Role of Gi/o-Src kinase-PI3K/Akt pathway and caveolin-1 in β2-adrenoceptor coupling to endothelial NO synthase in mouse pulmonary artery

Banquet, Sébastien; Delannoy, E; Agouni, Abdelali; Dessy, Chantal; Lacomme, Sabrina; Hubert, F.; Richard, Vincent; Müller, Bernard; Leblais, Véronique

doi:10.1016/j.cellsig.2011.02.008

Cited by 52 publications

(35 citation statements)

References 40 publications

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“…In SHR aortae, the remaining relaxations to acetylcholine in the presence of atropine were Banquet et al, 2011). The nicotine-induced relaxations were significantly prevented by incubation with LY294002 in WKY aortae and partially inhibited in SHR rats.…”

Section: Resultsmentioning

confidence: 87%

“…The aortic rings were incubated with vehicle, mecamylamine (nAChR inhibitor; 10 Ϫ4 M) (Bacher et al, 2009), atropine (mAChR inhibitor; 10 Ϫ5 M) (Clark, 1926), mecamylamine plus atropine, dihydro-␤-erthroidine hydrobromide (DH␤E; selective antagonist at ␣4-nAChRs; 10 Ϫ5 M) (Roegge and Levin, 2006), ␣-bungarotoxin (selective antagonist at ␣7-nAChRs; 10 Ϫ6 M) ), ␣-conotoxin (antagonist at ␣7 and ␣9 nAChRs; 10 Ϫ6 M) (Johnson et al, 1995), N -nitro-L-arginine methyl ester (L-NAME; NO synthase inhibitor; 10 Ϫ5 M) (Rees et al, 1990) (Gluais et al, 2005), and 6,12,19,20,25,26-hexahydro-5,27:13,18:21,24-trietheno-11,7-metheno-7H-dibenzo[b,n] Banquet et al, 2011).…”

Section: Methodsmentioning

confidence: 99%

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Activation of Nicotinic Receptors Can Contribute to Endothelium-Dependent Relaxations to Acetylcholine in the Rat Aorta

Zhang

Leung²,

Vanhoutte³

2012

J Pharmacol Exp Ther

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Acetylcholine causes endothelium-dependent relaxations in the rat aorta. Both muscarinic acetylcholine receptors (mAChRs) and nicotinic acetylcholine receptors (nAChRs) are expressed in endothelial cells. It is generally accepted that mAChRs are responsible for the endothelium-dependent relaxations evoked by acetylcholine. The present study was designed to investigate whether nAChRs can also be involved in such responses evoked by the cholinergic transmitter. Rings with or without endothelium of aortae of spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) normotensive rats were suspended in organ chambers for the measurement of isometric tension. In WKY aortae the muscarinic antagonist atropine abolished the relaxations to increasing concentrations of acetylcholine, confirming that mAChRs are responsible mainly for the response under control conditions. In SHR aortae, atropine caused only partial inhibition of the endothelium-dependent relaxations to acetylcholine; the remaining decreases in tension were inhibited by the nicotinic antagonist mecamylamine, which did not significantly affect the response in the absence of atropine in either SHR or WKY preparations. Thus, when mAChRs are inhibited, nAChRs mediate relaxation to the cholinergic transmitter in the SHR but not the WKY aorta. Nicotine, a direct agonist of the nicotinic receptor, induced endothelium-dependent relaxations in both SHR and WKY rats via the activation of ␣7-nAChRs, but not by mecamylamine-sensitive nicotinic receptors (␣3 subtype). The acetylcholine-induced, atropine-insensitive relaxations and those to nicotine both involve the phosphatidylinositol 3-kinase/AKT pathway. The present study demonstrates that the activation of nAChRs can contribute to acetylcholine-induced, endothelium-dependent relaxations in the aortae of hypertensive animals and suggests that these receptors may contribute to the endothelium-dependent regulation of vascular tone.

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Section: Resultsmentioning

confidence: 87%

Section: Methodsmentioning

confidence: 99%

Activation of Nicotinic Receptors Can Contribute to Endothelium-Dependent Relaxations to Acetylcholine in the Rat Aorta

Zhang

Leung²,

Vanhoutte³

2012

J Pharmacol Exp Ther

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“…The results shown here suggest that CAV1 exerts a negative effect on CDC42, which is dependent on the phosphorylation state of CAV1. Recently, it has been reported that CAV1 exerts a negative effect on the activity of the eNOS in mouse pulmonary arteries where NOS3 is inactivated in association with nonphosphorylated CAV1; this negative effect is vanquished when CAV1 is phosphorylated by c-Src (Banquet et al 2011). With regard to CDC42 and CAV1, we obtained similar results because CAV1 and CDC42 are associated even when CAV1 is not phosphorylated; in contrast, the phosphorylation of CAV1 on Tyr14 by a member of the SKF overcame the negative effects, permitting the dissociation of these proteins and, perhaps, the activation of CDC42.…”

