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

1997 ◽  
Vol 56 (6) ◽  
pp. 1513-1526 ◽  
Author(s):  
Edith Gomez ◽  
Gérard Morel ◽  
Annie Cavalier ◽  
Marie-Odile Liénard ◽  
France Haour ◽  
...  
Keyword(s):  
Interleukin 1 ◽  
Receptor Expression ◽  
Type I ◽  
Type Ii

scholarly journals In vivo interleukin-1 (IL-1) administration indirectly promotes type II IL-1 receptor expression on hematopoietic bone marrow cells: novel mechanism for the hematopoietic effects of IL-1

Blood ◽  
1991 ◽  
Vol 78 (11) ◽  
pp. 2841-2847 ◽  
Author(s):  
CM Dubois ◽  
FW Ruscetti ◽  
JR Keller ◽  
JJ Oppenheim ◽  
K Hestdal ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Bone Marrow Cells ◽  
Direct Action ◽  
Interleukin 1 ◽  
Receptor Expression ◽  
Type I ◽  
Type Ii ◽  
Hematopoietic Growth Factors ◽  
Accessory Cells

Abstract Interleukin-1 (IL-1) has profound stimulatory effects on hematopoiesis but the mechanism(s) of action remain unknown. The direct action of IL- 1 on hematopoietic progenitor cells requires the presence of a specific IL-1 receptor (IL-1R). In this report, we tested the effect of in vivo IL-1 treatment on the expression of IL-1R on bone marrow (BM) cells. Injection of mice with IL-1 results in a marked upregulation of IL-1R on light-density BM cells as on a subpopulation enriched for myeloid precursors. Pretreatment of mice with anti-type I IL-1R antibody (35F5), which has been shown to prevent the radioprotective effect of IL-1, also blocked IL-1-induced IL-1R expression on BM cells. This antibody did not directly bind and block IL-1 binding to the type II IL- 1R expressed on hematopoietic cells, suggesting that IL-1R upregulation by IL-1 is indirect. It is therefore possible that IL-1 acts on type I IL-1R-expressing accessory cells such as stromal cells or T cells to induce production of hematopoietic growth factors (HGFs). In support of this, granulocyte colony-stimulating factor administration can induce the increase of IL-1R on BM cells. Thus, the increased expression of IL- 1R on hematopoietic BM cells by IL-1 is indirect, probably mediated in part through endogenous HGF production. These results also suggest that the restorative hematopoietic effect of IL-1 occurs through both indirect and direct mechanisms.

scholarly journals In vivo interleukin-1 (IL-1) administration indirectly promotes type II IL-1 receptor expression on hematopoietic bone marrow cells: novel mechanism for the hematopoietic effects of IL-1

Blood ◽  
1991 ◽  
Vol 78 (11) ◽  
pp. 2841-2847
Author(s):  
CM Dubois ◽  
FW Ruscetti ◽  
JR Keller ◽  
JJ Oppenheim ◽  
K Hestdal ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Bone Marrow Cells ◽  
Direct Action ◽  
Interleukin 1 ◽  
Receptor Expression ◽  
Type I ◽  
Type Ii ◽  
Hematopoietic Growth Factors ◽  
Accessory Cells

Interleukin-1 (IL-1) has profound stimulatory effects on hematopoiesis but the mechanism(s) of action remain unknown. The direct action of IL- 1 on hematopoietic progenitor cells requires the presence of a specific IL-1 receptor (IL-1R). In this report, we tested the effect of in vivo IL-1 treatment on the expression of IL-1R on bone marrow (BM) cells. Injection of mice with IL-1 results in a marked upregulation of IL-1R on light-density BM cells as on a subpopulation enriched for myeloid precursors. Pretreatment of mice with anti-type I IL-1R antibody (35F5), which has been shown to prevent the radioprotective effect of IL-1, also blocked IL-1-induced IL-1R expression on BM cells. This antibody did not directly bind and block IL-1 binding to the type II IL- 1R expressed on hematopoietic cells, suggesting that IL-1R upregulation by IL-1 is indirect. It is therefore possible that IL-1 acts on type I IL-1R-expressing accessory cells such as stromal cells or T cells to induce production of hematopoietic growth factors (HGFs). In support of this, granulocyte colony-stimulating factor administration can induce the increase of IL-1R on BM cells. Thus, the increased expression of IL- 1R on hematopoietic BM cells by IL-1 is indirect, probably mediated in part through endogenous HGF production. These results also suggest that the restorative hematopoietic effect of IL-1 occurs through both indirect and direct mechanisms.

scholarly journals Independent binding of interleukin-1 alpha and interleukin-1 beta to type I and type II interleukin-1 receptors.

1993 ◽  
Vol 268 (4) ◽  
pp. 2513-2524
Author(s):  
J. Slack ◽  
C.J. McMahan ◽  
S. Waugh ◽  
K. Schooley ◽  
M.K. Spriggs ◽  
...  
Keyword(s):  
Interleukin 1 ◽  
Type I ◽  
Type Ii ◽  
Interleukin 1 Beta

scholarly journals A chimeric type II/type I interleukin-1 receptor can mediate interleukin-1 induction of gene expression in T cells

1993 ◽  
Vol 268 (14) ◽  
pp. 10490-10494
Author(s):  
A. Heguy ◽  
C.T. Baldari ◽  
S. Censini ◽  
P. Ghiara ◽  
J.L. Telford
Keyword(s):  
Gene Expression ◽  
T Cells ◽  
Interleukin 1 ◽  
Type I ◽  
Type Ii

FRI-317-Progression of fatty liver disease to steatohepatitis and liver fibrosis is associated with altered Oncostatin M type I and type II receptor expression

2019 ◽  
Vol 70 (1) ◽  
pp. e536
Author(s):  
Philipp Lederer ◽  
Martin Roderfeld ◽  
Daniela Kroy ◽  
Elke Roeb ◽  
Andreas Geier ◽  
...  
Keyword(s):  
Liver Disease ◽  
Liver Fibrosis ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Receptor Expression ◽  
Oncostatin M ◽  
Type I ◽  
Type Ii

Type II interleukin-1 receptor expression is reduced in monocytes/macrophages and atherosclerotic lesions

2011 ◽  
Vol 1811 (9) ◽  
pp. 556-563 ◽  
Author(s):  
Jordi Pou ◽  
José Martínez-González ◽  
Alba Rebollo ◽  
Cristina Rodríguez ◽  
Ricardo Rodríguez-Calvo ◽  
...  
Keyword(s):  
Interleukin 1 ◽  
Receptor Expression ◽  
Type Ii ◽  
Atherosclerotic Lesions

Interleukin-1 alpha stimulates dopamine release by activating type II protein kinase A in PC-12 cells

1995 ◽  
Vol 269 (6) ◽  
pp. E1083-E1088
Author(s):  
A. Joseph ◽  
A. Kumar ◽  
N. A. O'Connell ◽  
R. K. Agarwal ◽  
A. R. Gwosdow
Keyword(s):  
Protein Kinase ◽  
Protein Kinase A ◽  
Dopamine Release ◽  
Interleukin 1 ◽  
Intracellular Camp ◽  
Type I ◽  
Camp Accumulation ◽  
Type Ii ◽  
Pc 12 Cells ◽  
Kinase A

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.

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

1992 ◽  
Vol 153 (3) ◽  
pp. 583-588 ◽  
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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