Atrial Natriuretic Peptide

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Influence of Atrial Natriuretic Peptide on inflammatory pathways in the lung

Influence of Atrial Natriuretic Peptide on inflammatory pathways in the lung

The atrial natriuretic peptide was first described by de Bold et al in 1981 (de Bold et al., 1981), who discovered the natriuretic and diuretic capability of an atrial extract injected in rats. The biological agent found responsible for this effect was a small cyclic peptide of 28 amino acids named atrial natriuretic peptide. In the following years other members of the so called natriuretic peptide family were discovered. BNP was isolated from porcine brain first and therefore named brain natriuretic peptide (Sudoh et al., 1988). Along the lines of the first two peptides, the third discovered family member was named C-type natriuretic peptide (CNP) (Sudoh et al., 1990). In 1992, another natriuretic peptide, dendroaspis natriuretic peptide (DNP) was first isolated from the venom of the green mamba (Dendroaspis angusticeps) (Piao et al., 2004) and recently discovered also in humans (Richards et al., 2002). In addition, Urodilatin, which has four additional amino acids in comparison to ANP, is a product of alternative processing of pro-ANP by renal cells (Forssmann et al., 1998). ANP and BNP are mainly expressed in cardiac tissue, ANP in the atrium and BNP in the ventricle, while CNP is mainly expressed in the central nervous system and in the endothelium (Pandey, 2005).
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Cytoprotective and Anti-Inflammatory Properties of the Atrial Natriuretic Peptide during Ischemia/Reperfusion and Endotoxemia

Cytoprotective and Anti-Inflammatory Properties of the Atrial Natriuretic Peptide during Ischemia/Reperfusion and Endotoxemia

Due to our findings that ANP pretreatment in vivo reduces apoptosis in liver tissue after IR we finally aimed to elucidate functional consequences of this effect in the liver. The data of Gerwig et al. (Gerwig,T. et al., 2003a) clearly demonstrate a decrease in necrotic cell death in combination with anti-apoptotic effects in ANP-preconditioned livers. In contrast, we were not able to show anti-necrotic effects of the peptide in vivo. Interestingly, Cursio et al. found out that an application of caspase-inhibitors blocks apoptosis in liver tissue thereby assuring survival of 95 % of the animals after lethal warm liver ischemia, and assigning the major role in cell death during IR to apoptosis (Cursio,R. et al., 1999a). However, they furthermore showed that despite a complete inhibition of caspases, the activity of transaminases, though drastically reduced, remains relatively high. Apoptotic cell death is therefore assumed to be accompanied by necrosis of liver cells during IR. Regarding the nonexisting improvement of bile flow after transplantation, the results of Mueller et al. are interesting to discuss (Mueller,T.H. et al., 2004a). They demonstrated improved survival of rats after liver transplantation provoked by application of a caspase-3- inhibitor but could not observe any melioration regarding bile flow after transplantation. In our setting, ANP preconditioning in vivo only reduced caspase-3-like activity after ischemia to about 60%. This inhibitory effect might not be strong enough to have an influence on the amount of necrotic cells pointing to a possible explanation for the inability of ANP to influence transaminase activity.
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Characterisation of Anti-Apoptotic Signalling Pathways in Hepatocytes activated by alpha-Lipoic Acid and Atrial Natriuretic Peptide

Characterisation of Anti-Apoptotic Signalling Pathways in Hepatocytes activated by alpha-Lipoic Acid and Atrial Natriuretic Peptide

Under certain conditions cAMP-dependent protein kinase (protein kinase A, PKA) can act as a target molecule for cGMP (173). For example, Schumacher et al. displayed that the stimulation of testosterone production by ANP in isolated mouse Leyding cells results from activation of PKA in a cGMP-dependent manner (304). Furthermore it has been shown in mice that in the absence of PKGI NO can relax vessels via cGMP-dependent PKA activation (305). Recently Aizawa et al. described that the ANP homologue CNP (C-type natriuretic peptide) mediates transcriptional inhibition controlled by NF-κB via a cGMP-dependent activation of PKA (216). Data presented by Gerwig T support further evidence for a crosstalk of cGMP with the cAMP/PKA pathway: liver perfusion with the PKA inhibitor Rp-8-Br-cAMPS abrogated the antiapoptotic effects of ANP and treatment of hepatocytes with the hormone enhanced PKA activity (217).
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Influence of the Atrial Natriuretic Peptide on TNF- αα α -activated human endothelial cells

