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

Abstract

Postoperative-fluid retention is a severe complication frequently reported in patients undergoing major surgical procedures. The complex network of molecules involved in such a severe surgery-induced condition remains poorly understood. Inflammation has been proposed among the various causes of fluid retention. Since TNF-α is one of the main proinflammatory cytokine initially released after major surgery, it is reasonable to assume its involvement in fluid overload. Here, we showed that TNF-α selectively regulates key molecules involved in fluids balance, such as natriuretic peptides (NPs) and aquaporins, in human bronchial epithelial cells BEAS-2B. In particular, we found that TNF-α induced a decrease of arial natriuretic peptide, natriuretic peptide receptor-1, aquaporin-1 and aquaporin-5 and an increase of brain natriuretic peptide with a different involvement of nuclear factor-κB and mitogen-activated protein kinases signaling pathway activation. Moreover, the observed changes in NPs expression, demonstrate inflammation as an additional cause of brain natriuretic peptide elevation, adding an important piece of information in the novel area of study regarding NPs and inflammation. Finally, we suggest that inflammation is one of the mechanisms of Aquaporin-1 and aquaporin-5 expression regulation. Therefore, in this exploratory study, we speculate that TNF-α might be involved in postoperative-fluid retention related to major surgery.

Endothelial Aquaporins and Hypomethylation: Potential Implications for Atherosclerosis and Cardiovascular Disease

“…This led us to investigate the role of TNF-α in the ADA-induced downregulation of the AQP1 and AQP5 expression. The results, depicted in Figure 4 B, show that TNF-α treatment downregulates the expression of both AQP1 and AQP5 (0.183 ± 0.01 and 0.083 ± 0.01-fold p < 0.001, respectively), as previously reported [ 42 ]. In addition, the expression levels of AQP1 and AQP5 were also drastically decreased under SAH accumulation conditions (0.184 ± 0.02 and 0.074 ± 0.01-fold; p < 0.001, respectively).…”

“…The pro-inflammatory mediator TNF-α is implicated in the regulation of the expression levels of the AQP1 and AQP5 [ 42 , 43 ]. Interestingly, we recently reported a link between ADA-induced hypomethylation and the increase of TNF-α levels in cultured human endothelial cells [ 33 ].…”

Status of hydration assessed by bioelectrical impedance analysis: a valuable predictive factor for radiation-induced oral mucositis in head and neck cancer patients

“…The changes in hydration during inflammation also occur through changes in aquaporin function. In an in vitro study performed on human bronchial epithelial cells (BEAS-2B), Mezzasoma et al [27] demonstrated that, in inflammation, TNFα induced a decrease of atrial natriuretic peptide, natriuretic peptide receptor-1, aquaporin-1 and aquaporin-5 and an increase of brain natriuretic peptide with involvement of different NFκB and mitogen-activated protein kinases signaling pathway activation.…”

Ectopic expression of aquaporin-5 in noncancerous epithelial MDCK cells changes cellular morphology and actin fiber formation without inducing epithelial-to-mesenchymal transition

“…However, no increase of mesenchymal markers was detected for the second clone tested. Although BEAS-2B are noncancerous cells, they are easily differentiated and have endogenous AQP5 expression (28). These observations emphasize that the cellular environment may be of high importance to how AQP5 affects cell behavior.…”