Abstract
Dietary salt intake has been linked to hypertension and cardiovascular disease. Accumulating evidence has indicated that salt-sensitive individuals on high salt intake are more likely to develop renal fibrosis. Epithelial-to-mesenchymal transition (EMT) participates in the development and progression of renal fibrosis in humans and animals. The objective of this study was to investigate the impact of a high-salt diet on EMT in Dahl salt-sensitive (SS) rats. Twenty-four male SS and consomic SS-13BN rats were randomized to a normal diet or a high-salt diet. After 4 weeks, systolic blood pressure (SBP) and albuminuria were analyzed, and renal fibrosis was histopathologically evaluated. Tubular EMT was evaluated using immunohistochemistry and real-time PCR with E-cadherin and alpha smooth muscle actin (α-SMA). After 4 weeks, SBP and albuminuria were significantly increased in the SS high-salt group compared with the normal diet group. Dietary salt intake induced renal fibrosis and tubular EMT as identified by reduced expression of E-cadherin and enhanced expression of α-SMA in SS rats. Both blood pressure and renal interstitial fibrosis were negatively correlated with E-cadherin but positively correlated with α-SMA. Salt intake induced tubular EMT and renal injury in SS rats, and this relationship might depend on the increase in blood pressure.
Highlights
Salt has been linked to hypertension for many years [1]
Tubular Epithelial-to-mesenchymal transition (EMT) To demonstrate EMT in tubular epithelial cells, we examined the expression of E-cadherin, a phenotypic marker of epithelial cells, and alpha smooth muscle actin (a-SMA), a phenotypic marker of myofibroblast cells
We found that after salt loading, when the blood pressure in SS rats rose to 184 mmHg we could observe the occurrence of EMT
Summary
It was thought that volume overload induced by salt retention was the main underlying mechanism, and that this in turn was the driving factor for left ventricular hypertrophy. Evidence has accumulated that dietary salt intake by itself, even without causing hypertension or volume overload, might be deleterious, resulting in cardiac remodeling, fibrosis, and left ventricular hypertrophy [2]. Salt-sensitive subjects on a high-salt diet showed increased microalbuminuria, elevated renal vascular resistance, and decreased filtration fractions [7,8]. Rapid development of renal injury is a prominent feature of salt-induced hypertension in Dahl salt-sensitive (SS) rats. The mechanisms underlying the induction of renal injury, especially renal fibrosis, in salt-sensitive subjects on a high-salt diet are not fully understood
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