A5006256064- Cardiac Fibrosis and Remodeling
- Signaling Pathways in Disease
- Cardiomyopathy and Myosin Studies
- Heart Failure Treatment and Management
- Cardiovascular Function and Risk Factors
- RNA Research and Splicing
- RNA and protein synthesis mechanisms
- Receptor Mechanisms and Signaling
- Cardiovascular, Neuropeptides, and Oxidative Stress Research
- Nitric Oxide and Endothelin Effects
- Cardiac Structural Anomalies and Repair
- NF-κB Signaling Pathways
- Renin-Angiotensin System Studies
- Tissue Engineering and Regenerative Medicine
- Vasculitis and related conditions
- Renal Diseases and Glomerulopathies
- Parathyroid Disorders and Treatments
- Pharmacological Effects and Assays
- Gout, Hyperuricemia, Uric Acid
- Muscle Physiology and Disorders
- Neuropeptides and Animal Physiology
- Congenital heart defects research
- Viral Infections and Immunology Research
- Cardiac electrophysiology and arrhythmias
- Apelin-related biomedical research
Oulu University Hospital
2014-2024
University of Oulu
2009-2022
Matrix Research (United States)
2011
Orion Corporation (Finland)
2011
Institute for Biomedicine
2010
Semmelweis University
2001-2003
University of Pecs
2002-2003
Hungarian Academy of Sciences
2003
The orphan receptor APJ and its recently identified endogenous ligand, apelin, exhibit high levels of mRNA expression in the heart. However, functional importance apelin cardiovascular system is not known. In isolated perfused rat hearts, infusion (0.01 to 10 nmol/L) induced a dose-dependent positive inotropic effect (EC 50 : 33.1±1.5 pmol/L). Moreover, preload-induced increase dP/dt max was significantly augmented ( P <0.05) presence apelin. Inhibition phospholipase C (PLC) with U-73122...
Nephritis is a common manifestation of IgA vasculitis and morphologically indistinguishable from nephropathy. While MEST-C scores are predictive kidney outcomes in nephropathy, their value nephritis has not been investigated large multiethnic cohorts.
In overloaded heart the cardiomyocytes adapt to increased mechanical and neurohumoral stress by activation of hypertrophic program, resulting in morphological changes individual cells specific gene expression. Accumulating evidence suggests an important role for zinc finger transcription factor GATA-4 agonist-induced cardiac hypertrophy. However, its stretch-induced cardiomyocyte hypertrophy is not known. We employed vitro stretch model cultured used rat B-type natriuretic peptide promoter...
Mechanical forces are able to activate hypertrophic growth of cardiomyocytes in the overloaded myocardium. However, transcriptional profiles triggered by mechanical stretch cardiac myocytes not fully understood. Here, we performed first genome-wide time series study gene expression changes stretched cultured neonatal rat ventricular (NRVM)s, resulting 205, 579, 737, 621, and 1542 differentially expressed (>2-fold, P < 0.05) genes response 1, 4, 12, 24, 48 hours cyclic stretch. We used...
Background —The signaling cascades responsible for the activation of transcription factors in hypertrophic growth cardiac myocytes during hemodynamic overload are largely unknown. Several genes upregulated hypertrophied heart, including B-type natriuretic peptide (BNP) gene, controlled by cardiac-restricted zinc finger factor GATA4. Methods and Results —An vivo model intravenous administration arginine 8 -vasopressin (AVP) up to 4 hours conscious normotensive rats was used study mechanisms...
The expression of cardiac hormones, atrial natriuretic peptide and B-type peptide, is induced by wall stretch responds to various hypertrophic agonists such as endothelin-1. In myocytes, endothelin-1 induces GATA-4 binding the gene, but signaling pathways involved in endothelin-1-induced activation are unknown. Mitogen-activated protein kinase stimulated response extracellular stimuli, they modulate function several transcription activators. Here we show that inhibition p38 with SB203580...
Abstract The induction of atrial and ventricular B-type natriuretic peptide (BNP) gene expression is one the earliest events occurring during hemodynamic overload. To examine molecular mechanisms for increased BNP cardiac overload, we studied compared with that (ANP) in a modified perfused rat heart preparation. An increase right pressure 5 mm Hg resulted 1.4-fold ( P <.05) 2.2-fold <.01) mRNA levels after 1 2 hours, respectively, whereas ANP remained unchanged. Stretching up to hours...
Atrial natriuretic peptide (ANP), B-type (BNP), and C-type are the known members of mammalian system. Like ANP, BNP is a diuretic hormone that also causes peripheral vasodilation inhibition sympathetic renin-angiotensin systems. Although originally isolated from porcine brain, gene expressed in specific manner cardiac myocytes both atria ventricles, but it mainly released ventricles. The major determinant secretion wall stretch, levels mRNA increase substantially response to overload. In...
B-type natriuretic peptide (BNP) is an endogenous produced under physiological and pathological conditions mainly by ventricular myocytes. It has natriuretic, diuretic, blood pressure-lowering, antifibrotic actions that could mediate cardiorenal protection in cardiovascular diseases. In the present study, we used BNP gene transfer to examine functional structural effects of on left (LV) remodeling.Human was overexpressed using adenovirus-mediated delivery normal rat hearts during remodeling...
