Molecular characterization and functional expression of equine interleukin-1 type I and type II receptor cDNAs

A recent study from this laboratory [A. R. Gwosdow, N. A. O'Connell, and A. B. Abou-Samra. Am. J. Physiol. 263 (Endocrinol. Metab. 26): E461-E466, 1992] showed that the inflammatory mediator interleukin-1 alpha (IL-1 alpha) stimulates catecholamine release from primary cultures of rat adrenal cells. The present studies were conducted to determine whether 1) IL-1 alpha stimulates catecholamine/dopamine release from the adrenal medullary cell line PC-12 and 2) the adenosine 3',5'-cyclic monophosphate (cAMP)-protein kinase A (PKA) pathway is involved in IL-1 alpha-induced dopamine release from PC-12 cells. The results indicate that IL-1 alpha significantly (P < 0.05) elevated dopamine release after a 24-h incubation period. IL-1 alpha did not stimulate cAMP accumulation at any time period between 5 min and 2 h. In contrast, forskolin-treated cells elevated (P < 0.05) intracellular cAMP levels and increased dopamine release. Because IL-1 alpha did not affect cAMP accumulation, the effect of IL-1 alpha on PKA activity was investigated. IL-1 alpha increased (P < 0.05) PKA activity at 15 and 30 min and returned to control levels by 1 h. Forskolin also increased (P < 0.05) PKA activity. The type of PKA activated (P < 0.05) by IL-1 alpha was type II PKA. In contrast, forskolin activated (P < 0.05) type I and type II PKA. Inhibition of PKA with the PKA inhibitor H-8 blocked PKA activity and dopamine secretion by both IL-1 alpha and forskolin in PC-12 cells. These observations demonstrate that 1) IL-1 alpha stimulated dopamine release from PC-12 cells by activating PKA, 2) the mechanism of IL-1 alpha activation of PKA does not involve detectable increases in intracellular cAMP accumulation, and 3) IL-1 alpha activates type II PKA, which is used by IL-1 alpha to stimulate dopamine secretion from PC-12 cells.

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Human aortic endothelial cells express the type I but not the type II receptor for interleukin-1 (IL-1)

Journal of Cellular Physiology ◽

10.1002/jcp.1041530320 ◽

1992 ◽

Vol 153 (3) ◽

pp. 583-588 ◽

Cited By ~ 16

Author(s):

Ann L. Akeson ◽

Laura B. Mosher ◽

Connie W. Woods ◽

Kendra K. Schroeder ◽

Terry L. Bowlin

Keyword(s):

Endothelial Cells ◽

Interleukin 1 ◽

Type I ◽

Type Ii ◽

Aortic Endothelial Cells ◽

Human Aortic Endothelial Cells ◽

Aortic Endothelial

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Type I and Type II Interleukin-1 Receptor Expression in Rat, Mouse, and Human Testes1

Biology of Reproduction ◽

10.1095/biolreprod56.6.1513 ◽

1997 ◽

Vol 56 (6) ◽

pp. 1513-1526 ◽

Cited By ~ 29

Author(s):

Edith Gomez ◽

Gérard Morel ◽

Annie Cavalier ◽

Marie-Odile Liénard ◽

France Haour ◽

...

Keyword(s):

Interleukin 1 ◽

Receptor Expression ◽

Type I ◽

Type Ii

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Isolation and molecular characterization of type I and type II feline coronavirus in Malaysia

Virology Journal ◽

10.1186/1743-422x-9-278 ◽

2012 ◽

Vol 9 (1) ◽

pp. 278 ◽

Cited By ~ 8

Author(s):

Amer Alazawy ◽

Siti Suri Arshad ◽

Abdul Rahman Omar ◽

Mohd Hair Bejo ◽

Faruku Bande ◽

...

Keyword(s):

Molecular Characterization ◽

Type I ◽

Type Ii ◽

Feline Coronavirus

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The type II "receptor" as a decoy target for interleukin 1 in polymorphonuclear leukocytes: characterization of induction by dexamethasone and ligand binding properties of the released decoy receptor.

Journal of Experimental Medicine ◽

10.1084/jem.179.2.739 ◽

1994 ◽

Vol 179 (2) ◽

pp. 739-743 ◽

Cited By ~ 127

Author(s):

F Re ◽

M Muzio ◽

M De Rossi ◽

N Polentarutti ◽

J G Giri ◽

...

