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Unravelling Cellular Mechanisms of Stem Cell Senescence: An Aid from Natural Bioactive Molecules.

ABSTRACT: Cellular senescence plays a role in the onset of age-related pathologies and in the loss of tissue homeostasis. Natural compounds of food or plants exert an important antioxidant activity, counteracting the formation of harmful free radicals. In the presence of an intense stressing event, cells activate specific responses to counteract senescence or cell death. In the present paper, we aimed at evaluating the levels of expression of specific markers of senescence, in order to demonstrate that extracts from Myrtus Communis L. can prevent premature senescence in ADSCs exposed to oxidative stress. Cells were cultured in the presence of Myrtus extracts for 12-24 and 48 h and then incubated with H2O2 to induce senescence. We then evaluated the expression of senescence-related markers p16, p19, p21, p53, TERT, c-Myc, and the senescence-associated ?-Galactoidase activity. Our results showed that pre-treatment with Myrtus extracts protects cells from premature senescence, by regulating the cell cycle, and inducing the expression of TERT and c-Myc. These findings suggest a potential application of these natural compounds in the prevention and treatment of various diseases, counteracting premature senescence and preserving tissue functions.

SUBMITTER: Cruciani S

PROVIDER: S-EPMC7150900 | biostudies-literature | 2020 Mar

REPOSITORIES: biostudies-literature

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Unravelling Cellular Mechanisms of Stem Cell Senescence: An Aid from Natural Bioactive Molecules.

Cruciani Sara S Garroni Giuseppe G Ginesu Giorgio Carlo GC Fadda Angela A Ventura Carlo C Maioli Margherita M

Biology 20200320 3

Cellular senescence plays a role in the onset of age-related pathologies and in the loss of tissue homeostasis. Natural compounds of food or plants exert an important antioxidant activity, counteracting the formation of harmful free radicals. In the presence of an intense stressing event, cells activate specific responses to counteract senescence or cell death. In the present paper, we aimed at evaluating the levels of expression of specific markers of senescence, in order to demonstrate that ex ...[more]

PMID: 32244882

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Project description:BackgroundNeural stem cells (NSCs), especially human NSCs, undergo cellular senescence characterized by an irreversible proliferation arrest and loss of stemness after prolonged culture. While compelling correlative data have been generated to support the oxidative stress theory as one of the primary determinants of cellular senescence of NSCs, a direct cause-and-effect relationship between the accumulation of oxidation-mediated damage and cellular senescence of NSCs has yet to be firmly established. Human SOD1 (hSOD1) is susceptible to oxidation. Once oxidized, it undergoes aberrant misfolding and gains toxic properties associated with age-related neurodegenerative disorders. The present study aims to examine the role of oxidized hSOD1 in the senescence of NSCs.MethodsNSCs prepared from transgenic mice expressing the wild-type hSOD1 gene were maintained in culture through repeated passages. Extracellular vesicles (EVs) were isolated from culture media at each passage. To selectively knock down oxidized SOD1 in NSCs and EVs, we used a peptide-directed chaperone-mediated protein degradation system named CT4 that we developed recently.ResultsIn NSCs expressing the hSOD1 from passage 5, we detected a significant increase of oxidized hSOD1 and an increased expression of biomarkers of cellular senescence, including upregulation of P53 and SA-β-Gal and cytoplasmic translocation of HMGB1. The removal of oxidized SOD1 remarkably increased the proliferation and stemness of the NSCs. Meanwhile, EVs derived from senescent NSCs carrying the wild-type hSOD1 contained high levels of oxidized hSOD1, which could accelerate the senescence of young NSCs and induce the death of cultured neurons. The removal of oxidized hSOD1 from the EVs abolished their senescence-inducing activity. Blocking oxidized SOD1 on EVs with the SOD1 binding domain of the CT4 peptide mitigated its toxicity to neurons.ConclusionOxidized hSOD1 is a causal factor in the cellular senescence of NSCs. The removal of oxidized hSOD1 is a strategy to rejuvenate NSCs and to improve the quality of EVs derived from senescent cells.

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Unravelling Cellular Mechanisms of Stem Cell Senescence: An Aid from Natural Bioactive Molecules.

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Unravelling Cellular Mechanisms of Stem Cell Senescence: An Aid from Natural Bioactive Molecules.

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