Arginine vasopressin stimulates human mesangial cell production of endothelin.

Bakris, George L.; Fairbanks, Richard; Traish, Abdul

doi:10.1172/jci115113

Cited by 72 publications

(17 citation statements)

References 27 publications

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“…These changes in ECE activity were the consequence of a decrease in ECE-1 protein content, probably as a result of a decreased expression of its mRNA. demonstrated ET-1 synthesis by HMC [31][32][33][34], in our experimental conditions, HMC synthesized minimal amounts of ET-1. In fact, no immunoreactive ET-1 was detected in the supernatants of HMC alone and only a minimal expression of prepro-ET-1 mRNA appeared in these cells, independently of the presence or absence of HuVEC.…”

Section: Discussionmentioning

confidence: 93%

Crosstalk Between Mesangial and Endothelial Cells: Angiotensin II Down-Regulates Endothelin-Converting Enzyme 1

López‐Ongil¹,

Díez-Marqués

Griera

et al. 2005

Cell Physiol Biochem

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Objective: Since mesangial and endothelial cells interact in the kidney, the present experiments were designed to analyze the ability of human mesangial cells (HMC) to modulate endothelin-1 (ET-1) synthesis by human umbilical vein endothelial cells (HuVEC). Methods and Results: The supernatants of HuVEC/HMC contained significantly lower amounts of ET-1 than those of HuVEC alone. This effect was not due to a decreased prepro-ET-1 mRNA expression and was only partially the consequence of HMC-dependent ET-1 degradation. Therefore, we tested the influence of the coculture on endothelin-converting enzyme-1 (ECE-1), and found a significant reduction of its mRNA and protein levels as well as a decreased activity in HuVEC/HMC as compared to HuVEC alone. Using a pharmacological blockade approach (sulotrobam, BN52021, losartan or catalase), losartan was shown to completely abolish down-regulation of ECE-1 observed in HuVEC/HMC. Angiotensin II (AII) induced a dose and time-dependent inhibition of ECE-1 expression in HuVEC. Conclusions: These results support the importance of cross-talk among different cell types in the regulation of vascular or renal function. ET-1, and particularly ECE-1, might constitute a target in this regulation. In addition, locally synthesized AII could be one of the mediators involved in the down-regulation of ECE-1.

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Section: Discussionmentioning

confidence: 93%

Crosstalk Between Mesangial and Endothelial Cells: Angiotensin II Down-Regulates Endothelin-Converting Enzyme 1

López‐Ongil¹,

Díez-Marqués

Griera

et al. 2005

Cell Physiol Biochem

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“…They suggested that ET-1 production by IMCD cells serves an autocrine function. Furthermore, other experiments have shown that angiotensin II [8] and arginine vasopressin (AVP) [8,9] are able to increase ET-1 release. Thus, it is possible that raised angiotensin II levels in CHF lead to increased production of ET-1 by the collecting ducts.…”

Section: Oooooooooooooooooooooomentioning

confidence: 99%

Downregulation of Endothelin B Receptors in Cardiomyopathic Hamsters

Wong

et al. 1998

Cardiology

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The mechanisms responsible for abnormal fluid retention in congestive heart failure (CHF) are unclear. Studies were conducted to elucidate how endothelin (ET) may contribute to salt and water retention. Cardiomyopathic (CM) hamsters with moderate heart failure were employed for in vivo and in vitro trials. Clearance methods were used to compare the level of renal function in CM hamsters and control animals. Radioligand binding studies were also performed to determine ET receptor distribution in the inner medullary collecting ducts. CM hamsters exhibited an attenuated response to ANF infusion (FE_Na: 2.7 ± 0.5 vs. 5.9 ± 0.8%, p < 0.01; FE_H2O: 1.7 ± 0.3 vs. 3.2 ± 0.4%, p < 0.01; U_cGMP: 11.2 ± 2.3 vs. 16.6 ± 2.0 pmol/min, p < 0.05) and a decrease in total ET receptor density (532 ± 77 vs. 959 ± 154 fmol/mg protein, p < 0.005). Particularly ET_B receptors were significantly reduced (214 ± 26 vs. 483 ± 88 fmol/mg protein, p < 0.003). Enalapril therapy simultaneously restored the natriuretic and diuretic effects of ANF and ET receptor density in the diseased animals. These studies suggest that the renin-angiotensin-aldosterone system and ET hormonal system act together, via ET_B receptor downregulation, to promote the abnormal fluid retention observed in CHF.

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“…The binding data were comparable in their sensitivity for ET levels. However, the DCC assay is advantageous since it neither requires the secondary antibody conjugates nor the additional incubation time (16)(17)(18)(19)(20)(21)(22)(23)(24) h) and the subsequent washing of the precipitated material and centrifugation. The DCC assay is sensitive (1 pmol/ml), reproducible (<6% variation) and the intra-assay and inter-assay variations are less than 10%.…”

Section: Cross-reactivity Of the Antibodies With Big Endothelin (B-et)mentioning

confidence: 99%

“…Although initially demonstrated in porcine aortic endothelial cells, it is now known that several other cell types synthesize and release endothelin (5, 6,15,16), suggesting that endothelin may participate in autocrine and paracrine modulation of cell growth and function in many tissues. The role of ETs in regulation of cell function remains the subject of active investigation.…”

mentioning

confidence: 99%

Monoclonal Antibodies to Human Endothelin-1: Characterization and Utilization in Radioimmunoassay and Immunocytochemistry

Traish

Morán²,

Daley³

et al. 1992

Hybridoma

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A host of monoclonal antibodies directed against human endothelin-1 (ET-1) has been developed and characterized. The antibodies reacted with ET-1 specifically and with high affinity, as determined by competition analysis and sucrose density gradients. The antibodies did not cross-react with neuropeptide YY, beta-endorphin, calcitonin gene-related peptide, secretin or somatostatin. The antibodies cross-reacted with big endothelin (B-ET), endothelin-2 (ET-2), vasointestinal constrictor peptide (VIC), and endothelin-3 (ET-3) albeit with varying affinity but did not cross-react with sarafotoxin (SRTX-6b). None of the antibodies reacted with the C-terminal hexapeptide (HXPT) of ET-1, indicating that the epitopes are not located within this region of ET-1. The monoclonal antibodies exhibited binding activity in dilutions ranging from 1:1000, to 1:10(6). The isotypes of the monoclonal antibodies were determined by competition binding assay. Six of the monoclonal antibodies were of the IgG gamma 1, two were IgM and one of the IgG gamma 2a subclass. The antibodies detected immunoreactive ETs by radioimmunoassay and in immunocytochemical localization, suggesting the potential use of these antibodies as tools to determine the concentration of ETs in biological fluids and in immunocytochemical localization of ETs in specific cell types in various tissues.

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Arginine vasopressin stimulates human mesangial cell production of endothelin.

Abstract: Endothelin (ET) is a vasoactive peptide produced by both endothelial and epithelial cells with documented mitogenic action on mesangial cells. The present studies were designed to test the hypothesis that ET is also produced by human mesangial cells (HMC)

Cited by 72 publications

References 27 publications

Crosstalk Between Mesangial and Endothelial Cells: Angiotensin II Down-Regulates Endothelin-Converting Enzyme 1

Crosstalk Between Mesangial and Endothelial Cells: Angiotensin II Down-Regulates Endothelin-Converting Enzyme 1

Downregulation of Endothelin B Receptors in Cardiomyopathic Hamsters

Monoclonal Antibodies to Human Endothelin-1: Characterization and Utilization in Radioimmunoassay and Immunocytochemistry

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