Influence of the Atrial Natriuretic Peptide on TNF- αα α -activated human endothelial cells

Interestingly, in the last years natriuretic peptides and their receptors were found to be expressed in diverse tissues besides the cardiovascular and renal system. Vollmar and coworkers were able to show that ANP and its receptors are expressed in thymus (Vollmar and Schulz 1990a), as well as in macrophages (Vollmar and Schulz 1994; Vollmar and Schulz 1995, Kiemer and Vollmar 1997). It could be demonstrated that ANP inhibits thymocyte proliferation and thymopoesis (Vollmar et al. 1996; Vollmar 1997). Moreover, ANP seems to provide antiinflammatory action since it was shown to attenuate the induction of the inducible nitric oxide synthase (iNOS), a central proinflammatory enzyme, in an autocrine fashion (Kiemer and Vollmar 1997; Kiemer and Vollmar 1998; Kiemer and Vollmar 2001a; Kiemer and Vollmar 2001b). Additionally, ANP was found to attenuate the induction of other inflammatory mediators, such as cyclooxygenase-2 (Kiemer et al. 2002b) and TNF- α (Kiemer et al. 2000a; Tsukagoshi et al. 2001). The inhibitory action of ANP on the inflammatory mediator TNF- α could also be observed in LPS-stimulated macrophages (Kiemer et al. 2000a) as well as in reperfused livers (Kiemer et al. 2000b). Another interesting aspect to be mentioned is that ANP is able to induce the heat shock protein HSP70 in rat livers (Kiemer et al. 2002a) providing a cytoprotective potential of this natriuretic peptide.
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Prevention of Ischemia-Reperfusion Injury in the Rat Liver by Atrial Natriuretic Peptide

Prevention of Ischemia-Reperfusion Injury in the Rat Liver by Atrial Natriuretic Peptide

Caspases are a family of proteases that act in a cascade triggered by apoptotic signals. These enzymes are highly conserved cysteine proteases that specifically and efficiently cleave target substrates after the carboxy terminus of aspartate (Nicholson et al., 1997). The activation of the downstream caspase-3, considered as one of the major effector caspases (Hengartner, 2000), can be measured by applying the synthetic peptide substrate DEVD (asp-glu-val-asp). It is coupled to a fluorophor that is cleaved after the aspartate residue by the activated enzyme leading to increased fluorescence (Thornberry, 1994). Because other downstream caspases such as caspase-7 have similar substrate specifity, this assay does not exclusively demonstrate caspase-3 activity. Therefore, the measured activity is termed “caspase-3-like activity” regarding caspase-3 as the major effector caspase. To make detection possible, the DEVD substrate is labeled with a fluorescent molecule, 7-amino-4-trifluoromethyl coumarin (AFC). The liberation of this fluorophore shows a blue to green shift in fluorescence at an extinction wavelength of 390 nm and an emission wavelength of 505 nm. AFC as fluorophore is highly sensitive and sufficiently stable to handle.
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Cardiovascular effects of C-type natriuretic peptide (CNP) overexpression in
transgenic animals

Cardiovascular effects of C-type natriuretic peptide (CNP) overexpression in transgenic animals

Natriuretic peptide family consists of three structurally related peptides: atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) and C-type natriuretic peptide (CNP). In contrast to ANP and BNP, which are produced mainly in cardiac atria and ventricles, respectively, CNP occurs in a wide variety of tissues (1), and is commonly considered to be an endothelial hormone. The biological actions of natriuretic peptides are mediated by three different membrane-bound receptor subtypes, natriuretic peptide receptor A, B, and C (NPRA, NPRB and NPRC) (2). NPRA and NPRB are guanylyl cyclase (GC)-coupled receptors, which can convert guanosine triphosphate (GTP) to guanosine 3’,5’-cyclic monophosphate (cGMP). NPRC is a single transmembrane receptor with a short 37-amino- acid intracellular tail that lacks GC activity. ANP and BNP are ligands of NPRA, while CNP preferentially binds to NPRB. NPRC has similar affinity to all three natriuretic peptides and is commonly considered a clearance receptor.
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Co-expression of natriuretic peptide receptors and its implications on receptor regulation in smooth muscle cells of the aorta

Co-expression of natriuretic peptide receptors and its implications on receptor regulation in smooth muscle cells of the aorta

