6 research outputs found
Correlation of Midkine Serum Level with Pro- and Anti-Inflamatory Cytokines in Multiple Sclerosis
Background: Midkine (MK) is a heparin-binding growth factor with promoting effects in inflammatory responses through enhancing leukocytes migration. Objective: To study the correlation between MK serum levels and concentration of inflammatory cytokines in Multiple Sclerosis (MS) patients. Methods: We evaluated the MK level and its relationship with inflammatory cytokines (IL-17 and IL-23) and anti-inflammatory ones (IL-10 and TGF-beta) in multiple sclerosis (MS) patients. The serum concentrations of MK and cytokines were assessed by ELISA in 32 MS patients in comparison with 32 healthy subjects. Results: Our data showed that the MK concentration in MS patients is lower than healthy controls (341.15 +/- 40.71 Pg/ml vs. 620.15 +/- 98.61 Pg/ml, respectively, p= 0.015). We also observed a significant decrease in IL-10, IL-23, and TGF-beta cytokine levels in MS patients. There was a significant correlation between MK and IL-23 concentrations in our study (r = + 0.829, p <= 0.001). Conclusion: These results confirm a role for MK in inflammatory reactions in MS
Senescence-associated oxidative DNA damage promotes the generation of neoplastic cells
Studies on human fibroblasts have led to viewing senescence as a barrier against tumorigenesis. Using keratinocytes, we show here that partially transformed and tumorigenic cells systematically and spontaneously emerge from senescent cultures. We show that these emerging cells are generated from senescent cells, which are still competent for replication, by an unusual budding-mitosis mechanism. We further present data implicating reactive oxygen species that accumulate during senescence as a potential mutagenic motor of this post-senescence emergence. We conclude that senescence and its associated oxidative stress could be a tumor-promoting state for epithelial cells, potentially explaining why the incidence of carcinogenesis dramatically increases with advanced age. ©2009 American Association for Cancer Research.SCOPUS: ar.jinfo:eu-repo/semantics/publishe