Prostaglandin E-2-stimulated secretion of protein in the salivary glands of the lone star tick via a phosphoinositide signaling pathway

J Yuan, A S Bowman, M Aljamali, M R Payne, J S Tucker, J W Dillwith, R C Essenberg, J R Sauer

Research output: Contribution to journalArticle

17 Citations (Scopus)

Abstract

Previous studies identified a prostaglandin E-2 (PGE(2)) receptor in the salivary glands of partially fed female lone star ticks, Amblyomma americanum (L.). In the present studies, protein secretion from dispersed salivary gland acini was shown to be specific for PGE(2), as compared with PGF(2 alpha) or the thromboxane analog U-46619, in accordance with their respective binding affinities for the PGE(2) receptor. Furthermore, the selective PGE(2) EP1 receptor agonist, 17-phenyl trinor PGE(2), was as effective as PGE(2) in stimulating secretion of anticoagulant protein. Calcium ionophore A-23187 (1 to 100 mu M) stimulated secretion of anticoagulant protein in a dose-dependent manner but the voltage-gated Ca2+-channel blocker verapamil (1 to 1000 mu M) and the receptor-mediated Ca2+-entry antagonist, SK&F 96365 (1 and 10 mu M), and 5 mM ethylene glycol bis(beta-aminoethyl ether)-N,NN',N'-tetraacetic acid (EGTA) had no appreciable effect on inhibiting PGE(2)-stimulated secretion of anticoagulant protein. PGE(2) (0.1 mu M) and the nonhydrolyzable analog of guanosine triphosphate (GTP), GTP gamma S (10 mu M), directly activated phospholipase C (PLC) in a membrane-enriched fraction of the salivary glands after PLC was first incubated with the PGE(2) EP1 receptor antagonist AH-6809, which presumably antagonized endogenous PGE(2) (0.3 mu M) in the broken-cell-membrane-enriched fraction. TMB-8, an antagonist of intracellular inositol trisphosphate (IP3) receptors, inhibited PGE(2)-stimulated secretion. The results support the hypothesis that PGE(2) stimulates secretion of tick salivary gland protein via a phosphoinositide signaling pathway and mobilization of intracellular Ca2+. (C) 2000 Elsevier Science Ltd. All rights reserved.

Original languageEnglish
Pages (from-to)1099-1106
Number of pages8
JournalInsect Biochemistry and Molecular Biology
Volume30
Publication statusPublished - 2000

Keywords

  • tick salivary glands
  • exocytosis
  • calcium
  • PGE(2) receptor
  • PROSTANOID RECEPTORS
  • ARACHIDONIC-ACID
  • PHOSPHOLIPASE-C
  • CALCIUM-ENTRY
  • FEMALE TICK
  • CELLS
  • E-2

Cite this

Prostaglandin E-2-stimulated secretion of protein in the salivary glands of the lone star tick via a phosphoinositide signaling pathway. / Yuan, J ; Bowman, A S ; Aljamali, M ; Payne, M R ; Tucker, J S ; Dillwith, J W ; Essenberg, R C ; Sauer, J R .

In: Insect Biochemistry and Molecular Biology, Vol. 30, 2000, p. 1099-1106.

Research output: Contribution to journalArticle

Yuan, J ; Bowman, A S ; Aljamali, M ; Payne, M R ; Tucker, J S ; Dillwith, J W ; Essenberg, R C ; Sauer, J R . / Prostaglandin E-2-stimulated secretion of protein in the salivary glands of the lone star tick via a phosphoinositide signaling pathway. In: Insect Biochemistry and Molecular Biology. 2000 ; Vol. 30. pp. 1099-1106.
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abstract = "Previous studies identified a prostaglandin E-2 (PGE(2)) receptor in the salivary glands of partially fed female lone star ticks, Amblyomma americanum (L.). In the present studies, protein secretion from dispersed salivary gland acini was shown to be specific for PGE(2), as compared with PGF(2 alpha) or the thromboxane analog U-46619, in accordance with their respective binding affinities for the PGE(2) receptor. Furthermore, the selective PGE(2) EP1 receptor agonist, 17-phenyl trinor PGE(2), was as effective as PGE(2) in stimulating secretion of anticoagulant protein. Calcium ionophore A-23187 (1 to 100 mu M) stimulated secretion of anticoagulant protein in a dose-dependent manner but the voltage-gated Ca2+-channel blocker verapamil (1 to 1000 mu M) and the receptor-mediated Ca2+-entry antagonist, SK&F 96365 (1 and 10 mu M), and 5 mM ethylene glycol bis(beta-aminoethyl ether)-N,NN',N'-tetraacetic acid (EGTA) had no appreciable effect on inhibiting PGE(2)-stimulated secretion of anticoagulant protein. PGE(2) (0.1 mu M) and the nonhydrolyzable analog of guanosine triphosphate (GTP), GTP gamma S (10 mu M), directly activated phospholipase C (PLC) in a membrane-enriched fraction of the salivary glands after PLC was first incubated with the PGE(2) EP1 receptor antagonist AH-6809, which presumably antagonized endogenous PGE(2) (0.3 mu M) in the broken-cell-membrane-enriched fraction. TMB-8, an antagonist of intracellular inositol trisphosphate (IP3) receptors, inhibited PGE(2)-stimulated secretion. The results support the hypothesis that PGE(2) stimulates secretion of tick salivary gland protein via a phosphoinositide signaling pathway and mobilization of intracellular Ca2+. (C) 2000 Elsevier Science Ltd. All rights reserved.",
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T1 - Prostaglandin E-2-stimulated secretion of protein in the salivary glands of the lone star tick via a phosphoinositide signaling pathway

