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1. RhoA-ROCK signaling is involved in contraction-mediated inhibition of SERCA2a expression in cardiomyocytes

Author

A. Muller, Warner S. Simonides, Cornelis van Hardeveld, Cora M.L. Beckers, Geerten P. van Nieuw Amerongen, Walter Paulus, Marian J. Zuidwijk, Ronald Vlasblom, Physiology, Anatomy and neurosciences, and ICaR - Heartfailure and pulmonary arterial hypertension

Subjects
RHOA, Signaling and Cell Physiology, Physiology, Clinical Biochemistry, Signal transduction, Sarcoplasmic Reticulum Calcium-Transporting ATPases, GATA4, Transcription (biology), Physiology (medical), ROCK, Serum response factor, Gene expression, Transcriptional regulation, Animals, Myocytes, Cardiac, Rats, Wistar, Transcription factor, Cells, Cultured, rho-Associated Kinases, biology, RhoA, Transcription regulation, Myocardial Contraction, Molecular biology, Rats, Animals, Newborn, Gene Expression Regulation, Myocardin, embryonic structures, cardiovascular system, biology.protein, SRF, rhoA GTP-Binding Protein, SERCA2a, circulatory and respiratory physiology
Abstract

In neonatal ventricular cardiomyocytes (NVCM), decreased contractile activity stimulates sarco-endoplasmic reticulum Ca(2+)-ATPase2a (SERCA2a), analogous to reduced myocardial load in vivo. This study investigated in contracting NVCM the role of load-dependent RhoA-ROCK signaling in SERCA2a regulation. Contractile arrest of NVCM resulted in low peri-nuclear localized RhoA levels relative to contracting NVCM. In arrested NVCM, ROCK activity was decreased (59%) and paralleled a loss in F-actin levels. Y-27632-induced ROCK inhibition in contracting NVCM increased SERCA2a messenger RNA expression by 150%. This stimulation was transcriptional, as evident from transfections with the SERCA2a promoter. A reciprocal effect of Y-27632 treatment on the promoter activity of atrial natriuretic factor was observed. SERCA2a transcription was not altered by co-transfection of the RhoA-ROCK-dependent serum response factor (SRF) alone or in combination with myocardin. Furthermore, GATA4, another ROCK-dependent transcription factor, induced rather than repressed SERCA2a transcription. This study shows that contractile activity suppresses SERCA2a gene expression via RhoA-ROCK-dependent transcription modulation. This modulation is likely to be accomplished by a transcription factor other than SRF, myocardin, or GATA4.

Published
2009
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2. The role of the Ferric Uptake Regulator (Fur) in regulation of Helicobacter pylori iron uptake

Author

Nicola Jane Hughes, Manfred Kist, Stuart A. Wainwright, Stefan Bereswill, Ernst J. Kuipers, Johannes G. Kusters, Ronald Vlasblom, Christina M. J. E. Vandenbroucke-Grauls, David J. Kelly, Jetta J. E. Bijlsma, Theo Hoogenboezem, Arnoud H. M. van Vliet, Jeroen Stoof, Gastroenterology & Hepatology, Erasmus School of Philosophy, and Medical Microbiology and Infection Prevention

Subjects
Transcription, Genetic, Iron, Recombinant Fusion Proteins, Mutant, lac operon, Receptors, Cell Surface, 03 medical and health sciences, Bacterial Proteins, Gene expression, medicine, Humans, Promoter Regions, Genetic, Psychological repression, Gene, 030304 developmental biology, 2. Zero hunger, Regulation of gene expression, 0303 health sciences, Helicobacter pylori, biology, 030306 microbiology, Escherichia coli Proteins, Gastroenterology, Biological Transport, Gene Expression Regulation, Bacterial, General Medicine, biology.organism_classification, Culture Media, Repressor Proteins, Infectious Diseases, Lac Operon, Biochemistry, Mutation, Ferric, Carrier Proteins, Bacteria, Bacterial Outer Membrane Proteins, medicine.drug
Abstract

Background. Availability of the essential nutrient iron is thought to vary greatly in the gastric mucosa, and thus the human gastric pathogen Helicobacter pylori requires regulatory responses to these environmental changes. Bacterial iron-responsive regulation is often mediated by Ferric Uptake Regulator (Fur) homologs, and in this study we have determined the role of H. pylori Fur in regulation of H. pylori iron uptake. Methods. Wild-type H. pylori and fur mutant derivatives were compared after growth in iron-restricted and iron-replete conditions. Iron-uptake was measured using 55Fe-labeled iron, whereas gene expression was monitored at the transcriptional level using Northern hybridization and lacZ reporter gene fusions. Results. Iron-uptake and total cellular iron content were approximately five-fold increased in the fur mutant compared with the wild-type strain, which indicated that in the fur mutant iron-uptake is not repressed by excess iron. A comprehensive screening of all H. pylori genes encoding putative iron-uptake proteins indicated that some of these H. pylori genes are constitutively expressed, while others are iron- and Fur-regulated. Conclusions. Iron uptake in H. pylori is in part differently regulated compared with other bacteria, since in H. pylori some iron-uptake systems are constitutively expressed. However, other iron uptake systems of H. pylori display the iron- and Fur-mediated repression that is common in bacteria. Taken together, this Fur-mediated modulation of iron-uptake capacity may be a specific adaptation to the conditions in the human stomach, where iron starvation and iron overload can be encountered in relatively short time intervals.

