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#28786077   2017/08/08 Save this To Up

The phosphodiesterase 5 inhibitor tadalafil regulates lipidic homeostasis in human skeletal muscle cell metabolism.

Tadalafil seems to ameliorate insulin resistance and glucose homeostasis in humans. We have previously reported that tadalafil targets human skeletal muscle cells with an insulin (I)-like effect. We aim to evaluate in human fetal skeletal muscle cells after tadalafil or I: (i) expression profile of I-regulated genes dedicated to cellular energy control, glycolitic activity or microtubule formation/vesicle transport, as GLUT4, PPARγ, HK2, IRS-1, KIF1C, and KIFAP3; (ii) GLUT4, Flotillin-1, and Caveolin-1 localization, all proteins involved in energy-dependent cell trafficking; (iii) activation of I-targeted paths, as IRS-1, PKB/AKT, mTOR, P70/S6K. Free fatty acids intracellular level was measured. Sildenafil or a cGMP synthetic analog were used for comparison; PDE5 and PDE11 gene expression was evaluated in human fetal skeletal muscle cells.

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#26468073   2015/10/15 Save this To Up

Bixa orellana leaf extract suppresses histamine-induced endothelial hyperpermeability via the PLC-NO-cGMP signaling cascade.

Histamine is established as a potent inflammatory mediator and it is known to increased endothelial permeability by promoting gap formation between endothelial cells. Previous studies have shown that aqueous extract of Bixa orellana leaves (AEBO) exhibits antihistamine activity in vivo, yet the mechanism of its action on endothelial barrier function remains unclear. Therefore, the current study aimed to determine the protective effect of AEBO against histamine-induced hyperpermeability in vitro.

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#26171055   2015/07/14 Save this To Up

Nitric oxide/cyclic guanosine monophosphate inducers sodium nitroprusside and L-arginine inhibit the proliferation of gastric cancer cells via the activation of type II cyclic guanosine monophosphate-dependent protein kinase.

Nitric oxide (NO) may activate soluble guanylyl cyclase (sGC), resulting in the increase of intracellular cyclic guanosine monophosphate (cGMP), a key molecule in the activation of type II cGMP-dependent protein kinase (PKG II). In our previous study, the membrane-permeable cGMP analogue 8-pCPT-cGMP was used to activate PKG II. The aim of the present study was to investigate whether NO/sGC-induced endogenous cGMP is able to activate PKG II and induce the corresponding effects. In the AGS gastric cancer cell line, the expression of PKG II was increased by infecting the cells with an adenoviral construct encoding PKG II cDNA (Ad-PKG II) and the activation of PKG II was induced by 8-pCPT-cGMP (positive control), the NO donor sodium nitroprusside (SNP) and the NO precursor L-arginine. ELISA was performed to detect the concentration of cGMP in AGS cells and the Cell Counting Kit-8 was used to analyze the proliferation of differently treated cells. Western blot analysis was used to detect the expression and phosphorylation of associated proteins. The results demonstrated that the level of cGMP was increased in cells treated with the NO donor or precursor. There was an obvious increase of Ser239 phosphorylation of the vasodilator-stimulated phosphoprotein, representing the increase in the activity of PKG II. The epidermal growth factor (EGF)-induced proliferation of AGS cells was inhibited by infection with Ad-PKG II and treatment with SNP or L-arginine. In addition, EGF-induced tyrosine phosphorylation of the EGF receptor (EGFR) and tyrosine/serine phosphorylation of extracellular signal-regulated kinase (ERK) were also inhibited by infection with Ad-PKG II and treatment with the NO donor or precursor. These data indicated that NO donors and precursors may activate the expression of PKG II, thereby blocking EGF-initiated signaling of the mitogen-activated protein kinase/ERK pathway and inhibiting EGF-induced proliferative activity through preventing the phosphorylation of EGFR at tyr1068.

1863 related Products with: Nitric oxide/cyclic guanosine monophosphate inducers sodium nitroprusside and L-arginine inhibit the proliferation of gastric cancer cells via the activation of type II cyclic guanosine monophosphate-dependent protein kinase.

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#25382303   2015/03/10 Save this To Up

Luteolin antagonizes angiotensin II-dependent proliferation and collagen synthesis of cultured rat cardiac fibroblasts.

The purpose of this study was to observe if luteolin could affect the behavior of cardiac fibroblasts (CFs) on myocardial fibrosis stimulated by angiotensin II (Ang II) and investigate the mechanism involved.

