Protein kinase C-beta/the 66-kDa isoform of the growth factor adaptor Shc oxidative stress pathway in mediating the production of the reactive oxygen species in premature infants exposed to hyperoxia

Abstract

Objective To study the possible mitochondria oxidative stress signal transduction pathway, which probably mediates the production of reactive oxygen species in premature infants exposed to hyperoxia. Methods Hyperoxia group: 20 cases of premature infants whose gestational age was below 34 weeks were diagnosed as respiratory failure(treated with exposed to over 400 mL/L oxygen 48-69 h) in Department of Neonatology, the Affiliated Hospital of Luzhou Medical College, from Jul.to Dec.2012.Control group: 20 cases of premature infants with the same gestatio-nal age were diagnosed as no respiratory failure(exposed to air over 48 h in the same room simultaneously). The expression of protein kinase C-beta(PKCβ)/the 66-kDa isoform of the growth factor adaptor Shc(p66Shc)/prolyl isomerase1(Pin1)/phosphorylated the 66-kDa isoform of the growth factor adaptor Shc-Ser36(p66Shc-Ser36) were detected by immunohistochemistry and the production of mitochondrial reactive oxygen was detected by fluorescence microscope in the peripheral blood mononuclear cell of hyperoxia group and control group. Results Compared with the control group, the expressions of PKCβ, p66Shc, Pin1, phosphorylated p66Shc-Ser36 and the production of reactive oxygen in hype-roxia group were significantly increased(t=21.139, 5.592, 7.476, 16.895, 10.586, all P<0.001). There were positive correlations between the production of reactive oxygen and the expressions of PKCβ, p66Shc, Pin1, phosphorylated p66Shc-Ser36 in hyperoxia group(r=0.893, 0.795, 0.681, 0.663, all P<0.001). Conclusion PKCβ/p66Shc oxidative stress pathway might mediate the production of reactive oxygen species in premature infants exposed to hyperoxia. Key words: Protein kinase C-beta/the 66-kDa isoform of the growth factor adaptor Shc; Hyperoxia; Reactive oxygen species; Infant, premature