Fig. 4

Cigarette smoke exposure promoted SERPINB2 expression levels in endometrial stem cells. We postulated that SERPINB2 functions as a key regulator of smoking-induced toxic response (A). Cells were treated with cigarette smoke extract at 0.5, 1, 3, or 5% for 72 h. Real-time PCR and western blotting were conducted to investigate the effects of cigarette smoke exposure on the mRNA and protein levels of SERPINB2 (B). GEO respiratory metadata were analyzed to investigate interactions between elevated SERPINB2 expression and exposures to toxic agents, such as radiation, heavy metals, air pollution, and toxic substances (C). Differentially activated genes in toxicant exposed lung cells and nonexposed lung cells were analyzed using IPA software to investigate the activation statuses (intermediate, inactive, or activate) of SERPINB2 (GSE62564)-associated signaling molecules/transcription factors (D). Differentially activated genes in toxicant exposed liver cells and nonexposed liver cells were analyzed using IPA software to investigate the activation status of SERPINB2 (GSE62564)-associated signaling molecules/transcription factors (E). β-actin was used as the internal control, and PPIA as the housekeeping gene for real-time PCR. All experiments were performed in triplicate. Data are presented as means ± SDs. *, p < 0.05; **, p < 0.005; and ***, p < 0.001 (two-sample t test)