|
|
Blood, 1 February 2006, Vol. 107, No. 3, pp. 1178-1183.
Prepublished online as a Blood First Edition Paper on October 13, 2005; DOI 10.1182/blood-2005-07-2692.
 Previous Article | Next Article 
Submitted July 7, 2005
Accepted September 23, 2005
Interaction between integrin  9 1 and vascular cell adhesion molecule-1 (VCAM-1) inhibits neutrophil apoptosis
Ewan A Ross, Mike R Douglas, See Heng Wong, Emma J Ross, S J Curnow, Gerard B Nash, Ed Rainger, Dagmar Scheel-Toellner, Janet M Lord, Mike Salmon, and Christopher D Buckley*
Division of Immunity and Infection, MRC Centre for Immune Regulation, Institute for Biomedical Research, University of Birmingham, Birmingham, United Kingdom
Division of Neurosciences, MRC Centre for Immune Regulation, Institute for Biomedical Research, University of Birmingham, Birmingham, United Kingdom
Division of Medical Sciences, MRC Centre for Immune Regulation, Institute for Biomedical Research, University of Birmingham, Birmingham, United Kingdom
* Corresponding author; email: c.d.buckley{at}bham.ac.uk.
According to the prevailing paradigm neutrophils are short-lived cells that undergo spontaneous apoptosis within 24 hours of their release from the bone marrow. However, neutrophil survival can be significantly prolonged within inflamed tissue by cytokines, inflammatory mediators and hypoxia. During screening experiments aimed at identifying the effect of the adhesive microenvironment on neutrophil survival, we found that VCAM-1 (CD106) was able to delay both spontaneous and Fas-induced apoptosis. VCAM-1 mediated survival was as efficient as that induced by the cytokine IFN- and provided an additive, increased delay in apoptosis when given in combination with IFN-. VCAM-1 delivered its anti-apoptotic effect through binding the integrin  91. The 91 signaling pathway shares significant features with the IFN- survival signaling pathway; requiring PI3 Kinase, NF- B activation as well as de novo protein synthesis, but the kinetics of NF-B activation by VCAM-1 were slower and more sustained compared to IFN-. This study demonstrates a novel functional role for 91 in neutrophil biology and suggests that adhesive signaling pathways provides an important extrinsic checkpoint for the resolution of inflammatory responses in tissues
 CiteULike  Connotea  Del.icio.us  Digg  Reddit  Technorati What's this?
This article has been cited by other articles:
|
|
|
|
 
X. Wu, R. Guo, P. Chen, Q. Wang, and P. N. Cunningham
TNF induces caspase-dependent inflammation in renal endothelial cells through a Rho- and myosin light chain kinase-dependent mechanism
Am J Physiol Renal Physiol,
August 1, 2009;
297(2):
F316 - F326.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
S. K. Gupta and N. E. Vlahakis
Integrin {alpha}9{beta}1 mediates enhanced cell migration through nitric oxide synthase activity regulated by Src tyrosine kinase
J. Cell Sci.,
June 15, 2009;
122(12):
2043 - 2054.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
A. Planaguma, S. Kazani, G. Marigowda, O. Haworth, T. J. Mariani, E. Israel, E. R. Bleecker, D. Curran-Everett, S. C. Erzurum, W. J. Calhoun, et al.
Airway Lipoxin A4 Generation and Lipoxin A4 Receptor Expression Are Decreased in Severe Asthma
Am. J. Respir. Crit. Care Med.,
September 15, 2008;
178(6):
574 - 582.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
E. Pluskota, D. A. Soloviev, D. Szpak, C. Weber, and E. F. Plow
Neutrophil Apoptosis: Selective Regulation by Different Ligands of Integrin {alpha}M{beta}2
J. Immunol.,
September 1, 2008;
181(5):
3609 - 3619.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
