Die Kontamination des Wassers und die Infektionsrate bei der Wassergeburt

Thöni, A.; Zech, Nicolas H.; Moroder, Luca; Ploner, Ferdinand

doi:10.1159/000098123

Cited by 16 publications

(11 citation statements)

References 18 publications

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“…Especially in the gastrointestinal tract serotonin plays an important role, here it stimulates intestinal peristalsis and intestinal secretion. In the lung serotonin is involved in the pathogenesis of pulmonary hypertension, during hypoxia the intravascular serotonin concentration increases which then results in a rise in 5-HT 2B receptor signaling of endothelial cells from pulmonary arteries consequently increasing vascular resistance [35] [36] [37]. In addition serotonin as well induces pulmonary artery remodeling by hypertrophy of smooth muscle cells, this goes in parallel to the enhanced expression of the serotonin transporter (SERT) [38] [39] [40].…”

Section: Discussionmentioning

confidence: 99%

Tumor Necrosis Factor Alpha Induces a Serotonin Dependent Early Increase in Ciliary Beat Frequency and Epithelial Transport Velocity in Murine Tracheae

et al. 2014

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The tracheal epithelium prevents via its highly effective clearance mechanism the contamination of the lower airways by pathogens. This mechanism is driven by ciliary bearing cells which are not only in contact with the gas phase; in addition they are also influenced by inflammatory mediators. These mediators can alter the protective function of the epithelium. Since the pro-inflammatoric cytokine tumor necrosis factor-α (TNF-α) plays a pivotal role within the inflammatory cascade, we investigated its effect onto the tracheal epithelium measured by its ciliary beat frequency and the particle transport velocity. In organ explant experiments the ciliary beat frequency and the particle transport velocity were measured under the application of TNF-α using tracheae from male C57BL6J mice. We observed a dose dependent TNF-α induced increase of both particle transport velocity and ciliary beat frequency. Knock out mice experiments made evident that the increase was depended on the expression of tumor necrosis factor receptor 1 (TNF-R1). The increases in ciliary beat frequency as well as the accelerated particle transport velocity were either inhibited by the unspecific serotonin antagonist methysergide or by cyproheptadine a specific 5-HT2 receptor antagonist. Thus, acetylcholine antagonists or nitric oxide synthase (NOS) inhibitors failed to inhibit the TNF-α induced activation. In conclusion, TNF-α may play a pivotal role in the protection of lower airways by inducing ciliary activity and increase in particle transport velocity via TNF-R1 and 5-HT2 receptor.

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Section: Discussionmentioning

confidence: 99%

Tumor Necrosis Factor Alpha Induces a Serotonin Dependent Early Increase in Ciliary Beat Frequency and Epithelial Transport Velocity in Murine Tracheae

et al. 2014

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“…Just as agonists of the 5-HT 2B receptor have been observed to lead to HVD, many of these agonists have also been implicated in fibrotic responses and ECM alterations that lead to other pathologies such as ventricular hypertrophy (Jaffre, Callebert et al 2004; Jaffre, Bonnin et al 2009) and pulmonary arterial fibrosis and hypertension (Esteve, Launay et al 2007). Correspondingly, genetic deletion of 5-HT 2B receptor expression in mice has been shown to lead to incomplete cardiac development characterized by ventricular dilation and a lack of tissue integrity (Nebigil, Choi et al 2000; Nebigil, Hickel et al 2001).…”

Section: 5-ht2b Receptor As a Novel Treatment Strategymentioning

confidence: 99%

Serotonin receptors and heart valve disease—It was meant 2B

Hutcheson

Setola

Roth

et al. 2011

Pharmacology & Therapeutics

194

153

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Carcinoid heart disease was one of the first valvular pathologies studied in molecular detail, and early research identified serotonin produced by oncogenic enterochromaffin cells as the likely culprit in causing changes in heart valve tissue. Researchers and physicians in the mid-1960s noted a connection between the use of several ergot-derived medications with structures similar to serotonin and the development of heart valve pathologies similar to those observed in carcinoid patients. The exact serotonergic target that mediated valvular pathogenesis remained a mystery for many years until similar cases were reported in patients using the popular diet drug Fen-Phen in the late 1990s. The Fen-Phen episode sparked renewed interest in serotonin-mediated valve disease, and studies led to the identification of the 5-HT2B receptor as the likely molecular target leading to heart valve tissue fibrosis. Subsequent studies have identified numerous other activators of the 5-HT2B receptor, and consequently, the use of many of these molecules has been linked to heart valve disease. Herein, we: review the molecular properties of the 5-HT2B receptor including factors that differentiate the 5-HT2B receptor from other 5-HT receptor subtypes, discuss the studies that led to the identification of the 5-HT2B receptor as the mediator of heart valve disease, present current efforts to identify potential valvulopathogens by screening for 5-HT2B receptor activity, and speculate on potential therapeutic benefits of 5-HT2B receptor targeting.

