Differential expression of Livin, caspase-3, and second mitochondria-derived activator of caspases in chronic rhinosinusitis with nasal polyps.

Abstract

The pathogenesis of human chronic rhinosinusitis with nasal polyps (CRSwNP) remains undetermined. Livin is a member of the inhibitor of the apoptosis protein family proteins. Caspase-3 and second mitochondria-derived activator of caspases (Smac) are critical in the induction of apoptosis. However, little is known about their roles in CRSwNP. We aimed to investigate the expression and role of Livin, caspase-3, and Smac in CRSwNP. Basic research and descriptive study. Fuzhou General Hospital, Fuzhou, Fujian, China. The immunohistochemistry method was employed for detecting Livin, caspase-3, and Smac protein expression, and real-time polymerase chain reaction was used for assaying mRNA expression of Livin, caspase-3, and Smac in CRSwNP and controls. Moreover, the effects of various stimulators on Livin were evaluated on human nasal epithelial cells (HNECs) culture. Then, the effects of Livin on caspase-3 and Smac were observed on the culture of HNECs. Stronger protein and mRNA expression of Livin was observed in CRSwNP, especially eosinophilic CRSwNP, weaker protein and mRNA expression of caspase-3 and Smac was observed in CRSwNP, and Livin expression was negatively related to caspase-3 or Smac expression, respectively. Livin mRNA was augmented by interleukin (IL)-4, IL-17A, and IL-1β but suppressed by interferon-γ. Caspase-3 and Smac mRNA expression were inhibited by Livin. Upregulation of Livin and downregulation of caspase-3 and Smac were observed in CRSwNP, especially in eosinophilic CRSwNP. Livin may exert its anti-apoptosis effect by suppressing caspase-3 and Smac in CRSwNP. IL-4, IL-17A, and IL-1β may be critical for Livin expression.