The family of these natriuretic peptides consists of atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) and C-type natriuretic peptide (CNP). Structurally related but genetically distinct, these hormones (ANP, BNP) or paracrine factors (CNP) regulate blood pressure and blood volume and play a crucial role in modulating ventricular hypertrophy, fat metabolism, bone growth and pulmonary hypertension among others (Maack, Suzuki et al. 1987; Stein and Levin 1998; Kuhn 2004; Potter, Abbey-Hosch et al. 2006). Both ANP and BNP are synthesized in atrial cardiomyocytes and secreted into circulation in response to cardiac wall stretch. Thus they exert important cardiovascular functions by acting as true endocrinal factors (Brenner, Ballermann et al. 1990; Ruskoaho 1992). By contrast, the third member, CNP, is mainly produced in vascular endothelial cells and chondrocytes while also found in high concentrations in brain tissue. It exhibits various local and paracrine functions in the cardiovascular system as well as outside of it (Sudoh, Minamino et al. 1990; Suga, Nakao et al. 1992; Hagiwara, Sakaguchi et al. 1994). For the sake of completeness another peptide of this family, urodilantin, should be mentioned. This peptide represents an elongated form of ANP, produced exclusively in the kidney (Schulz-Knappe, Forssmann et al. 1988).
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Circulating MicroRNA-21 Correlates With Left Atrial Low-Voltage Areas and Is Associated With Procedure Outcome in Patients Undergoing Atrial Fibrillation Ablation

Circulating MicroRNA-21 Correlates With Left Atrial Low-Voltage Areas and Is Associated With Procedure Outcome in Patients Undergoing Atrial Fibrillation Ablation

tissue concentration and extent of atrial fibrosis deter- mined by immunostainings of left atrial appendages. In addition, we found a significant correlation between miR-21 serum concentrations and 1-year out- come after catheter ablation in patients with persistent AF. Circulating miR-21 might, therefore, be useful for the stratification of patients and to plan the proce- dure (eg, to perform a pulmonary vein isolation only in patients with very low miR-21 serum concentrations or to plan extensive substrate modification in patients with high miR-21 levels), although this needs to be con- firmed in further studies.
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TGF? Is Specifically Upregulated on Circulating CD14++ CD16+ and CD14+ CD16++ Monocytes in Patients with Atrial Fibrillation and Severe Atrial Fibrosis

TGF? Is Specifically Upregulated on Circulating CD14++ CD16+ and CD14+ CD16++ Monocytes in Patients with Atrial Fibrillation and Severe Atrial Fibrosis

20 Huo Y, Gaspar T, Pohl M, Sitzy J, Richter U, Neudeck S, Mayer J, Kronborg MB, Piorkowski C: Prevalence and predictors of low voltage zones in the left atrium in patients with atrial fibrillation. Europace 2017; DOI:10.1093/europace/eux082. 21 Heinzmann D, Bangert A, Muller AM, von Ungern-Sternberg SN, Emschermann F, Schonberger T, Chatterjee M, Mack AF, Klingel K, Kandolf R, Malesevic M, Borst O, Gawaz M, Langer HF, Katus H, Fischer G, May AE, Kaya Z, Seizer P: The Novel Extracellular Cyclophilin A (CyPA) - Inhibitor MM284 Reduces Myocardial Inflammation and Remodeling in a Mouse Model of Troponin I -Induced Myocarditis. PLoS One 2015;10:e0124606.
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Aqueous solid-phase peptide synthesis (ASPPS): A novel concept of peptide synthesis

Aqueous solid-phase peptide synthesis (ASPPS): A novel concept of peptide synthesis

into the ASPPS-based peptide assembly. To that end, all the by-products originating from incomplete couplings are labelled with charged Sulfo-tags and can be easily removed upon successive IEC after cleavage from solid support. Our studies showed that this method could also be applied to Fmoc-based peptide synthesis. This method allows tailoring of purification strategy depending on required peptide purity grade. It can be applied solely or serve as a pre- purification system to simplify and optimize the following HPLC separation. In addition, the same method could be used to refine the wastewater.
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Role of microRNAs in Atrial Fibrillation: Establishment of Technological Pipeline

Role of microRNAs in Atrial Fibrillation: Establishment of Technological Pipeline

