Molecular Mechanisms Involved in the Control of Differential Cytokine Expression in Human Monocytes

1997 ◽  
pp. 13-18
Author(s):  
L. M. L. Tuyt ◽  
W. H. A. Dokter ◽  
E. Vellenga
Keyword(s):  
Molecular Mechanisms ◽  
Cytokine Expression ◽  
Human Monocytes

Alteration of Actin Organization by Jaspamide Inhibits Ruffling, but not Phagocytosis or Oxidative Burst, in HL-60 Cells and Human Monocytes

Blood ◽  
1999 ◽  
Vol 93 (11) ◽  
pp. 3994-4005 ◽  
Author(s):  
Ina Fabian ◽  
Drora Halperin ◽  
Smadar Lefter ◽  
Leonid Mittelman ◽  
Rom T. Altstock ◽  
...  
Keyword(s):  
Oxidative Burst ◽  
Phagocytic Activity ◽  
Mammalian Cells ◽  
Molecular Mechanisms ◽  
Cyclic Peptide ◽  
De Novo ◽  
Human Monocytes ◽  
Actin Organization ◽  
Fibrous Network ◽  
Intracellular Movement

Abstract Jaspamide, a naturally occurring cyclic peptide isolated from the marine sponge Hemiastrella minor, has fungicidal and growth-inhibiting activities. Exposure of promyelocytic HL-60 cells and human monocytes to jaspamide induces a dramatic reorganization of actin from a typical fibrous network to focal aggregates. HL-60 cells exposed to 5 × 10−8 mol/L or 10−7 mol/L jaspamide exhibited a reduced proliferation rate. In addition, 10−7mol/L jaspamide induced maturation of HL-60 cells as indicated by the appearance of a lobulated nucleus in 55% ± 5% of the cells and immunophenotypic maturation of the leukemia cells (upregulation of CD16 and CD14 B antigens). Further characterization has shown that F-actin is aggregated both in HL-60 cells and in human monocytes exposed to 10−7 mol/L jaspamide. Well-spread cultured human monocytes contracted and adopted round shapes after treatment with jaspamide. Moreover, a dose-dependent increase in both total actin and de novo synthesized portions of the soluble actin was observed in jaspamide-treated HL-60 cells. Jaspamide treatment inhibits ruffling and intracellular movement in HL-60 cells and monocytes, but does not affect phagocytic activity or respiratory burst activity. The consequential effects of jaspamide-induced actin reorganization on ruffling, versus its negligible effect on phagocytosis and oxidative burst, may shed light on molecular mechanisms of actin involvement in these processes. Jaspamide disrupts the actin cytoskeleton of normal and malignant mammalian cells with no significant effect on phagocytic activity and may, therefore, be considered as a novel therapeutic agent.

scholarly journals Ghrelin inhibits leptin- and activation-induced proinflammatory cytokine expression by human monocytes and T cells

2004 ◽  
Vol 114 (1) ◽  
pp. 57-66 ◽  
Author(s):  
Vishwa Deep Dixit ◽  
Eric M. Schaffer ◽  
Robert S. Pyle ◽  
Gary D. Collins ◽  
Senthil K. Sakthivel ◽  
...  
Keyword(s):  
T Cells ◽  
Proinflammatory Cytokine ◽  
Cytokine Expression ◽  
Human Monocytes ◽  
Proinflammatory Cytokine Expression

Alteration of Actin Organization by Jaspamide Inhibits Ruffling, but not Phagocytosis or Oxidative Burst, in HL-60 Cells and Human Monocytes

Blood ◽  
1999 ◽  
Vol 93 (11) ◽  
pp. 3994-4005
Author(s):  
Ina Fabian ◽  
Drora Halperin ◽  
Smadar Lefter ◽  
Leonid Mittelman ◽  
Rom T. Altstock ◽  
...  
Keyword(s):  
Oxidative Burst ◽  
Phagocytic Activity ◽  
Mammalian Cells ◽  
Molecular Mechanisms ◽  
Cyclic Peptide ◽  
De Novo ◽  
Human Monocytes ◽  
Actin Organization ◽  
Fibrous Network ◽  
Intracellular Movement

