Prostanoid‐induced contraction of human bronchial smooth muscle is mediated by TP‐receptors

Coleman, Robert A.; Sheldrick, R.L.G.

doi:10.1111/j.1476-5381.1989.tb11869.x

Cited by 132 publications

(87 citation statements)

References 10 publications

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“…48 Some of these effects may be due to interaction with receptors for other prostanoids, as PGD 2 has a relatively high affinity for FP receptors 32,49 and PGD 2 -mediated bronchoconstriction has been reported to be due to stimulation of TP receptors. 33,34 In contrast, some other effects of PGD 2 , such as those on epithelial cell ion transport, 50 are difficult to explain on the basis of classic prostanoid receptors and may be due to stimulation of DP 2 receptors.…”

Section: Discussionmentioning

confidence: 99%

Prostaglandin D2 is a potent chemoattractant for human eosinophils that acts via a novel DP receptor

Monneret

Gravel

Diamond

et al. 2001

Blood

309

286

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Prostaglandin D 2 (PGD 2 ) is released following exposure of asthmatics to allergen and acts via the adenylyl cyclase-coupled receptor for PGD 2 (DP receptor). In this study, it is reported that human eosinophils possess this receptor, which would be expected to inhibit their activation. In contrast, it was found that prostaglandin D 2 is a potent stimulator of eosinophil chemotaxis, actin polymerization, CD11b expression, and Lselectin shedding. These responses are specific for eosinophils, as neutrophils display little or no response to prostaglandin D 2 . They were not due to interaction with receptors for other prostanoids, as prostaglandins E 2 and F 2␣ , U46619 (a thromboxane A 2 analogue), and carbaprostacyclin (a prostacyclin analogue) displayed little or no activity. Furthermore, they were not shared by the selective DP receptor agonist BW245C and were not prevented by the selective DP receptor antagonist BWA868C, indicating that they were not mediated by DP receptors. In contrast, the prostaglandin D 2 metabolite 13,14-dihydro-15-oxoprostaglandin D 2 induced eosinophil activation but did not stimulate DP receptor-mediated adenosine 3,5-cyclic monophosphate (cAMP) formation. These results indicate that in addition to the classic inhibitory DP 1 receptor, eosinophils possess a second, novel DP 2 receptor that is associated with PGD 2 -induced cell activation. These 2 receptors appear to interact to regulate eosinophil responses to PGD 2 , as blockade of DP 1 receptor-mediated cAMP production by BWA868C resulted in enhanced DP 2 receptor-mediated stimulation of CD11b expression. The balance between DP 1 and DP 2 receptors could determine the degree to which prostaglandin D 2 can activate eosinophils and may play a role in eosinophil recruitment in asthma. (Blood. 2001;98:1942-1948

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Section: Discussionmentioning

confidence: 99%

Prostaglandin D2 is a potent chemoattractant for human eosinophils that acts via a novel DP receptor

Monneret

Gravel

Diamond

et al. 2001

Blood

309

286

View full text Add to dashboard Cite

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“…Moreover, the increased excretion of the PGD 2 metabolite may indicate an important role for PGD 2 in the bronchoconstrictive response to mannitol. PGD 2 , as well as 9a,11b-PGF 2 , are potent bronchoconstrictors in man [17], mainly acting on the TP-receptor [18,19]. Pretreatment with selective TP-receptor antagonists attenuated both PGD 2 -and allergen-induced, but not histamine-induced, bronchoconstriction [20][21][22].…”

Section: Discussionmentioning

confidence: 99%

Evidence of mast cell activation and leukotriene release after mannitol inhalation

Brannan

Gulliksson²,

Anderson³

et al. 2003

Eur Respir J

155

108

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The aim of this study was to investigate if mannitol inhalation, as a model of exercise-induced bronchoconstriction (EIB), causes mast cell activation and release of mediators of bronchoconstriction.Urinary excretion of previously identified mediators of EIB was investigated in association with mannitol-induced bronchoconstriction. Twelve asthmatic and nine nonasthmatic subjects inhaled mannitol and urine was collected 60 min before and for 90 min after challenge. The urinary concentrations of leukotriene (LT)E 4 , the prostaglandin (PG)D 2 metabolite and the mast cell marker 9a,11b-PGF 2 were measured by enzyme immunoassay. N t -methylhistamine was measured by radioimmunoassay.In asthmatic subjects, inhalation of a mean¡SEM dose of 272¡56 mg mannitol induced a reduction in forced expiratory volume in one second (FEV1) of 34.5¡2.1%. This was associated with increases in urinary 9a,11b-PGF 2 (91.9¡8.2 versus 66.9¡ 6.6 ng?mmol creatinine -1 , peak versus baseline) and LTE 4 (51.3¡7.5 versus 32.9¡4.7). In nonasthmatic subjects, the reduction in FEV1 was 1.0¡0.5% after inhaling 635 mg of mannitol. Although smaller than in the asthmatics, significant increases of urinary 9a,11b-PGF 2 (68.4¡6.9 versus 56.0¡5.8 ng?mmol creatinine -1 ) and LTE 4 (58.5¡5.3 versus 43.0¡3.3 ng?mmol creatinine -1 ) were observed in the nonasthmatic subjects. There was also a small increase in urinary excretion of N t -methylhistamine in the nonasthmatics, but not in the asthmatics.The increased urinary levels of 9a,11b-prostaglandin F 2 support mast cell activation with release of mediators following inhalation of mannitol. Increased bronchial responsiveness to the released mediators could explain the exclusive bronchoconstriction in asthmatic subjects. Eur Respir J 2003; 22: 491-496.

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“…AH6809, a well characterized antagonist for EP 1 and EP 2 -mediated signaling (54,55), was used to treat MLO-Y4 cells. As shown in Fig.…”

Section: Blocking Ep 2 Receptor Activation Suppresses the Stimulatorymentioning

confidence: 99%

Effects of Mechanical Strain on the Function of Gap Junctions in Osteocytes Are Mediated through the Prostaglandin EP2 Receptor

Cherian

Cheng

et al. 2003

Journal of Biological Chemistry

191

146

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Fluid flow conditioned medium and PGE 2 stimulated cAMP production and PKA activity suggesting that PGE 2 released by mechanically stimulated cells is responsible for the activation of cAMP and PKA. The adenylate cyclase activators, forskolin and 8-bromo-cAMP, enhanced intercellular connectivity, the number of functional gap junctions, and Cx43 protein expression, whereas the PKA inhibitor, H89, inhibited the stimulatory effect of PGE 2 on gap junctions. These studies suggest that the EP 2 receptor mediates the effects of autocrine PGE 2 on the osteocyte gap junction in response to fluid flow-induced shear stress. These data support the hypothesis that the EP 2 receptor, cAMP, and PKA are critical components of the signaling cascade between mechanical strain and gap junction-mediated communication between osteocytes.

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Prostanoid‐induced contraction of human bronchial smooth muscle is mediated by TP‐receptors

Cited by 132 publications

References 10 publications

Prostaglandin D2 is a potent chemoattractant for human eosinophils that acts via a novel DP receptor

Prostaglandin D2 is a potent chemoattractant for human eosinophils that acts via a novel DP receptor

Evidence of mast cell activation and leukotriene release after mannitol inhalation

Effects of Mechanical Strain on the Function of Gap Junctions in Osteocytes Are Mediated through the Prostaglandin EP2 Receptor

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