Published
2002
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3. RhoA-ROCK signaling is involved in contraction-mediated inhibition of SERCA2a expression in cardiomyocytes.

Author

Vlasblom, Ronald, Muller, Alice, Beckers, Cora M. L., van Nieuw Amerongen, Geerten P., Zuidwijk, Marian J., van Hardeveld, Cornelis, Paulus, Walter J., and Simonides, Warner S.

Subjects
HEART cells, CELLULAR signal transduction, ENDOPLASMIC reticulum, MESSENGER RNA, GENE expression
Abstract

In neonatal ventricular cardiomyocytes (NVCM), decreased contractile activity stimulates sarco-endoplasmic reticulum Ca2+-ATPase2a (SERCA2a), analogous to reduced myocardial load in vivo. This study investigated in contracting NVCM the role of load-dependent RhoA-ROCK signaling in SERCA2a regulation. Contractile arrest of NVCM resulted in low peri-nuclear localized RhoA levels relative to contracting NVCM. In arrested NVCM, ROCK activity was decreased (59%) and paralleled a loss in F-actin levels. Y-27632-induced ROCK inhibition in contracting NVCM increased SERCA2a messenger RNA expression by 150%. This stimulation was transcriptional, as evident from transfections with the SERCA2a promoter. A reciprocal effect of Y-27632 treatment on the promoter activity of atrial natriuretic factor was observed. SERCA2a transcription was not altered by co-transfection of the RhoA-ROCK-dependent serum response factor (SRF) alone or in combination with myocardin. Furthermore, GATA4, another ROCK-dependent transcription factor, induced rather than repressed SERCA2a transcription. This study shows that contractile activity suppresses SERCA2a gene expression via RhoA-ROCK-dependent transcription modulation. This modulation is likely to be accomplished by a transcription factor other than SRF, myocardin, or GATA4. [ABSTRACT FROM AUTHOR]

Published
2009
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4. Contractile arrest reveals calcium-dependent stimulation of SERCA2a mRNA expression in cultured ventricular cardiomyocytes

Author

Vlasblom, Ronald, Muller, Alice, Musters, René J.P., Zuidwijk, Marian J., van Hardeveld, Cornelis, Paulus, Walter J., and Simonides, Warner S.

Subjects
PROTEINS, PROSPECTING, BRAIN stimulation, HYPERTROPHY
Abstract

Objective: Downregulation of sarco-endoplasmic reticulum calcium ATPase 2a (SERCA2a) expression is a critical marker of pathological myocardial hypertrophy. The effects of calcium-dependent signaling and of contractile activity on the regulation of myocardial SERCA2a expression remain unclear. The present study dissociates effects of calcium-dependent signaling through calcineurin (CN) and calmodulin dependent protein kinase-II (CAMK-II), from effects of contractile activity in spontaneously contracting rat neonatal ventricular cardiomyocytes (NVCM) using 2,3-butanedione monoxime (BDM), which arrests contractions but maintains calcium fluxes. Methods: SERCA2a mRNA expression was analysed using Northern hybridisation in spontaneously contracting NVCM (control) and in NVCM treated with either BDM, L-type Ca2+-channel blocker (verapamil), CN-blocker (cyclosporin A; CsA), CAMK-II blocker (KN-93), or combinations thereof. Transient transfection of the CN-dependent transcription factor nuclear factor of activated T-lymphocytes (NFATc), coupled to GFP, was used to detect NFAT nuclear translocation. The effects of CN/CAMK-II-dependent signaling were further dissected into effects of the transcription factors NFATc4 and myocyte enhancer factor 2c (MEF2c) on the activity of various SERCA2a promoter fragments using transient transfection assays. Results: Treatment with BDM induced a 2.5-fold rise in SERCA2a mRNA, which was abolished by addition of verapamil and was reduced by addition of CsA (-40%) and KN-93 (-20%). NFAT nuclear translocation was similar in control and BDM-treated NVCM. SERCA2a promoter activity was stimulated by NFATc4 and MEF2c, but only when both factors were co-transfected. Conclusion: Following contractile arrest with BDM, upregulation of SERCA2a mRNA expression by CN/CAMK-II signaling becomes evident. This upregulation is likely the result of synergistic stimulation of SERCA2a promoter activity by NFATc4 and MEF2c. Contractile activity opposes this upregulation through distinct and independent pathways. [Copyright &y& Elsevier]

Published
2004
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