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“…At near-physiologic concentrations, 5-HT also acts as a mitogen for pulmonary arterial smooth muscle cells (PASMC) in culture [4]. Extensive clinical and experimental studies have implicated 5-HT in the pathologic pulmonary vascular smooth muscle remodeling that underlies idiopathic pulmonary arterial hypertension (PAH) [5, 6], a progressive disease that is ultimately fatal despite available therapies.…”

Section: Introductionmentioning

confidence: 99%

“…PASMC express not only 5-HT receptors (5-HTRs), but also the 5-HT transporter (SERT) [5], and the mitogenic effect of 5-HT on SMCs requires the combinatorial actions of SERT and 5-HT receptors [19]. SERT belongs to a monoamine transporter family that is known to actively move 5-HT intracellularly, and earlier we reported that 5-HT is actively transported intracellularly in pulmonary vascular cells [20].…”

Section: Introductionmentioning

confidence: 99%

Tissue transglutaminase promotes serotonin-induced AKT signaling and mitogenesis in pulmonary vascular smooth muscle cells

Penumatsa¹,

Abualkhair²,

Lin³

et al. 2014

Cellular Signalling

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Tissue transglutaminase 2 (TG2) is a multifunctional enzyme that cross-links proteins with monoamines such as serotonin (5-hydroxytryptamine, 5-HT) via a transglutamidation reaction, and is associated with pathophysiologic vascular responses. 5-HT is a mitogen for pulmonary artery smooth muscle cells (PASMC) that has been linked to the pulmonary vascular remodeling underlying pulmonary hypertension development. We previously reported that 5-HT-induced PASMC proliferation is inhibited by the TG2 inhibitor monodansylcadaverine (MDC); however, the mechanisms are poorly understood. In the present study we hypothesized that TG2 contributes to 5-HT-induced signaling pathways of PASMC. Pre-treatment of bovine distal PASMC with varying concentrations of the inhibitor MDC led to differential inhibition of 5-HT-stimulated AKT and ROCK activation, while p-P38 was unaffected. Concentration response studies showed significant inhibition of AKT activation at 50 μM MDC, along with inhibition of the AKT downstream targets mTOR, p-S6 Kinase and p-S6. Furthermore, TG2 depletion by siRNA led to reduced 5-HT-induced AKT activation. Immunoprecipitation studies showed that 5-HT treatment led to increased levels of serotonylated AKT and increased TG2-AKT complex formations which were inhibited by MDC. Overexpression of TG2 point mutant cDNAs in PASMC showed that the TG2 C277V transamidation mutant blunted 5-HT-induced AKT activation and 5-HT-induced PASMC mitogenesis. Finally, 5-HT-induced AKT activation was blunted in SERT genetic knock-out rat cells, but not in their wild-type counterpart. The SERT inhibitor imipramine similarly blocked AKT activation. These results indicate that TG2 contributes to 5-HT-induced distal PASMC proliferation via promotion of AKT signaling, likely via its serotonylation. Taken together, these results provide new insight into how TG2 may participate in vascular smooth muscle remodeling.

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Die Kontamination des Wassers und die Infektionsrate bei der Wassergeburt

Cited by 16 publications

References 18 publications

Tumor Necrosis Factor Alpha Induces a Serotonin Dependent Early Increase in Ciliary Beat Frequency and Epithelial Transport Velocity in Murine Tracheae

Tumor Necrosis Factor Alpha Induces a Serotonin Dependent Early Increase in Ciliary Beat Frequency and Epithelial Transport Velocity in Murine Tracheae

Serotonin receptors and heart valve disease—It was meant 2B

Tissue transglutaminase promotes serotonin-induced AKT signaling and mitogenesis in pulmonary vascular smooth muscle cells

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