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Sphingosine-1-phosphate and endothelin-1 induce the expression of rgs16 protein in cardiac myocytes by transcriptional activation of the rgs16 gene

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Sphingosine-1-phosphate and endothelin-1 induce the expression of rgs16 protein in cardiac myocytes by transcriptional activation of the rgs16 gene. / Stuebe, Sabine; Wieland, Thomas; Kraemer, Elisabeth; Stritzky, Alexandra v; Schroeder, Diana; Seekamp, Sünje; Vogt, Andreas; Chen, Ching-Kang; Patten, Monica.

In: N-S ARCH PHARMACOL, Vol. 376, No. 5, 01.2008, p. 363-373.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Stuebe, S, Wieland, T, Kraemer, E, Stritzky, AV, Schroeder, D, Seekamp, S, Vogt, A, Chen, C-K & Patten, M 2008, 'Sphingosine-1-phosphate and endothelin-1 induce the expression of rgs16 protein in cardiac myocytes by transcriptional activation of the rgs16 gene', N-S ARCH PHARMACOL, vol. 376, no. 5, pp. 363-373. https://doi.org/10.1007/s00210-007-0214-2

APA

Stuebe, S., Wieland, T., Kraemer, E., Stritzky, A. V., Schroeder, D., Seekamp, S., Vogt, A., Chen, C-K., & Patten, M. (2008). Sphingosine-1-phosphate and endothelin-1 induce the expression of rgs16 protein in cardiac myocytes by transcriptional activation of the rgs16 gene. N-S ARCH PHARMACOL, 376(5), 363-373. https://doi.org/10.1007/s00210-007-0214-2

Vancouver

Stuebe S, Wieland T, Kraemer E, Stritzky AV, Schroeder D, Seekamp S et al. Sphingosine-1-phosphate and endothelin-1 induce the expression of rgs16 protein in cardiac myocytes by transcriptional activation of the rgs16 gene. N-S ARCH PHARMACOL. 2008 Jan;376(5):363-373. https://doi.org/10.1007/s00210-007-0214-2

Bibtex

@article{f1cabc6fc0f64e6498c676aae3541a3f,
title = "Sphingosine-1-phosphate and endothelin-1 induce the expression of rgs16 protein in cardiac myocytes by transcriptional activation of the rgs16 gene",
abstract = "The expression of the negative Regulator of G protein signaling 16 (RGS16) is rapidly induced in cardiomyocytes by various stimuli. To identify the promoter of the mouse RGS16 gene, a 1.8-kb deoxyribonucleic acid fragment 5' of the RGS16-coding region was subcloned into a firefly-luciferase reporter vector and four overlapping fragments were analyzed. The luciferase production was quantified in neonatal rat cardiac myocytes (NRCM). A 0.6-kb fragment that induced a tenfold increase in luciferase activity contained the minimal promoter sequence. Its activity was twofold stimulated by fetal calf serum, endothelin-1 (ET-1), and sphingosine 1-phosphate (S1P), which stimuli also elevated the level of RGS16 protein. Stimulation of NRCM with ET-1 induced activation of the monomeric GTPases RhoA and Rac1, whereas S1P and the selective S1P1 receptor agonist SEW2871 only induced a pronounced activation of Rac1. In accordance, the treatment with the Rho-, Rac-, and Cdc42-inactivating Clostridium difficile Toxin B (TcdB) 10463 inhibited ET-1 and S1P-induced transcriptional activation. The ET-1-induced activation was insensitive to pertussis toxin but selectively suppressed by the RhoA-C-specific C2I-C3 ADP-ribosyl transferase and the ET(B) receptor antagonist BQ788. The S1P-induced activation was specifically inhibited by pertussis toxin and the Rac-inactivating TcdB 1470. All stimulated transcriptional activity was abolished by the negative transcription factor Yin Yang 1 (YY1), which binds to a consensus sequence within the minimal promoter. Taken together, our data show that most likely ET(B)- and S1P1-receptors induce RGS16 protein expression in cardiac myocytes by increasing the transcriptional activity of the rgs16 gene. This activation is mediated by heterotrimeric G proteins, Rho GTPases, and is under negative control of the transcription factor YY1.",
keywords = "Animals, Animals, Newborn, Bacterial Proteins/pharmacology, Bacterial Toxins/pharmacology, Cattle, Cells, Cultured, Endothelin-1/physiology, Fetal Blood/metabolism, Gene Expression Regulation, Luciferases/metabolism, Lysophospholipids/physiology, Mice, Myocytes, Cardiac, Pertussis Toxin/pharmacology, Promoter Regions, Genetic, RGS Proteins/metabolism, Rats, Sphingosine/analogs & derivatives, Transcription, Genetic, YY1 Transcription Factor/metabolism, rac1 GTP-Binding Protein/metabolism, rhoA GTP-Binding Protein/metabolism",
author = "Sabine Stuebe and Thomas Wieland and Elisabeth Kraemer and Stritzky, {Alexandra v} and Diana Schroeder and S{\"u}nje Seekamp and Andreas Vogt and Ching-Kang Chen and Monica Patten",
year = "2008",
month = jan,
doi = "10.1007/s00210-007-0214-2",
language = "English",
volume = "376",
pages = "363--373",
journal = "N-S ARCH PHARMACOL",
issn = "0028-1298",
publisher = "Springer",
number = "5",