Jaspamide, a naturally occurring cyclic peptide isolated from the marine sponge Hemiastrella minor, has fungicidal and growth-inhibiting activities. Exposure of promyelocytic HL-60 cells and human monocytes to jaspamide induces a dramatic reorganization of actin from a typical fibrous network to focal aggregates. HL-60 cells exposed to 5 × 10−8 mol/L or 10−7 mol/L jaspamide exhibited a reduced proliferation rate. In addition, 10−7mol/L jaspamide induced maturation of HL-60 cells as indicated by the appearance of a lobulated nucleus in 55% ± 5% of the cells and immunophenotypic maturation of the leukemia cells (upregulation of CD16 and CD14 B antigens). Further characterization has shown that F-actin is aggregated both in HL-60 cells and in human monocytes exposed to 10−7 mol/L jaspamide. Well-spread cultured human monocytes contracted and adopted round shapes after treatment with jaspamide. Moreover, a dose-dependent increase in both total actin and de novo synthesized portions of the soluble actin was observed in jaspamide-treated HL-60 cells. Jaspamide treatment inhibits ruffling and intracellular movement in HL-60 cells and monocytes, but does not affect phagocytic activity or respiratory burst activity. The consequential effects of jaspamide-induced actin reorganization on ruffling, versus its negligible effect on phagocytosis and oxidative burst, may shed light on molecular mechanisms of actin involvement in these processes. Jaspamide disrupts the actin cytoskeleton of normal and malignant mammalian cells with no significant effect on phagocytic activity and may, therefore, be considered as a novel therapeutic agent.

Molecular Mechanisms of Apoptosis Induced by an Immunomodulating Peptide on Human Monocytes

2000 ◽  
Vol 379 (2) ◽  
pp. 353-362 ◽  
Author(s):  
Juan A. Osés-Prieto ◽  
Natalia López-Moratalla ◽  
Esteban Santiago ◽  
Jean P. Jaffrézou ◽  
Maria J. López-Zabalza
Keyword(s):  
Molecular Mechanisms ◽  
Human Monocytes ◽  
Immunomodulating Peptide

Abstract 15252: Ischemic-Trained Monocytes Improve Arteriogenesis During Hindlimb Ischemia

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Gustavo Falero-Diaz ◽  
Catarina d Barboza ◽  
Felipe Pires ◽  
Roberto I Vazquez-Padron ◽  
Omaida C Velazquez ◽  
...  
Keyword(s):  
Blood Flow ◽  
Molecular Mechanisms ◽  
Ischemia Reperfusion ◽  
Local Effect ◽  
Human Monocytes ◽  
Hindlimb Ischemia ◽  
Artery Ligation ◽  
Trained Immunity ◽  
Major Player ◽  
Before And After

Introduction: Recent studies have shown that innate response can build immunological memory. This process called “trained immunity” is an epigenetic reprogramming of the monocytes driven by a metabolism shift towards glycolysis. Hypothesis: Since HIF-1a is a major player in monocytes activation and also targets some epigenetic enzymes, we hypothesize that hypoxia/ischemia can lead to “trained immunity” improving arteriogenesis in a mouse model of hindlimb ischemia. Methods: Mice subjected to a unilateral single ischemia insult for 24hours (24h group: femoral artery ligation for 24 h) or by ischemia reperfusion cycles (Cycle group: ischemia-reperfusion in 4 cycles of 5 minutes) or non-ischemia (sham group), were used as donors in the monocyte transfer experiment. Recipient mice underwent to permanent hindlimb ischemia one day prior the tail vein injection of bone marrow (BM) monocytes from the ischemic leg. Laser Doppler assessed blood flow recovery before and after hindlimb ischemia. Arteriogenesis was quantified on recipient mice by assessing the diameter of gracilis collaterals. A 24h group monocytes from ischemia and non-ischemia leg was used as donors to test the systemic vs. local effect of the ischemic-trained monocytes. Lin- cells were used as a control. Cultured human monocytes were subjected to 24h hypoxia and gene expression for epigenetic enzymes was performed by real time rt-PCR Results: Blood flow recovery in recipients who received ischemic-trained monocytes (24h and cycle) improved overtime compared to sham. Arteriogenesis was significant greater in 24h group compared to sham. Surprisingly, the improvement in blood flow recovery was abolished using combined monocytes from ischemic and non-sichemic, suggesting that ischemia training has a local effect in the monocytes. The Lin- experiment confirmed that the ischemia training is monocyte specific. Moreover, hypoxia regulated epigenetic enzymes responsible for histones methylation in human monocytes. Conclusions: Monocytes can be trained by previous ischemia/hypoxia insult and improve arteriogenesis during hindlimb ischemia. The molecular mechanisms that lead the trained immunity by hypoxia still unknown, however epigenetic modifications might play a role in this process.

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