Dietary salt modulates renal production of transforming growth factor-β in rats

Ying, Wei‐Zhong; Sanders, Paul W.

doi:10.1152/ajprenal.1998.274.4.f635

Cited by 86 publications

(85 citation statements)

References 45 publications

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“…32 These effects of high salt intake on target organs are linked to the fibrogenic activity of transforming growth factor (TGF)-b1, as TGF-b1 production has been demonstrated to increase during high salt intake. 33,34 Indeed, the overexpression of TGF-b1 mRNA was demonstrated in the left ventricle and kidneys after a high-salt diet in animal studies. 31 The present study demonstrated a positive correlation between albuminuria and serum CRP levels in treated hypertensive patients.…”

Section: Discussionmentioning

confidence: 99%

Dietary salt intake is related to inflammation and albuminuria in primary hypertensive patients

et al. 2012

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BACKGROUND/OBJECTIVES:In this study, we hypothesized that dietary salt intake may be related with inflammation and albuminuria independently from blood pressure (BP) in non-diabetic hypertensive patients. SUBJECTS/METHODS: A total of 224 patients with primary hypertension were included in the study. Serum C-reactive protein (CRP) levels, 24-h urine sodium and albumin excretion were measured in all patients. The subjects were divided into tertiles according to the level of 24-h urinary sodium excretion: low-salt-intake group (n ¼ 76, mean urine sodium: 111.7 ± 29.1 mmol/24 h), mediumsalt-intake group (n ¼ 77, mean urine sodium: 166.1 ± 16.3 mmol/24 h) and high-salt-intake group (n ¼ 71, mean urine sodium: 263.6±68.3 mmol/24 h). RESULTS: Systolic and diastolic BP measurements of patients were similar in the three salt-intake groups. CRP and urinary albumin levels were significantly higher in high-salt-intake group compared with medium-and low-salt-intake groups (P ¼ 0.0003 and P ¼ 0.001, respectively). CRP was positively correlated with 24-h urinary sodium excretion (r ¼ 0.28, P ¼ 0.0008) and albuminuria, whereas albuminuria was positively correlated with 24-h urinary sodium excretion (r ¼ 0.21, P ¼ 0.0002). Multiple regression analysis revealed that urinary sodium excretion was an independent predictor of both CRP and albuminuria. CONCLUSIONS: These findings suggest that high salt intake is associated with enhanced inflammation and target organ damage reflected by increased albuminuria in treated hypertensive patients independent of any BP effect. Keywords: albuminuria; hypertension; inflammation; salt intake INTRODUCTION Salt intake is an important factor in the genesis of primary hypertension. Epidemiological and clinical data have showed that high salt intake is associated with increased risk of cardiovascular diseases and stroke. 1 Recent work has provided further evidence that high dietary salt intake may even partly cause blood pressure (BP) -independent target organ damage including left ventricular hypertrophy and microalbuminuria. [2][3][4] Microalbuminuria is a significant predictor of endothelial dysfunction and an independent marker of cardiovascular diseases in patients with primary hypertension. 5,6 Several studies have demonstrated that high salt intake is positively related to urinary albumin excretion and this relation may be independent of BP. 3,4,7 The mechanisms responsible for this effect are unclear. In animal models, dietary salt overload has been demonstrated to contribute to renal injury documented by albuminuria and decreased glomerular filtration rate with a minimally increased arterial pressure. 8,9 Inflammatory mechanisms have been proposed to have a role in this nephrotoxic effect of salt excess. 9-13 The role of inflammation in the initiation and progression of cardiovascular diseases is increasingly recognized. 14,15 Studies in hypertensive individuals have shown increased plasma and vascular tissue levels of C-reactive protein (CRP) and several inflammatory cytokines, suggesting a...

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Section: Discussionmentioning

confidence: 99%

Dietary salt intake is related to inflammation and albuminuria in primary hypertensive patients

et al. 2012

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“…These findings suggest that the vascular smooth muscle hypertrophy and the ventricular hypertrophy in SHR-SP resulted directly from the severe hypertension, but that the renal damage may be associated not only with the hypertension but also with the local production of TGF-β. In addition, dietary salt has been reported to modulate production of TGF-β in the kidney (15,16). Ying and Sanders (15) reported that an increase in dietary salt produced sustained increases in expression of TGF-β1 mRNA in rat kidney, but no changes in serum concentration of TGF-β1.…”

Section: Discussionmentioning

confidence: 99%

Transforming Growth Factor-.BETA. Expression in Cardiovascular Organs in Stroke-Prone Spontaneously Hypertensive Rats with the Development of Hypertension.

et al. 2002

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“…TGF-␤1 protein levels in urine and conditioned medium were determined by enzyme immunoassay (TGF-␤1 Emax ImmunoAssay System; Promega) as described previously (26). Mesangial cells were treated with 0.1 or 1.0 M polyamide or 1.0 M mismatch in the presence of 1.0 M PMA for 24 h. Conditioned medium was collected and diluted with TGF-␤1 sample buffer.…”

Section: Measurement Of Tgf-␤1 Proteinmentioning

confidence: 99%

Development of Gene Silencing Pyrrole-Imidazole Polyamide Targeting the TGF-β1 Promoter for Treatment of Progressive Renal Diseases

Matsuda¹,

Fukuda²,

Ueno³

et al. 2006

Journal of the American Society of Nephrology

102

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Pyrrole-imidazole (Py-Im) polyamides are nuclease-resistant novel compounds that inhibit gene expression by binding to the minor groove of DNA. A Py-Im polyamide that targets rat TGF-␤1 was designed as a gene-silencing agent for progressive renal diseases, and the distribution and the effects of this polyamide on renal injury were examined in Dahl-salt sensitive (Dahl-S) rats. For identification of transcription factor binding elements for activation of the rat TGF-␤1 gene, recombinant TGF-␤1 reporter plasmids were transfected into HEK-293 cells, and promoter activity was measured. Py-Im polyamide was designed to the activator protein-1 binding site of the rat TGF-␤1 promoter. This Py-Im polyamide showed strong, fast, and specific binding to the target DNA in gel mobility shift and Biacore assays. Py-Im polyamide significantly inhibited TGF-␤1 promoter activity and expression of TGF-␤1 mRNA and protein in rat mesangial cells. Intravenously administered fluorescein-labeled polyamide distributed to the kidney of rats. Py-Im polyamide significantly inhibited expression of TGF-␤1 mRNA and protein in the renal cortex of Dahl-S rats and reduced the increase in urinary protein and albumin in Dahl-S rats independent of changes in blood pressure. These results indicate that Py-Im polyamide that targets TGF-␤1 will be a novel gene-silencing agent for the TGF-␤1-associated diseases, including progressive renal diseases.

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Dietary salt modulates renal production of transforming growth factor-β in rats

Cited by 86 publications

References 45 publications

Dietary salt intake is related to inflammation and albuminuria in primary hypertensive patients

Dietary salt intake is related to inflammation and albuminuria in primary hypertensive patients

Transforming Growth Factor-.BETA. Expression in Cardiovascular Organs in Stroke-Prone Spontaneously Hypertensive Rats with the Development of Hypertension.

Development of Gene Silencing Pyrrole-Imidazole Polyamide Targeting the TGF-β1 Promoter for Treatment of Progressive Renal Diseases

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