Classification of prostaglandin receptors based on coupling to signal transduction systems

Muallem, Shmuel; Merritt, Bradley S.; Green, J; Yamaguchi, Dean T.

doi:10.1042/bj2630769

Cited by 32 publications

(12 citation statements)

References 10 publications

(10 reference statements)

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“…Many signal transduction mechanisms activated by PGs have been described in bone cells (55). Many signal transduction mechanisms activated by PGs have been described in bone cells (55).…”

Section: Discussionmentioning

confidence: 99%

PGE2 Is Essential for Gap Junction-Mediated Intercellular Communication between Osteocyte-Like MLO-Y4 Cells in Response to Mechanical Strain

et al. 2001

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We have observed, in our previous studies, that fluid flow increases gap junction-mediated intercellular coupling and the expression of a gap junction protein, connexin 43, in osteocyte-like MLO-Y4 cells. Interestingly, this stimulation is further enhanced during the poststress period, indicating that a released factor(s) is likely to be involved. Here, we report that the conditioned medium obtained from the fluid flow-treated MLO-Y4 cells increased the number of functional gap junctions and connexin 43 protein. These changes are similar to those observed in MLO-Y4 cells directly exposed to fluid flow. Fluid flow was found to induce PGE(2) release and increase cyclooxygenase 2 expression. Treatment of the cells with PGE(2) had the same effect as fluid flow, suggesting that PGE(2) could be responsible for these autocrine effects. When PGE(2) was depleted from the fluid flow-conditioned medium, the stimulatory effect on gap junctions was partially, but significantly, decreased. Addition of the cyclooxygenase inhibitor, indomethacin, partially blocked the stimulatory effects of mechanical strain on gap junctions. Taken together, these studies suggest that the stimulatory effect of fluid flow on gap junctions is mediated, in part, by the release of PGE(2). Hence, PGE(2) is an essential mediator between mechanical strain and gap junctions in osteocyte-like cells.

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“…Many signal transduction mechanisms activated by PGs have been described in bone cells (55). Many signal transduction mechanisms activated by PGs have been described in bone cells (55).…”

Section: Discussionmentioning

confidence: 99%

PGE2 Is Essential for Gap Junction-Mediated Intercellular Communication between Osteocyte-Like MLO-Y4 Cells in Response to Mechanical Strain

et al. 2001

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“…[4][5][6][7][8] Based on the analysis of Coleman et al, 1,7 Eglin and Whiting, 3 and Muallem et al, 9 we know that prostanoid receptors differ in the second messengers that mediate their biological effects. Agonists acting on the EP 1 , FP, and TP receptors stimulate the IP 3 /DAG pathway and exert their effects through an increase in intracellular calcium.…”

Section: 3mentioning

confidence: 99%

Prostaglandin E ₂ –Induced Aldosterone Release Is Mediated by an EP ₂ Receptor

et al. 1998

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Abstract-Prostaglandin E 2 (PGE 2 ) is an endogenous hormone of adrenal zona glomerulosa cells and is released in response to stimulation by agonists such as angiotensin II (Ang II). It stimulates the release of aldosterone from cultured bovine adrenal zona glomerulosa cells. These studies were designed to determine whether this steroidogenic effect of PGE 2 was mediated by an EP 1 , EP 2 , or EP 3 receptor. Prostaglandin E 2 and 11-deoxy PGE 1 , an EP 2 -selective agonist, stimulated aldosterone release in a concentration-related manner with an ED 50 of 300 nmol/L for PGE 2 and 2 mol/L for 11-deoxy PGE 1 . The maximal effect of PGE 2 was less than that of angiotensin II. 17-Phenyl trinor PGE 2 , an EP 1 -selective agonist, required concentrations of 100 mol/L to stimulate aldosterone release and sulprostone, an EP 3 /EP 1 -selective agonist, failed to alter aldosterone release. The EP 1 -selective antagonist SC19220 failed to alter basal or PGE 2 -stimulated aldosterone release over a range of concentrations. PGE 2 and 11-deoxy PGE 1 also stimulated an increase in both intracellular and extracellular cAMP. This increase was time-and concentration-related. The ED 50 for PGE 2 was 9.8 mol/L. 17-Phenyl trinor PGE 2 and sulprostone were without effect. Using fura-2 loaded cells, PGE 2 (2 mol/L), dibutyryl cAMP (2 mmol/L), and Ang II (2 mol/L) increased intracellular calcium over basal concentrations by 5.5-fold, 3-fold, and 6.2-fold, respectively. Like PGE 2 , dibutyryl cAMP also stimulated aldosterone release. PGE 2 -and dibutyryl cAMP-induced aldosterone release were blocked by the calcium channel inhibitor diltiazem. These studies indicate that PGE 2 is a potent stimulus for aldosterone release and that the effect is mediated by EP 2 receptors. Both cAMP and calcium appear to mediate the steroidogenic effect of PGE 2 and calcium seems to be distal to cAMP. (Hypertension. 1998;31:575-581.)Key Words: zona glomerulosa Ⅲ cyclic AMP Ⅲ calcium Ⅲ receptors, prostanoid Ⅲ angiotensin II T here are five classes of prostanoid (P) receptors designated as EP, FP, DP, IP, and TP, corresponding to their naturally occurring agonists, prostaglandin E 2 , prostaglandin F 2␣ , prostaglandin D 2 , prostaglandin I 2 , and thromboxane A 2 , respectively.1 Synthetic and natural analogues of these prostaglandins also exist that possess selectivity at these five classes of receptors. 2,3The EP receptor has been subclassified into three subtypes: EP 1 , EP 2 , and EP 3 . [4][5][6][7][8] Based on the analysis of Coleman et al, 1,7 Eglin and Whiting, 3 and Muallem et al, 9 we know that prostanoid receptors differ in the second messengers that mediate their biological effects. Agonists acting on the EP 1 , FP, and TP receptors stimulate the IP 3 /DAG pathway and exert their effects through an increase in intracellular calcium. The EP 2 , DP, or IP receptor agonists stimulate adenylyl cyclase and the accumulation of cAMP. Finally, EP 3 receptor activation may increase IP 3 /DAG formation or inhibit adenylyl cyclase.There is considerable evid...

