NRF2 and PPAR-γ Pathways in Oligodendrocyte Progenitors: Focus on ROS Protection, Mitochondrial Biogenesis and Promotion of Cell Differentiation

Autor: Carmen Troiano, Mario Falchi, Maria Stefania Brignone, Sergio Visentin, Cristina Lanni, Chiara De Nuccio, Michela Rosini, Antonietta Bernardo, Anita Greco, Luisa Minghetti, Filippo Basagni, Melania Maria Serafini
Přispěvatelé: De Nuccio C., Bernardo A., Troiano C., Brignone M.S., Falchi M., Greco A., Rosini M., Basagni F., Lanni C., Serafini M.M., Minghetti L., Visentin S.
Jazyk: angličtina
Rok vydání: 2020
Předmět:
Cellular differentiation
Dimethyl Fumarate
Peroxisome proliferator-activated receptor
Mitochondrion
medicine.disease_cause
Antioxidants
lcsh:Chemistry
lcsh:QH301-705.5
Spectroscopy
chemistry.chemical_classification
Organelle Biogenesis
Cell Differentiation
General Medicine
Computer Science Applications
Cell biology
Mitochondria
Oligodendroglia
medicine.anatomical_structure
Signal Transduction
PPAR-γ
NF-E2-Related Factor 2
Neurogenesis
oligodendrocytes
Oxidative phosphorylation
Catalysis
Article
NRF2
Inorganic Chemistry
DMF
medicine
Animals
Humans
Physical and Theoretical Chemistry
Molecular Biology
Oligodendrocyte Precursor Cells
Pioglitazone
Tumor Necrosis Factor-alpha
Organic Chemistry
Oligodendrocyte differentiation
Oligodendrocyte
Rats
PPAR gamma
Oxidative Stress
chemistry
Mitochondrial biogenesis
lcsh:Biology (General)
lcsh:QD1-999
Reactive Oxygen Species
Oxidative stress
Zdroj: International Journal of Molecular Sciences
International Journal of Molecular Sciences, Vol 21, Iss 7216, p 7216 (2020)
Volume 21
Issue 19
ISSN: 1422-0067
Popis: An adequate protection from oxidative and inflammatory reactions, together with the promotion of oligodendrocyte progenitor (OP) differentiation, is needed to recover from myelin damage in demyelinating diseases. Mitochondria are targets of inflammatory and oxidative insults and are essential in oligodendrocyte differentiation. It is known that nuclear factor-erythroid 2-related factor/antioxidant responsive element (NRF2/ARE) and peroxisome proliferator-activated receptor gamma/PPAR-&gamma
response element (PPAR-&gamma
/PPRE) pathways control inflammation and overcome mitochondrial impairment. In this study, we analyzed the effects of activators of these pathways on mitochondrial features, protection from inflammatory/mitochondrial insults and cell differentiation in OP cultures, to depict the specificities and similarities of their actions. We used dimethyl-fumarate (DMF) and pioglitazone (pio) as agents activating NRF2 and PPAR-&gamma
respectively, and two synthetic hybrids acting differently on the NRF2/ARE pathway. Only DMF and compound 1 caused early effects on the mitochondria. Both DMF and pio induced mitochondrial biogenesis but different antioxidant repertoires. Moreover, pio induced OP differentiation more efficiently than DMF. Finally, DMF, pio and compound 1 protected from tumor necrosis factor-alpha (TNF-&alpha
) insult, with pio showing faster kinetics of action and compound 1 a higher activity than DMF. In conclusion, NRF2 and PPAR-&gamma
by inducing partially overlapping pathways accomplish complementary functions aimed at the preservation of mitochondrial function, the defense against oxidative stress and the promotion of OP differentiation.
Databáze: OpenAIRE
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