We administered ghrelin, a novel growth hormone-releasing hormone, to isolated perfused rat hearts, coronary arterioles, and cultured neonatal cardiomyocytes determine its effects on vascular tone, contractility, natriuretic peptide secretion gene expression. also determined cardiac levels of ghrelin whether the heart is source circulating peptide. Ghrelin dose dependently increased perfusion pressure (44 +/- 9%, P < 0.01), constricted arterioles (12 2%, 0.05), significantly enhanced...
Atrial natriuretic peptide (ANP), B-type (BNP), and C-type are the known members of mammalian system. Like ANP, BNP is a diuretic hormone that also causes peripheral vasodilation inhibition sympathetic renin-angiotensin systems. Although originally isolated from porcine brain, gene expressed in specific manner cardiac myocytes both atria ventricles, but it mainly released ventricles. The major determinant secretion wall stretch, levels mRNA increase substantially response to overload. In...
Abstract Aim: Accumulating evidence supports the concept that proinflammatory cytokines play an essential role in failing heart. We examined concomitant tumour necrosis factor‐like weak inducer of apoptosis (TWEAK)/Fn14 expression myocytes vitro as well vivo cardiac remodelling. Methods: assessed TWEAK and its receptor Fn14 response to angiotensin (Ang) II, myocardial infarction (MI) local adenovirus‐mediated p38 gene transfer . The effect various hypertrophic factors mechanical stretch was...
The precise function of angiotensin II type 2 receptor (AT2-R) in the mammalian heart vivo is unknown. Here, we investigated role AT2-R cardiac pressure overload.Rats were infused with vehicle, (Ang II), PD123319 (an antagonist), or combination Ang and via subcutaneously implanted osmotic minipumps for 12 72 hours. II-induced increases mean arterial pressure, left ventricular weight/body weight ratio, elevation skeletal alpha-actin beta-myosin heavy chain mRNA levels not altered by PD123319....
Mechanisms regulating stretch response in the left ventricle are investigated detail but not well understood atrial myocardium. Hypertrophic growth of myocardium contributes to pathogenesis fibrillation. In this study, we sought elucidate mechanisms stretch-induced activation key signaling pathways and hypertrophy-associated genes rat atria. Stretching isolated atria induced a rapid increase phosphorylation p38 MAPK ERK MAPK-dependent DNA binding activity transcription factors Elk-1 GATA-4....
Terminally differentiated cardiac myocytes adapt to mechanical and neurohumoral stress via morphological changes of individual cells accompanied by reactivation fetal pattern gene expression. Endothelin-1, a powerful paracrine mediator myocyte growth, induces similar in cultured as those seen hypertrophied heart <i>in vivo</i>. By using rat B-type natriuretic peptide promoter, we identified novel ETS binding sequence, on which nuclear protein is activated endothelin-1-treated myocytes. This...
Aims Activating transcription factor 3 (ATF3) is a stress-activated immediate early gene suggested to have both detrimental and cardioprotective role in the heart. Here we studied mechanisms of ATF3 activation by hypertrophic stimuli downstream targets rat cardiomyocytes. Methods Results When neonatal cardiomyocytes were exposed endothelin-1 (ET-1, 100 nM) mechanical stretching vitro, maximal increase expression occurred at 1 hour. Inhibition extracellular signal-regulated kinase (ERK)...
Abstract Background In Henoch–Schönlein nephritis (HSN), a risk factor for unfavorable outcome is prolonged proteinuria, but the value of renal biopsies in prognosis assessment debatable. Methods We evaluated serial from 26 HSN patients. Follow-up biopsy occurred at median 2.1 years after diagnostic biopsy. Patients formed two groups follow-up biopsy: patients without proteinuria (group I; n = 11) and with II; 15). Biopsies underwent evaluation according to three classifications:...
What is known and objective Calciphylaxis a rare potentially life-threatening cause of skin necrosis poorly recognized by clinicians in non-uraemic patients. Case description We report five cases warfarin-induced calciphylaxis patients with normal renal function. In four cases, sodium thiosulphate was successfully used as treatment. No other predisposing factors besides obesity warfarin were found these new conclusion Previously only few solely have been described. Treatment has shown...
Members of the mammalian protein kinase C (PKC) superfamily play key regulatory roles in multiple cellular processes. In heart, PKC signaling is involved hypertrophic agonist-induced gene expression and growth. To investigate specific function regulating cardiomyocyte growth, we used antisense oligonucleotides to inhibit α, major isozyme present neonatal heart. Transfection cultured cardiomyocytes with PKCα resulted a marked reduction both mRNA levels. treatment also reduced phenylephrine...
Tumor necrosis factor α-induced protein 3 gene (TNFAIP3, also called A20) haploinsufficiency (HA20) leads to autoinflammation and autoimmunity. We have recently shown that a p.(Lys91*) mutation in A20 disrupts nuclear κB signaling, impairs protein-protein interactions of A20, inflammasome activation.We now describe the clinical presentations drug responses family with HA20 mutation, consistent our previously reported diverse immunological functional findings.We report for first time...