AU - Yuan, J

AU - Bowman, A S

AU - Aljamali, M

AU - Payne, M R

AU - Tucker, J S

AU - Dillwith, J W

AU - Essenberg, R C

AU - Sauer, J R

PY - 2000

Y1 - 2000

N2 - Previous studies identified a prostaglandin E-2 (PGE(2)) receptor in the salivary glands of partially fed female lone star ticks, Amblyomma americanum (L.). In the present studies, protein secretion from dispersed salivary gland acini was shown to be specific for PGE(2), as compared with PGF(2 alpha) or the thromboxane analog U-46619, in accordance with their respective binding affinities for the PGE(2) receptor. Furthermore, the selective PGE(2) EP1 receptor agonist, 17-phenyl trinor PGE(2), was as effective as PGE(2) in stimulating secretion of anticoagulant protein. Calcium ionophore A-23187 (1 to 100 mu M) stimulated secretion of anticoagulant protein in a dose-dependent manner but the voltage-gated Ca2+-channel blocker verapamil (1 to 1000 mu M) and the receptor-mediated Ca2+-entry antagonist, SK&F 96365 (1 and 10 mu M), and 5 mM ethylene glycol bis(beta-aminoethyl ether)-N,NN',N'-tetraacetic acid (EGTA) had no appreciable effect on inhibiting PGE(2)-stimulated secretion of anticoagulant protein. PGE(2) (0.1 mu M) and the nonhydrolyzable analog of guanosine triphosphate (GTP), GTP gamma S (10 mu M), directly activated phospholipase C (PLC) in a membrane-enriched fraction of the salivary glands after PLC was first incubated with the PGE(2) EP1 receptor antagonist AH-6809, which presumably antagonized endogenous PGE(2) (0.3 mu M) in the broken-cell-membrane-enriched fraction. TMB-8, an antagonist of intracellular inositol trisphosphate (IP3) receptors, inhibited PGE(2)-stimulated secretion. The results support the hypothesis that PGE(2) stimulates secretion of tick salivary gland protein via a phosphoinositide signaling pathway and mobilization of intracellular Ca2+. (C) 2000 Elsevier Science Ltd. All rights reserved.

AB - Previous studies identified a prostaglandin E-2 (PGE(2)) receptor in the salivary glands of partially fed female lone star ticks, Amblyomma americanum (L.). In the present studies, protein secretion from dispersed salivary gland acini was shown to be specific for PGE(2), as compared with PGF(2 alpha) or the thromboxane analog U-46619, in accordance with their respective binding affinities for the PGE(2) receptor. Furthermore, the selective PGE(2) EP1 receptor agonist, 17-phenyl trinor PGE(2), was as effective as PGE(2) in stimulating secretion of anticoagulant protein. Calcium ionophore A-23187 (1 to 100 mu M) stimulated secretion of anticoagulant protein in a dose-dependent manner but the voltage-gated Ca2+-channel blocker verapamil (1 to 1000 mu M) and the receptor-mediated Ca2+-entry antagonist, SK&F 96365 (1 and 10 mu M), and 5 mM ethylene glycol bis(beta-aminoethyl ether)-N,NN',N'-tetraacetic acid (EGTA) had no appreciable effect on inhibiting PGE(2)-stimulated secretion of anticoagulant protein. PGE(2) (0.1 mu M) and the nonhydrolyzable analog of guanosine triphosphate (GTP), GTP gamma S (10 mu M), directly activated phospholipase C (PLC) in a membrane-enriched fraction of the salivary glands after PLC was first incubated with the PGE(2) EP1 receptor antagonist AH-6809, which presumably antagonized endogenous PGE(2) (0.3 mu M) in the broken-cell-membrane-enriched fraction. TMB-8, an antagonist of intracellular inositol trisphosphate (IP3) receptors, inhibited PGE(2)-stimulated secretion. The results support the hypothesis that PGE(2) stimulates secretion of tick salivary gland protein via a phosphoinositide signaling pathway and mobilization of intracellular Ca2+. (C) 2000 Elsevier Science Ltd. All rights reserved.

KW - tick salivary glands

KW - exocytosis

KW - calcium

KW - PGE(2) receptor

KW - PROSTANOID RECEPTORS

KW - ARACHIDONIC-ACID

KW - PHOSPHOLIPASE-C

KW - CALCIUM-ENTRY

KW - FEMALE TICK

KW - CELLS

KW - E-2

M3 - Article

VL - 30

SP - 1099

EP - 1106

JO - Insect Biochemistry and Molecular Biology

JF - Insect Biochemistry and Molecular Biology

SN - 0965-1748

ER -