Keyword(s):

Polymorphonuclear Leukocytes ◽

Interleukin 1 ◽

Soluble Form ◽

Type I ◽

Type Ii ◽

Membrane Expression ◽

Binding Properties ◽

Signaling Function ◽

Human Polymorphonuclear Leukocytes

Whereas the signaling function of the interleukin 1 (IL-1) receptor type I (IL-1R I) has been well documented, the type II "receptor" has been suggested to act as a decoy target for this cytokine. Since IL-1 may represent a key target of the immunomodulatory and antiinflammatory properties of glucocorticoids (GC), the aim of this study was to investigate the effects of dexamethasone (Dex) on IL-1R expression in human polymorphonuclear leukocytes (PMN), which express predominantly the type II molecule (IL-1R II). We found that Dex augments the levels of steady state transcripts encoding the IL-1R I and, most prominently, those of IL-1R II. Dex induced both transcripts via transcription-dependent mechanisms and by prolongation of the mRNAs half-lives. Inhibition of protein synthesis superinduced basal and Dex-augmented IL-1R II mRNA, whereas it completely inhibited the induction by Dex of IL-1R I transcripts. Induction of IL-1R II mRNA by Dex was associated with augmented membrane expression and release of the type II IL-1 binding molecule. This effect was mediated by the GC receptor. Other steroids (17 beta-estradiol, progesterone, and testosterone) were ineffective. The concentrations of IL-1 alpha and IL-1 receptor antagonist required to displace the binding of IL-1 beta to the soluble form of the decoy molecule induced by Dex from PMN were, respectively, 100 and 2 times higher compared with IL-1 beta. The induction by Dex of the type II receptor, a decoy molecule for IL-1, may contribute to the immunosuppressive and antiinflammatory activities of Dex.

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Hematopoietic growth factors upregulate the p65 type II interleukin-1 receptor on bone marrow progenitor cells in vitro

Blood ◽

10.1182/blood.v80.3.600.600 ◽

1992 ◽

Vol 80 (3) ◽

pp. 600-608 ◽

Cited By ~ 8

Author(s):

CM Dubois ◽

FW Ruscetti ◽

SE Jacobsen ◽

JJ Oppenheim ◽

JR Keller

Keyword(s):

Bone Marrow ◽

Growth Factors ◽

Progenitor Cells ◽

Specific Binding ◽

Interleukin 1 ◽

Scatchard Analysis ◽

Type I ◽

Type Ii ◽

Hematopoietic Growth Factors

Abstract Having previously shown that interleukin-1 (IL-1) induces the expression of IL-1 receptors (IL-1Rs) on bone marrow (BM) cells in vivo through an indirect mechanism, we studied whether hematopoietic growth factors (HGFs) could induce the expression of IL-1R on BM cells in vitro. In vitro treatment of light-density murine BM (LDBM) cells with either IL-3, IL-6, granulocyte--colony-stimulating factor (CSF), or granulocyte-macrophage--CSF caused a 5- to 10-fold upregulation of IL- 1R expression, whereas IL-1, IL-5, IL-7, and macrophage-CSF had no effect. Scatchard analysis showed one class of IL-1Rs on LDBM cells with an average of 66 +/- 20 sites per cells. After 24 hours of treatment with IL-3, the number of IL-1Rs increased to 413 +/- 125, without effecting the affinity. This effect required protein synthesis, but was independent of cell division. Purified lineage-negative progenitor cells (Lin-) did not express detectable levels of IL-1R, but 24 hours of treatment with IL-3, GM-CSF, and G-CSF stimulated IL-1-- specific binding. Autoradiographic analysis of Lin- cells showed that IL-1R induction by IL-3 occurs on undifferentiated blast cells. Affinity labeling of Lin- cells treated with HGFs showed an increase in a 65-Kd IL-1 binding protein that did not bind or compete with an anti- type I IL-1R antibody, suggesting that these cells expressed type II IL- 1R. These data suggest that IL-1 stimulation of myelopoiesis occurs by a mechanism involving IL-1R upregulation on hematopoietic progenitor cells by HGFs.

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