TNF-𝜶 Regulates Natriuretic Peptides and Aquaporins in Human Bronchial Epithelial Cells BEAS-2B

Figure 5

TNF-α modulation of BNP and NPR-1 expression may require activation of MAPKs pathway. BEAS-2B cells were treated with 10 ng/mL TNF-α alone or in combination with 10 μM SB 203580 (p38 MAPK inhibitor), SP 600125 (JNK 1/2 inhibitor), or U-0126 (ERK 1/2 inhibitor), for 24 h. Panels show: ((a), (b)) BNP, ((c), (d)) NPR-1 gene expression at mRNA ((a), (c)) and protein ((b), (d)) level, and (e) Phospho-p38 MAPK protein level. Western blots were obtained by using the specific rabbit polyclonal or monoclonal Abs. The blots were stripped of the bound Ab and reprobed with mouse anti-β-actin, to confirm equal loading. Western blots are representative of three separate experiments. All histograms indicate means±SD of three different cultures each one tested in quadruplicate and expressed as percentage of control. (^∗𝑃<0.05, ^∗∗𝑃<0.01, and ^∗∗∗𝑃<0.001 versus Controls) (^••𝑃<0.01 versus SB) (^§𝑃<0.05,^§§𝑃<0.01 versus SP) (^∘∘𝑃<0.01, ^∘∘∘𝑃<0.001 versus U-0126). C: Controls (untreated cells).

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