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“…Laminin-mediated cell adhesion mediated by the a61pl integrin receptor may be facilitated by receptor phosphorylation (Shaw et al, 1990). PGE, activates cAMP and therefore CAMP-dependent kinase (Mualem et al, 1989). A fibronectin receptor is also regulated by cAMP (Cheung and Juliano, 1985).…”

Section: Discussionmentioning

confidence: 99%

Prostaglandin E₂ receptor modulation affects tumor cell adhesion to laminin

Zhang¹,

Fulton²

1991

Journal Cellular Physiology

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We have shown previously that murine mammary adenocarcinoma cells both synthesize prostaglandin E2 (PGE2) and have a high affinity receptor for this ligand. Modulation of either PGE synthesis or PGE receptor function changes the metastatic potential of these cells. Because of the importance of laminin and laminin receptors to the metastatic process, we asked whether or not the PGE receptor participates in tumor cell-laminin interactions. As has been reported for many other tumor cells, laminin and the laminin-derived peptide PA22-2, containing the sequence IKVAV, mediate attachment of line 410.4 mammary tumor cells in vitro. We now demonstrate that the attachment of 410.4 cells to laminin or peptide PA22-2 was significantly inhibited by three PGE receptor antagonists, LE0101, SC19220, and sodium meclofenamate. LE0101 was most active, inhibiting tumor cell adhesion in a dose-dependent manner in the absence of nonspecific toxicity. These receptor antagonists had no effect on the PA22-2-mediated attachment of a PGE receptor negative tumor cell line, except at the highest concentration of LE0101 tested. No inhibition of adhesion to Type I collagen was seen. These results indicate that the PGE2 receptor modulates tumor cell adhesion to laminin which may subsequently affect the in vivo process of metastasis.

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Classification of prostaglandin receptors based on coupling to signal transduction systems

Cited by 32 publications

References 10 publications

PGE2 Is Essential for Gap Junction-Mediated Intercellular Communication between Osteocyte-Like MLO-Y4 Cells in Response to Mechanical Strain

PGE2 Is Essential for Gap Junction-Mediated Intercellular Communication between Osteocyte-Like MLO-Y4 Cells in Response to Mechanical Strain

Prostaglandin E ₂ –Induced Aldosterone Release Is Mediated by an EP ₂ Receptor

Prostaglandin E₂ receptor modulation affects tumor cell adhesion to laminin

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Classification of prostaglandin receptors based on coupling to signal transduction systems

Cited by 32 publications

References 10 publications

PGE2 Is Essential for Gap Junction-Mediated Intercellular Communication between Osteocyte-Like MLO-Y4 Cells in Response to Mechanical Strain

PGE2 Is Essential for Gap Junction-Mediated Intercellular Communication between Osteocyte-Like MLO-Y4 Cells in Response to Mechanical Strain

Prostaglandin E 2 –Induced Aldosterone Release Is Mediated by an EP 2 Receptor

Prostaglandin E2 receptor modulation affects tumor cell adhesion to laminin

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Prostaglandin E ₂ –Induced Aldosterone Release Is Mediated by an EP ₂ Receptor

Prostaglandin E₂ receptor modulation affects tumor cell adhesion to laminin