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Fig. 4 | Respiratory Research

Fig. 4

From: Human epididymis protein 4 aggravates airway inflammation and remodeling in chronic obstructive pulmonary disease

Fig. 4

HE4 affected IL-6 release in HBE cells through phosphorylation of NFκB-p65. A–C The transfection of siRNA in HBE cells significantly lowered HE4 mRNA expression (n = 3), secretory level (n = 3) and intracellular protein expression (n = 4). A, B, D Infecting lentivirus expressing HE4 markedly enhanced HE4 mRNA expression (n = 3), secretory level (n = 4) and intracellular protein expression (n = 4). The western blot images were shown and quantified by ImageJ. E, G HE4 knockdown mitigated IL-6 expression while HE4 overexpression augmented IL-6 expression in HBE cells both in mRNA level (n = 3) and secretory protein level (n = 4). F, H Intervening HE4 expression had no significant impact on IL-8 expression, although reducing HE4 expression can alleviate CSE-induced IL-8 elevation at mRNA level (n = 3–4). I, J Knockdown of HE4 expression reduced phosphorylation of NFκB-p65 relative to the expression of p65 (n = 4). K, L Overexpression of HE4 increased phosphorylation of NFκB-p65 (n = 5). Data are expressed as mean ± SEM. P-values were calculated using one-way ANOVA followed by Newman–Keuls test. *P < 0.05, **P < 0.01, and ***P < 0.001 represent significant differences. HE4, human epididymis protein 4; si, small interfering RNA; NC, negative control; Lv-GFP, lentivirus with empty vector carrying green fluorescent protein; Lv-HE4, lentivirus expressing HE4; CSE, cigarette smoke extract; HBE, human bronchial epithelial; IL-6, interleukin-6; IL-8, interleukin-8

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