}

RIS

TY - JOUR

T1 - Sphingosine-1-phosphate and endothelin-1 induce the expression of rgs16 protein in cardiac myocytes by transcriptional activation of the rgs16 gene

AU - Stuebe, Sabine

AU - Wieland, Thomas

AU - Kraemer, Elisabeth

AU - Stritzky, Alexandra v

AU - Schroeder, Diana

AU - Seekamp, Sünje

AU - Vogt, Andreas

AU - Chen, Ching-Kang

AU - Patten, Monica

PY - 2008/1

Y1 - 2008/1

N2 - The expression of the negative Regulator of G protein signaling 16 (RGS16) is rapidly induced in cardiomyocytes by various stimuli. To identify the promoter of the mouse RGS16 gene, a 1.8-kb deoxyribonucleic acid fragment 5' of the RGS16-coding region was subcloned into a firefly-luciferase reporter vector and four overlapping fragments were analyzed. The luciferase production was quantified in neonatal rat cardiac myocytes (NRCM). A 0.6-kb fragment that induced a tenfold increase in luciferase activity contained the minimal promoter sequence. Its activity was twofold stimulated by fetal calf serum, endothelin-1 (ET-1), and sphingosine 1-phosphate (S1P), which stimuli also elevated the level of RGS16 protein. Stimulation of NRCM with ET-1 induced activation of the monomeric GTPases RhoA and Rac1, whereas S1P and the selective S1P1 receptor agonist SEW2871 only induced a pronounced activation of Rac1. In accordance, the treatment with the Rho-, Rac-, and Cdc42-inactivating Clostridium difficile Toxin B (TcdB) 10463 inhibited ET-1 and S1P-induced transcriptional activation. The ET-1-induced activation was insensitive to pertussis toxin but selectively suppressed by the RhoA-C-specific C2I-C3 ADP-ribosyl transferase and the ET(B) receptor antagonist BQ788. The S1P-induced activation was specifically inhibited by pertussis toxin and the Rac-inactivating TcdB 1470. All stimulated transcriptional activity was abolished by the negative transcription factor Yin Yang 1 (YY1), which binds to a consensus sequence within the minimal promoter. Taken together, our data show that most likely ET(B)- and S1P1-receptors induce RGS16 protein expression in cardiac myocytes by increasing the transcriptional activity of the rgs16 gene. This activation is mediated by heterotrimeric G proteins, Rho GTPases, and is under negative control of the transcription factor YY1.

AB - The expression of the negative Regulator of G protein signaling 16 (RGS16) is rapidly induced in cardiomyocytes by various stimuli. To identify the promoter of the mouse RGS16 gene, a 1.8-kb deoxyribonucleic acid fragment 5' of the RGS16-coding region was subcloned into a firefly-luciferase reporter vector and four overlapping fragments were analyzed. The luciferase production was quantified in neonatal rat cardiac myocytes (NRCM). A 0.6-kb fragment that induced a tenfold increase in luciferase activity contained the minimal promoter sequence. Its activity was twofold stimulated by fetal calf serum, endothelin-1 (ET-1), and sphingosine 1-phosphate (S1P), which stimuli also elevated the level of RGS16 protein. Stimulation of NRCM with ET-1 induced activation of the monomeric GTPases RhoA and Rac1, whereas S1P and the selective S1P1 receptor agonist SEW2871 only induced a pronounced activation of Rac1. In accordance, the treatment with the Rho-, Rac-, and Cdc42-inactivating Clostridium difficile Toxin B (TcdB) 10463 inhibited ET-1 and S1P-induced transcriptional activation. The ET-1-induced activation was insensitive to pertussis toxin but selectively suppressed by the RhoA-C-specific C2I-C3 ADP-ribosyl transferase and the ET(B) receptor antagonist BQ788. The S1P-induced activation was specifically inhibited by pertussis toxin and the Rac-inactivating TcdB 1470. All stimulated transcriptional activity was abolished by the negative transcription factor Yin Yang 1 (YY1), which binds to a consensus sequence within the minimal promoter. Taken together, our data show that most likely ET(B)- and S1P1-receptors induce RGS16 protein expression in cardiac myocytes by increasing the transcriptional activity of the rgs16 gene. This activation is mediated by heterotrimeric G proteins, Rho GTPases, and is under negative control of the transcription factor YY1.

KW - Animals

KW - Animals, Newborn

KW - Bacterial Proteins/pharmacology

KW - Bacterial Toxins/pharmacology

KW - Cattle

KW - Cells, Cultured

KW - Endothelin-1/physiology

KW - Fetal Blood/metabolism

KW - Gene Expression Regulation

KW - Luciferases/metabolism

KW - Lysophospholipids/physiology

KW - Mice

KW - Myocytes, Cardiac

KW - Pertussis Toxin/pharmacology

KW - Promoter Regions, Genetic

KW - RGS Proteins/metabolism

KW - Rats

KW - Sphingosine/analogs & derivatives

KW - Transcription, Genetic

KW - YY1 Transcription Factor/metabolism

KW - rac1 GTP-Binding Protein/metabolism

KW - rhoA GTP-Binding Protein/metabolism

U2 - 10.1007/s00210-007-0214-2

DO - 10.1007/s00210-007-0214-2

M3 - SCORING: Journal article

C2 - 18046543

VL - 376

SP - 363

EP - 373

JO - N-S ARCH PHARMACOL

JF - N-S ARCH PHARMACOL

SN - 0028-1298

IS - 5

ER -