Key result
High dietary salt intake induced epithelial-to-mesenchymal transition and peritoneal fibrosis in a rat model, coinciding with upregulation of TGF-beta1 and IL-6.
Why the study?
Does high dietary salt intake induce epithelial-to-mesenchymal transition and fibrosis in the peritoneal membrane in rats?
RCT (n=28)
randomized
Does high dietary salt intake induce epithelial-to-mesenchymal transition and fibrosis in the peritoneal membrane in rats?
High dietary salt intake induces epithelial-to-mesenchymal transition and peritoneal fibrosis in a rat model, suggesting a direct profibrotic effect independent of volume overload.
Raises possibility of salt-mediated peritoneal injury in dialysis; hypothesis-generating pending human studies.
BACKGROUND: Dietary salt intake has been linked to hypertension and cardiovascular disease through volume-mediated effects. Accumulating evidence points to direct negative influence of salt intake independent of volume overload, such as cardiac and renal fibrosis, mediated through transforming growth factor beta (TGF-beta). Epithelial-to-mesenchymal transition (EMT) has been implicated as a key process in chronic fibrotic diseases, such as chronic kidney disease or heart failure. The potential role of dietary salt intake on cell transdifferentiation has never been investigated. This study analysed the effect of dietary salt intake on EMT and fibrosis in the peritoneal membrane (PM) in a rat model. METHODS: Twenty-eight Wistar rats were randomized to a normal salt (NS) or a high salt (HS) intake. NS and HS rats had free access to tap water or NaCl 2% as drinking water, respectively. After 2 weeks, samples of peritoneum were taken, and TGF-beta(1), Interleukin 6 (IL-6) and vascular endothelial growth factor (VEGF) mRNA expression were quantified with qRT-PCR. Fibrosis and submesothelial PM thickness were scored. EMT was evaluated using fluorescence staining with cytokeratin and alpha smooth muscle actin (alpha-SMA). RESULTS: Dietary salt intake caused peritoneal fibrosis and thickening of the submesothelial layer and induced EMT as identified by colocalization of cytokeratin and alpha-SMA in cells present in the submesothelial layer. Peritoneal TGF-beta(1) and IL-6 mRNA expression were upregulated in the HS group. CONCLUSION: High dietary salt intake induces EMT and peritoneal fibrosis, a process coinciding with upregulation of TGF-beta1.
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Pletinck et al. (2010) conducted an RCT in Peritoneal fibrosis and epithelial-to-mesenchymal transition (n=28). High salt intake vs. Normal salt intake (tap water) was evaluated on Epithelial-to-mesenchymal transition and fibrosis in the peritoneal membrane. High dietary salt intake induced epithelial-to-mesenchymal transition and peritoneal fibrosis in a rat model, coinciding with upregulation of TGF-beta1 and IL-6.
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