Atrial fibrillation is the leading cause of morbidity however, the pathophysiological mechanisms of AF are not well investigated. Molecular mechanisms to understand the underlying genetic aetiologies still needs to be identified. Various studies have concluded a definite relation between miRNAs and AF. miRNAs are substances that can be easily measured in available body fluids like blood and serum, making them perfect candidates for biomarker analysis. The method to establish the relationship between the miRNA and the disease begins with a wide range microarray search that might provide insights about dysregulated miRNAs. AF, as a disease, has other cardiovascular diseases as its risk factors and this arises complications in identifying a miRNA biomarker specific to AF only. The targets of these miRNAs are analysed through miRNA databases such as TargetScan, miRBase, etc. Based on a pathway analysis and possible role in heart function, a miRNA can be established as a personalised global biomarker for AF.
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jV-Trityl-Aminosäuren und -peptide 

jV-Trityl-Aminosäuren und -peptide 

wäßrig-alkoholischer NaOH wurde der Tritylrest abgespalten, bei der Verseifung des N- Trityl-Z-glutaminsäure-diäthylesters unter gleichen Be- dingungen konnte nach dem Ansäuern mit Wein[r]

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Die Darstellung höherer ringförmiger Peptide 

Die Darstellung höherer ringförmiger Peptide 

This work has been digitalized and published in 2013 by Verlag Zeitschrift für Naturforschung in cooperation with the Max Planck Society for the Advancement of Science under a Creative[r]

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Expression antimikrobieller Peptide in Bronchialkarzinomen

Expression antimikrobieller Peptide in Bronchialkarzinomen

Einige Peptide töten Bakterien, ohne die Membran zu permeabilisieren. Sie penetrieren Zellen und interagieren mit physiologischen Prozessen. Z.B. können Defensine Einzelstrang-DNA aufbrechen (Bateman et al 1991). Defensine und Histatine töten Pilze durch nichtlytische Freisetzung zellulären ATPs, welches sich anschließend an mutmaßliche purinerge Rezeptoren bindet und den zytotoxischen Weg aktiviert (Edgerton et al 2000). Defensine verhindern die Infektfähigkeit einiger Viren (Daher et al 1986, Aboudy et al 1994). Dieser Effekt wird durch das Binden des Peptids an die virale Hülle verursacht, während analog dazu unbehüllte Viren in ihrem infektiösen Potential nicht beeinflusst werden (Kamysz et al 2003).
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Antimikrobielle Peptide in induziertem Sputum

Antimikrobielle Peptide in induziertem Sputum

Entsprechend der Hauptfragestellung dieser Arbeit wurden die verschiedenen, im induzierten Sputum bestimmten Parameter zuerst bezüglich ihres Beitrags zur Trennung zwischen Rauchern u[r]

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Antibiotische Peptide in Phospholipiden: Strukturuntersuchungen mit Beugungsmethoden

Antibiotische Peptide in Phospholipiden: Strukturuntersuchungen mit Beugungsmethoden

uber einen Zeitraum mehrerer Stunden und Tage. Antibiotische Peptide, wie sie von Tieren und P anzen zur Verteidigung ihres Organismus gegen eindringende pathogene Mikroorga- nismen verwendet werden, toten Eindringlinge innerhalb kurzester Zeit ab. Der Zeitrahmen liegt hier im Bereich weniger Minuten. Damit ist bereits ein wichtiger Aspekt eines antibio- tischen Peptids genannt. Die Zeit, die das Peptid zum Wirken braucht sollte deutlich kurzer sein, als die Zellteilungsrate eines typischen Bakteriums (im Fall Escherichia coli sind das ca. 20 min). Das Zellinnere ist wegen der schnellen Wirkung als Ziel demnach weniger geeignet, als eine direkte Wechselwirkung mit dem Zellaueren, also den Lipiden der Zellmembrane. Da Zellmembrane in lebenden Organismen allgegenwartig sind, also auch in den Wirtszellen, mu das Peptid zwischen Wirts- und Mikrobenzellmembran unterscheiden konnen. Das Pep- tid sollte also seine Wirkung auf Molekule entfalten, die in prokaryotischen Mikrobenzellen allgegenwartig anzutre en sind, aber nur selten oder nie in den eukaryotischen Wirtszel- len. Denkbar ist eine Unterscheidung uber die Lipidzusammensetzung der Zellmembran. Ein
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publish.UP Entwicklung influenzabindender Peptide für die Biosensorik

