Sex-specific up-regulation of p50-associated COX-2 extragenic RNA (PACER) lncRNA in periodontitis

A number of recent studies have shown dysregulation of some long non-coding RNAs (lncRNAs) in affected tissues or peripheral blood of patients with periodontitis. In the current study, we investigated the role of TNF and HNRNPL related immunoregulatory (THRIL) and p50-associated COX-2 extragenic RNA (PACER) lncRNAs in periodontitis. We assessed expression of these lncRNAs in 30 affected tissue, 30 control tissue samples, 23 blood samples from patients and 18 blood samples from healthy controls. Expression of PACER was higher in total blood samples of patients compared with controls (Posterior beta of RE = 5.143, P value = 0.001). However, when assessing its expression in a gender-based manner, the difference in the expression of this lncRNA was significant only among male subgroups (Posterior beta of RE = 7.16, P value < 0.0001). Moreover, expression of PACER was significantly higher in female subjects compared with male subjects (Posterior beta of RE = 3.098, P value < 0.0001). There was no significant difference in tissue expression of PACER between study subgroups. Expression of THRIL was not significantly different between blood/tissue samples of cases and controls. However, expression of this lncRNA was higher in blood of female subjects compared with male subjects (Posterior beta of RE = 4.353, P value = 0.002). Tissue expression of THRIL was correlated with blood levels of this lncRNA (r = 0.33, P < 0.0001) and with the tissue levels of PACER (r = 0.3, P < 0.0001). Moreover, blood levels of these lncRNAs were correlated with each other (r = 0.34, P < 0.0001). However, there was no significant correlation between blood and tissue levels of PACER. Expression of these lncRNAs were not correlated with age either in males or in females. Taken together, we demonstrated a sex-based up-regulation of PACER in blood samples of patients with periodontitis which implies possible participation of this lncRNA in the pathobiology of periodontitis.