Unit:
Κατεύθυνση Κλινική Βιοχημεία - Μοριακή ΔιαγνωστικήLibrary of the School of Science
Author:
Konstantinou Angeliki
Supervisors info:
Δ. Σίδερης, Αναπληρωτής Καθηγητής, Τμήμα Βιολογίας, ΕΚΠΑ
Δ. Κλέτσας, Ερευνητής Α΄, ΕΚΕΦΕ Δημόκριτος
Α. Σκορίλας, Καθηγητής, Τμήμα Βιολογίας, ΕΚΠΑ
Original Title:
ΣΥΓΚΡΙΤΙΚΗ ΜΕΛΕΤΗ ΤΗΣ ΡΥΘΜΙΣΗΣ ΤΟΥ ΚΥΤΤΑΡΙΚΟΥ ΠΟΛΛΑΠΛΑΣΙΑΣΜΟΥ ΚΑΙ ΓΗΡΑΝΣΗΣ ΦΥΣΙΟΛΟΓΙΚΩΝ ΙΝΟΒΛΑΣΤΩΝ ΥΠΟ ΤΗΝ ΕΠΙΔΡΑΣΗ ΟΞΕΙΔΩΤΙΚΟΥ ΣΤΡΕΣ ΚΑΙ ΚΥΤΟΚΙΝΩΝ
Translated title:
ΣΥΓΚΡΙΤΙΚΗ ΜΕΛΕΤΗ ΤΗΣ ΡΥΘΜΙΣΗΣ ΤΟΥ ΚΥΤΤΑΡΙΚΟΥ ΠΟΛΛΑΠΛΑΣΙΑΣΜΟΥ ΚΑΙ ΓΗΡΑΝΣΗΣ ΦΥΣΙΟΛΟΓΙΚΩΝ ΙΝΟΒΛΑΣΤΩΝ ΥΠΟ ΤΗΝ ΕΠΙΔΡΑΣΗ ΟΞΕΙΔΩΤΙΚΟΥ ΣΤΡΕΣ ΚΑΙ ΚΥΤΟΚΙΝΩΝ
Summary:
Reactive oxygen species (ROS), produced in the cells as a byproduct of various biochemical reactions, represent pivotal regulators of homeostasis. Under normal conditions they control important cellular functions, such as cellular signaling and proliferation, while at higher concentrations (a condition termed oxidative stress) they provoke damage in cellular macromolecules, leading to an inhibition of proliferation or evεn cell death. In addition, continuous exposure to non-cytotoxic concentrations of ROS can lead to premature senescence. Finally, many inflammatory cytokines can provoke oxidative stress and premature senescence.
In this work we studied the effect of the inflammatory cytokine TNF-α on human dermal fibroblasts, in comparison with a classical oxidative stress, i.e. the exposure of cells to H2O2. We found that high H2O2 concentrations are cytotoxic and inhibits cell proliferation. In contrast, TNF-α does not provoke ROS induction, is not cytotoxic and does not inhibit fibroblast proliferation. Oxidative stress, as is already mentioned in the literature, provokes premature senescence. Premature senescence is also provoked after a long-term exposure to TNF-α. These senescent cells express the classical senescent phenotype and gene expression profile, i.e. a catabolic phenotype. However, the TNF-α induced senescence is not due to an oxidative stress, as has been hypothesized in the literature. This mechanism is currently under investigation.
Main subject category:
Science
Keywords:
Reactive oxygen species (ROS), premature senescence, oxidative stress, tumor necrosis factor-α (TNF-α)
