Long Non-Coding Rna Snhg29 Regulates Cell Senescence Via P53/P21 Signaling In Spontaneous Preterm Birth

Introduction: Spontaneous preterm birth affects>5-18% of pregnancies and causes infant morbidity and mortality. Long non-coding RNAs can regulate gene expression and have been associated with preterm birth. In this study, we investigated whether the long non-coding RNA SNHG29 was associated with spontaneous preterm birth.Methods: We collected the placentas from women who underwent preterm/full-term birth with/without labor. We determined the levels of expression of SNHG29 in the placental tissues using quantitative real-time polymerase chain reaction. We generated a senescence model by treating HTR8/SVneo cells with 200 mu M H2O2 for 2 h. The degree of senescence induced in cells depleted of or overexpressing SNHG29 was determined by measuring senescence-associated gene expression and beta-galactosidase activity.Results: SNHG29 was overexpressed in the placentas of women who delivered preterm with labor and in HTR8/SVneo cells treated with H2O2 (p < 0.05). The levels of mRNA of p53 and p21, protein levels of p53, phosphop53, p2land phospho-p21, and beta-galactosidase activity was decreased in HTR8/SVneo cells depleted of SNHG29, while the opposite trend was observed in HTR8/SVneo cells overexpressing SNHG29 (p < 0.05). We observed an increase in the expression of IL-8 and TNF-alpha in senescent HTR8/SVneo cells (p < 0.05).Discussion: SNHG29 was overexpressed in placentas from women who delivered preterm with labor compared to those in women who underwent preterm birth without labor and full-term birth with/without labor. High levels of SNHG29 enhanced senescence in vivo. The increase in pro-inflammatory cytokine expression and release by senescent cells may be pivotal to the pathophysiology of spontaneous preterm birth.