced by HHC only required HSF-1 and HSP-70. Moreover, suppression of autophagy induction showed the significance of this process for adapting C. elegans to cope with thermal stress. Conclusion: This study demonstrates that CGA-induced thermotolerance in C. elegans is mediated by HIF-1 and downstream, by HSF-1, HSPs and autophagy resembling HHC.
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Background: Chlorogenic acid (CGA) is a polyphenol widely distributed in plants and plant-derived food with antioxidant and protective activities against cell stress. Caenorhabditis elegans is a model organism particularly useful for understanding the molecular and biochemical mechanisms associated with aging and stress in mammals. In C. elegans, CGA was shown to improve resistance to thermal, while the underlying mechanisms that lead to this effect require further understanding.
Purpose: The present study was conducted to investigate the underlying molecular mechanisms behind CGA response conferring thermotolerance to C. elegans.
Methods and results: Signaling pathways that could be involved in the CGA-induced thermotolerance were evaluated in C. elegans strains with loss-of-function mutation. CGA-induced thermotolerance required hypoxiainducible factor HIF-1 but no insulin pathway. CGA exposition (1.4 μM CGA for 18 h) before thermal stress treatment increased HIF-1 levels and activity. HIF-1 activation could be partly attributed to an increase in radical oxygen species and a decrease in superoxide dismutase activity. In addition, CGA exposition before thermal stress also increased autophagy just as hormetic heat condition (HHC), worms incubated at 36 °C for 1 h. RNAi experiments evidenced that autophagy was increased by CGA via HIF-1, heat-shock transcription factor HSF-1 and heat-shock protein HSP-16 and HSP-70. In contrast, autophagy induced by HHC only required HSF-1 and HSP-70. Moreover, suppression of autophagy induction showed the significance of this process for adapting C.
elegans to cope with thermal stress.
Conclusion: This study demonstrates that CGA-induced thermotolerance in C. elegans is mediated by HIF-1 and downstream, by HSF-1, HSPs and autophagy resembling HHC.

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