Section: Discussionmentioning

confidence: 99%

“…Western blot images are representative of three independent experiments. Lee et al 2000, Cao et al 2002, Banquet et al 2011. The presence of c-Src has been shown in mammalian sperm, and its inhibition by SU6656, an inhibitor of SFK, blocks sperm processes related to tyrosine phosphorylation such as capacitation, motility hyperactivation, and the AR (Baker et al 2006, Mitchell et al 2008, Krapf et al 2010, Tapia et al 2011.…”

Section: Cav1 Is Phosphorylated By Kinases Belonging To the Src Familymentioning

confidence: 99%

The association between CDC42 and caveolin-1 is involved in the regulation of capacitation and acrosome reaction of guinea pig and mouse sperm

Baltiérrez-Hoyos

Roa-Espitia²,

Hernández‐González³

2012

Reproduction

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In the mammalian sperm, the acrosome reaction (AR) is considered to be a regulated secretion that is an essential requirement for physiological fertilization. The AR is the all-or-nothing secretion system that allows for multiple membrane fusion events. It is a Ca 2C -regulated exocytosis reaction that has also been shown to be regulated by several signaling pathways. CDC42 has a central role in the regulated exocytosis through the activation of SNARE proteins and actin polymerization. Furthermore, the lipid raft protein caveolin-1 (CAV1) functions as a scaffold and guanine nucleotide dissociation inhibitor protein for CDC42, which is inactivated when associated with CAV1. CDC42 and other RHO proteins have been shown to localize in the acrosome region of mammalian sperm; however, their relationship with the AR is unknown. Here, we present the first evidence that CDC42 and CAV1 could be involved in the regulation of capacitation and the AR. Our findings show that CDC42 is activated early during capacitation, reaching an activation maximum after 20 min of capacitation. Spontaneous and progesterone-induced ARs were inhibited when sperm were capacitated in presence of secramine A, a specific CDC42 inhibitor. CAV1 and CDC42 were co-immunoprecipitated from the membranes of noncapacitated sperm; this association was reduced in capacitated sperm, and our data suggest that the phosphorylation (Tyr14) of CAV1 by c-Src is involved in such reductions. We suggest that CDC42 activation is favored by the disruption of the CAV1-CDC42 interaction, allowing for its participation in the regulation of capacitation and the AR.

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“…H 2 O 2 can also induce the activation of NF-kB through the PI3-K/Akt pathway (42). Procaterol can elicit an endothelial nitric oxide synthase (eNOS)-dependent relaxation through the PI3-K/Akt pathway in mouse pulmonary artery (43). So procaterol can not inhibit the activation of the PI3-K/Akt pathway.…”

Section: Discussionmentioning

confidence: 99%

Procaterol but Not Dexamethasone Protects 16HBE Cells From H2O2-Induced Oxidative Stress

et al. 2014

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Abstract.Oxidative stress is an important pathophysiological factor of asthma and chronic obstructive pulmonary disease (COPD). We hypothesized that procaterol and dexamethasone might treat inflammation through inhibiting oxidative stress in vitro. This study evaluated procaterol and dexamethasone in the hydrogen peroxide (H 2 O 2 )-induced immortal human bronchial epithelial cell model of oxidative stress and investigated the underlying mechanisms. Results showed that exposure to 125 mM H 2 O 2 for 2 h led to a 50% reduction in the cell viability, significantly increased the percentage of apoptosis, and elevated levels of malondialdehyde and reactive oxygen species. Pretreatment with procaterol (25 -200 nM) could reduce these effects in a dosedependent manner. In contrast, pretreatment with dexamethasone (100 nM, 1000 nM) was inefficient. Pretreatment with procaterol plus dexamethasone (100 nM procaterol + 1000 nM dexamethasone) was effective, but the combined effect was not more effective than the sole pretreatment with 100 nM procaterol. The nuclear factor kappa-B (NF-kB) pathway was involved in the pathogenic mechanisms of H 2 O 2 . Procaterol may indirectly inhibit H 2 O 2 -induced activation of the NF-kB pathway due to its capability of antioxidation. Glucocorticoids may be not recommended to treat asthma or COPD complicated with severe oxidative stress.

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Role of Gi/o-Src kinase-PI3K/Akt pathway and caveolin-1 in β2-adrenoceptor coupling to endothelial NO synthase in mouse pulmonary artery

Cited by 52 publications

References 40 publications

Activation of Nicotinic Receptors Can Contribute to Endothelium-Dependent Relaxations to Acetylcholine in the Rat Aorta

Activation of Nicotinic Receptors Can Contribute to Endothelium-Dependent Relaxations to Acetylcholine in the Rat Aorta

The association between CDC42 and caveolin-1 is involved in the regulation of capacitation and acrosome reaction of guinea pig and mouse sperm

Procaterol but Not Dexamethasone Protects 16HBE Cells From H2O2-Induced Oxidative Stress

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