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#24977346   2014/11/08 Save this To Up

Cross regulation between cGMP-dependent protein kinase and Akt in vasodilatation of porcine pulmonary artery.

cGMP-dependent protein kinase (PKG) plays a crucial role in vasodilatation induced by cGMP-elevating agents. Akt has been demonstrated to be involved in modulating vasoreactivity. The present study was to determine the interaction between PKG and Akt and their influences on nitric oxide (NO)-induced vasodilatation. Isolated fourth-generation porcine pulmonary arteries were dissected from the lung and cut into rings in ice-cold modified Krebs-Ringer bicarbonate buffer. The relaxant responses of vessels were determined by organ chamber technique, cGMP was assayed by using enzyme-linked immunosorbent assay kit, the protein levels of phosphorylated Akt were examined by Western blotting, and the activity of phosphodiesterase type 5 (PDE5) was assayed by measuring the rate of cGMP degradation. Incubation with DETA NONOate (a stable NO donor) and 8-Br-cGMP (a cell membrane permeable analog of cGMP) attenuated Akt phosphorylation at Ser-473, which was prevented by Rp-8-Br-PET-cGMPS (a specific inhibitor of PKG) and calyculin A (an inhibitor of protein phosphatase 1 and 2A) but not by okadaic acid (a selective inhibitor of protein phosphatase 2A). Inhibition of Akt enhanced the relaxation and cGMP elevation of porcine pulmonary arteries induced by DETA NONOate or sodium nitroprusside, which was prevented by zaprinast, a specific inhibitor of PDE5. Incubation with LY294002 or Akt inhibitor reduced PDE5 activity in porcine pulmonary arteries. The present study indicates that PKG may attenuate Akt phosphorylation through protein phosphatase 1, which leads to an augmented cGMP elevation by inhibition of PDE5. The increased cGMP in turn activates PKG. Such a positive feedback may play an important role in NO-induced pulmonary vasodilatation.

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#24906916   2014/08/02 Save this To Up

cIMP synthesized by sGC as a mediator of hypoxic contraction of coronary arteries.

cGMP is considered the only mediator synthesized by soluble guanylyl cyclase (sGC) in response to nitric oxide (NO). However, purified sGC can synthesize several other cyclic nucleotides, including inosine 3',5'-cyclic monophosphate (cIMP). The present study was designed to determine the role of cIMP in hypoxic contractions of isolated porcine coronary arteries. Vascular responses were examined by measuring isometric tension. Cyclic nucleotides were assayed by HPLC tandem mass spectroscopy. Rho kinase (ROCK) activity was determined by measuring the phosphorylation of myosin phosphatase target subunit 1 using Western blot analysis and an ELISA kit. The level of cIMP, but not that of cGMP, was elevated by hypoxia in arteries with, but not in those without, endothelium [except if treated with diethylenetriamine (DETA) NONOate]; the increases in cIMP were inhibited by the sGC inhibitor 1H-[1,2,4]oxadiazolo[4,3,-a]quinoxalin-1-one (ODQ). Hypoxia (Po2: 25-30 mmHg) augmented contractions of arteries with and without endothelium if treated with DETA NONOate; these hypoxic contractions were blocked by ODQ. In arteries without endothelium, hypoxic augmentation of contraction was also obtained with exogenous cIMP. In arteries with endothelium, hypoxic augmentation of contraction was further enhanced by inosine 5'-triphosphate, the precursor for cIMP. The augmentation of contraction caused by hypoxia or cIMP was accompanied by increased phosphorylation of myosin phosphatase target subunit 1 at Thr(853), which was prevented by the ROCK inhibitor Y-27632. ROCK activity in the supernatant of isolated arteries was stimulated by cIMP in a concentration-dependent fashion. These results demonstrate that cIMP synthesized by sGC is the likely mediator of hypoxic augmentation of coronary vasoconstriction, in part by activating ROCK.

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#24826884   2014/06/13 Save this To Up

Interlude of cGMP and cGMP/protein kinase G type 1 in pancreatic adenocarcinoma cells.

cAMP and cGMP signaling is important both for normal and cancer cells. This signaling is controlled by adenylyl and guanylyl cyclases and cyclic nucleotide phosphodiesterases. One of the direct targets for cGMP is protein kinase G (PKG). The main aim of this work was to investigate cGMP and PKG signaling in pancreatic adenocarcinoma (PDAC) cells.

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#23353150   2013/01/28 Save this To Up

[Calcineurin/NFAT signaling pathway mediates endothelin-1-induced pulmonary artery smooth muscle cell proliferation by regulating phosphodiesterase-5].

To examine whether calcineurin/NFAT signaling pathway mediates endothelin-1 (ET-1)-induced proliferation of pulmonary artery smooth muscle cells (PASMCs) by regulating phosphodiesterase-5 (PDE5) and the effect of the selective calcineurin inhibitor cyclosporine A and PDE5 inhibitor sildenafil on ET-1-induced PASMC proliferation.

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#22122966   2011/12/22 Save this To Up

Inhibition of phosphoinositide 3-kinase potentiates relaxation of porcine coronary arteries induced by nitroglycerin by decreasing phosphodiesterase type 5 activity.

Vessel tension can be modulated by phosphoinositide 3-kinase (PI3K) acting on l-type calcium channel, rho kinase and phosphodiesterase (PDE) type 3 in smooth muscle cells. Inhibition of PI3K could increase the relaxation of porcine coronary arteries to nitroglycerin independent of this pathway, and the aim of the present study was therefore to determine the underlying mechanisms.

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#21635258   2011/06/03 Save this To Up

Gnaphaliin A and B relax smooth muscle of guinea-pig trachea and rat aorta via phosphodiesterase inhibition.

To explore the relaxant mechanism of action of gnaphaliin A and gnaphaliin B in guinea-pig trachea and rat aorta, and to investigate the theoretical and experimental phosphodiesterase (PDE) inhibitory activity of these flavones.

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