publish.UP Entwicklung influenzabindender Peptide für die Biosensorik

Die Funktionalität des Peptids PeB hängt stark von dessen Präsentation auf der Oberfläche und dem verwendeten Linkermolekül ab. Die Immobilisierungsmethoden, die auf einer Kopplung über N-terminale primäre oder sekundäre Amine beruhen, ermöglichen allesamt die Virusdetektion. Kopplungen über die freie Thiolgruppe eines Cysteins ermöglichen in einigen Fällen die Influenzadetektion. Die Immobilisierung der Peptide über einen Biotin-Linker (N-/ C-terminal) und anschließender nichtkovalenter Kopplung des Peptids an Neutravidin führt zum vollständigen Funktionsverlust und ist damit für das untersuchte Bindungssystem ungeeignet. Dies kann einerseits sterische Gründe haben. Wichtige Motive der Peptidsequenz könnten durch die Immobilisierung in der Bindungstasche des Neutravidins vergraben werden, obwohl hier zusätzlich ein C16-Spacer (Ttds) zwischen erster AS und Biotin eingefügt wurde. Andererseits wurde eine direkte Interaktion des Peptids mit Neutravidin im Spezifitätstest nicht beobachtet. Dennoch können schwache Interaktionen mit Neutravidin nicht ausgeschlossen werden, da diese nun durch die Fixierung des Peptids in der Bindungstasche entropisch begünstigt wären.
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New perspectives in oral peptide delivery

New perspectives in oral peptide delivery

There are many challenges to overcome when dealing with the oral delivery of peptides. The development of orally delivered peptides to replace injections remains a challenge, which would not only help improve the lives of patients, but also reduce healthcare costs worldwide. Orally delivered insulin is an ex- ample of this ultimate objective, providing undisputed thera- peutic advantages for non-invasive chronic use. However, the improvement of life quality and the safety of patients must be the driving force of oral delivery peptide research. The solution to such a complex problem requires approaches from various disciplines, with formulation and chemical modification being vital.
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Mesoporöse Silikananopartikel als Trägermaterial für therapeutische Peptide

Mesoporöse Silikananopartikel als Trägermaterial für therapeutische Peptide

verwendet wurden, um im Bereich der biokompatiblen Partikelkonzentrationen zu bleiben. Nach 24 h zeigt sich eine leichte Reduktion der Infektion um ~ 20%. Der Unterschied zum freien VIR576 ist allerdings noch sehr groß. Nach 48 h zeigen die peptidbeladenen MSN200c die gleiche Inhibierung der Infektion wie die freie Peptidlösung. Die Kontrolle der unbeladenen MSN200c zeigt für die ersten zwei Zeitpunkte keine Inhibierung der Infektion und für den 48 h Zeitpunkt eine sehr leichte Inhibierung. Dieses Experiment zeigt, dass die Funktionalität des von den MSN200c freigesetzten VIR-576 erhalten bleibt und nach ausreichend langen Zeiträumen genug freies Peptid vorhanden ist, um die Infektion der Zellen zu inhibieren. Das zeigt, dass mesoporöse Silikananopartikel als Trägermaterial für antivirale Peptide prinzipiell für die Therapie von HIV-Infektionen anwendbar sind. Produktiv infizierte Zellen haben im Durchschnitt eine Lebensdauer von 2,2 Tagen (Halbwertszeit t1/2 = 1,6 Tage) und Plasmavirionen eine mittlere Lebensdauer von 0,3 Tagen (t1/2 = 0,24 Tage). Die geschätzte durchschnittliche HIV-1- Gesamtproduktion liegt bei 10,3 × 10 9 Virionen pro Tag. Die Ergebnisse dieser Studie
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Einfluss natriuretischer Peptide auf die endotheliale Glykokalyx

Einfluss natriuretischer Peptide auf die endotheliale Glykokalyx

Heparansulfat wurde nicht verhindert, jedoch der Effekt auf das Syndekan-Shedding halbiert. Alle drei natriuretischen Peptide verursachten eine Zunahme der Netto- Filtration von Perfusat im Koronarsystem. Dieses konnte direkt in Form des sogenannten Transsudat-Flusses bestimmt werden. Gleichsam wie die hydraulische Leitfähigkeit erhöhte sich die Extravasation von Hydroxyethylstärke (Molekulargewicht 130.000), d.h. auch die Permeabilität für Kolloide nahm zu. Überraschend war, dass die im Transsudat gemessene Konzentration von HES in den Versuchsgruppen ANP, CNP und ANP + AT III den Wert der Effluat- konzentration um Werte bis zu 20 Prozent überstieg – und damit die HES- Konzentration im interstitiellen Kompartiment höher wurde als im intravaskulären Raum. Dies lässt auf eine „Ventilfunktion“ am venulären Kapillarende schließen, die eine Rückkehr von Kolloid aus dem Interstitium in das Gefäßlumen erschwert. Elektronenmikroskopische Aufnahmen der Glykokalyx stützen die gewonnenen Ergebnisse.
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