Interferon γ–Inducible Protein 10 Selectively Inhibits Proliferation and Induces Apoptosis in Endothelial Cells

2006 ◽  
Vol 13 (1) ◽  
pp. 125-133 ◽  
Author(s):  
Elizabeth D. Feldman ◽  
David M. Weinreich ◽  
Nancy M. Carroll ◽  
Monika L. Burness ◽  
Andrew L. Feldman ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Interferon Γ ◽  
Inducible Protein

Rapid chemokine secretion from endothelial cells originates from 2 distinct compartments

Blood ◽  
2004 ◽  
Vol 104 (2) ◽  
pp. 314-320 ◽  
Author(s):  
Inger Øynebråten ◽  
Oddmund Bakke ◽  
Per Brandtzaeg ◽  
Finn-Eirik Johansen ◽  
Guttorm Haraldsen
Keyword(s):  
Endothelial Cells ◽  
T Cell ◽  
Innate Immune System ◽  
Intracellular Localization ◽  
Interferon Γ ◽  
Innate Immune ◽  
Monocyte Chemoattractant Protein 1 ◽  
Monocyte Chemoattractant ◽  
Rapid Release ◽  
Inducible Protein

Abstract The neutrophil-attracting chemokine interleukin 8 (IL-8) is stored in the Weibel-Palade body (WPB) of endothelial cells (ECs) from which it can be rapidly released after exposure to the secretagogues histamine or thrombin. In this manner, IL-8 may enable rapid recruitment of leukocytes to inflammatory sites. To explore the possible storage of EC-derived chemokines that may attract other subsets of leukocytes, we examined the intracellular localization and secretagogue responsiveness of growth-related oncogene α (GROα), monocyte chemoattractant protein-1 (MCP-1), eotaxin-3, interferon-γ-inducible protein 10 (IP-10), and regulated on activation, normal T-cell expressed and secreted (RANTES). While eotaxin-3, GROα, and MCP-1 were rapidly released from ECs, the release of the T-cell attractors RANTES and IP-10 was not sensitive to the secretagogues. Moreover, of the 3 former chemokines, only eotaxin-3 was stored in WPBs. GROα and MCP-1 resided mainly in smaller vesicles compatible with sorting to a different, histamine-responsive compartment, which has been described in ECs although not reported to contain chemokines. In conclusion, we propose that rapid release of chemokines is restricted to those primarily recruiting leukocytes of the innate immune system, and that their storage in ECs is not restricted to the WPB compartment. (Blood. 2004;104:314-320)

scholarly journals Host interferon-γ inducible protein contributes to Brucella survival

2012 ◽  
Vol 2 ◽  
Author(s):  
Jennifer A. Ritchie ◽  
Adam Rupper ◽  
James A. Cardelli ◽  
Bryan H. Bellaire
Keyword(s):  
Interferon Γ ◽  
Inducible Protein

scholarly journals Endothelial Cells Require STAT3 for Protection against Endotoxin-induced Inf lammation

2003 ◽  
Vol 198 (10) ◽  
pp. 1517-1525 ◽  
Author(s):  
Arihiro Kano ◽  
Michael J. Wolfgang ◽  
Qian Gao ◽  
Joerg Jacoby ◽  
Gui-Xuan Chai ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Transforming Growth Factor ◽  
Endotoxic Shock ◽  
Transforming Growth Factor Β ◽  
Organ Damage ◽  
Interleukin 10 ◽  
Interferon Γ ◽  
Protective Function ◽  
Lps Challenge

Endothelial cells (ECs) are believed to be an important component in the protection from lipopolysaccharide (LPS)-induced endotoxic shock. However, the cellular and molecular mechanism is not well defined. Here, we report that signal transducer and activator of transcription (STAT) 3 is an essential regulator of the antiinflammatory function of ECs in systemic immunity. Because STAT3 deficiency results in early embryonic lethality, we have generated mice with a conditional STAT3 deletion in endothelium (STAT3E−/−). STAT3E−/− mice are healthy and fertile, and isolated ECs initiate normal tube formation in vitro. Conditional endothelial but not organ-specific (i.e., hepatocyte or cardiomyocyte) STAT3 knockout mice show an increased susceptibility to lethality after LPS challenge. The LPS response in STAT3E−/− mice shows exaggerated inflammation and leukocyte infiltration in multiple organs combined with elevated activity of serum alanine aminotransferase and aspartate aminotransferase, indicating organ damage. Concomitantly, proinflammatory cytokines are produced at an exaggerated level and for a prolonged period. This defect cannot be explained by lack of antiinflammatory cytokines, such as interleukin 10 and transforming growth factor β. Instead, we have shown that a soluble activity derived from endothelia and dependent on STAT3 is critical for suppression of interferon γ. These data define STAT3 signaling within endothelia as a critical antiinflammatory mediator and provide new insight to the protective function of ECs in inflammation.

scholarly journals Endogenous CXCL10/Interferon‐γ‐Inducible Protein (IP)‐10 orchestrates myocardial infarct healing

2008 ◽  
Vol 22 (S1) ◽  
Author(s):  
Marcin J. Bujak ◽  
Thorsten Leucker ◽  
Pawel Zymek ◽  
Vikas Veeranna ◽  
Peter Huebener ◽  
...  
Keyword(s):  
Myocardial Infarct ◽  
Interferon Γ ◽  
Infarct Healing ◽  
Inducible Protein
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