|
|
Prepublished online as a Blood First Edition Paper on July 25, 2002; DOI 10.1182/blood-2002-01-0303.

Submitted January 31, 2002
Accepted June 30, 2002
Differential movements of VE-cadherin and PECAM-1 during transmigration of polymorphonuclear leukocytes through human umbilical vein endothelium
Wen-Hong Su, Hsiun-ing Chen, and Chauying J Jen*
Institute of Basic Medical Sciences, National Cheng Kung University, Tainan, Taiwan; Department of Physiology, National Cheng Kung University, Tainan, Taiwan
Department of Physiology, National Cheng Kung University, Tainan, Taiwan; Institute of Basic Medical Sciences, National Cheng Kung University, Tainan, Taiwan
* Corresponding author; email: jen{at}mail.ncku.edu.tw.
Most existing evidence regarding junction protein movements during transendothelial migration of leukocytes comes from taking post-fixation snap shots of the transendothelial migration process that happens on a cultured endothelial monolayer. In this study, we used junction protein-specific antibodies that did not interfere the transendothelial migration to examine the real-time movements of vascular endothelial-cadherin (VE-cadherin) and platelet/endothelial cell adhesion molecule-1 (PECAM-1) during transmigration of polymorphonuclear leukocytes (PMNs) either through a cultured endothelial monolayer or through the endothelium of a dissected human umbilical vein tissue. In either experimental model system, both junction proteins showed relative movements, not transient disappearance, at the PMN transmigration sites. VE-cadherin moved away to different ends of the transmigration site, whereas PECAM-1 opened to surround the periphery of a transmigrating PMN. Junction proteins usually moved back to their original positions when the PMN transmigration process was completed in less than 2 min. The relative positions of some junction proteins might rearrange to form a new inter-endothelial contour after PMNs had transmigrated through multi-cellular corners. Although transmigrated PMNs maintained good mobility, they only moved laterally underneath the vascular endothelium instead of deeply into the vascular tissue. In conclusion, our results obtained from using either cultured cells or vascular tissues showed that VE-cadherin-containing adherent junctions were relocated aside, not opened or disrupted, while PECAM-1-containing junctions were opened, during PMN transendothelial migration.

CiteULike Connotea Del.icio.us Digg Reddit Technorati What's this?
This article has been cited by other articles:

|
 |

|
 |
 
A. Rabodzey, P. Alcaide, F. W. Luscinskas, and B. Ladoux
Mechanical Forces Induced by the Transendothelial Migration of Human Neutrophils
Biophys. J.,
August 1, 2008;
95(3):
1428 - 1438.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
D. Vestweber
VE-Cadherin: The Major Endothelial Adhesion Molecule Controlling Cellular Junctions and Blood Vessel Formation
Arterioscler. Thromb. Vasc. Biol.,
February 1, 2008;
28(2):
223 - 232.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
W.-H. Su, H.-i. Chen, and C. J. Jen
Polymorphonuclear leukocyte transverse migration induces rapid alterations in endothelial focal contacts
J. Leukoc. Biol.,
September 1, 2007;
82(3):
542 - 550.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
M. Sircar, P. F. Bradfield, M. Aurrand-Lions, R. J. Fish, P. Alcaide, L. Yang, G. Newton, D. Lamont, S. Sehrawat, T. Mayadas, et al.
Neutrophil Transmigration under Shear Flow Conditions In Vitro Is Junctional Adhesion Molecule-C Independent
J. Immunol.,
May 1, 2007;
178(9):
5879 - 5887.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
N. Kogata, Y. Arai, J. T. Pearson, K. Hashimoto, K. Hidaka, T. Koyama, S. Somekawa, Y. Nakaoka, M. Ogawa, R. H. Adams, et al.
Cardiac Ischemia Activates Vascular Endothelial Cadherin Promoter in Both Preexisting Vascular Cells and Bone Marrow Cells Involved in Neovascularization
Circ. Res.,
April 14, 2006;
98(7):
897 - 904.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
E. Cernuda-Morollon and A. J. Ridley
Rho GTPases and Leukocyte Adhesion Receptor Expression and Function in Endothelial Cells
Circ. Res.,
March 31, 2006;
98(6):
757 - 767.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
A. Soghomonians, T. L. Thirkill, N. F. Mariano, A. I. Barakat, and G. C. Douglas
Effect of Aqueous Tobacco Smoke Extract and Shear Stress on PECAM-1 Expression and Cell Motility in Human Uterine Endothelial Cells
Toxicol. Sci.,
October 1, 2004;
81(2):
408 - 418.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
R. M. Rao, T. V. Betz, D. J. Lamont, M. B. Kim, S. K. Shaw, R. M. Froio, F. Baleux, F. Arenzana-Seisdedos, R. Alon, and F. W. Luscinskas
Elastase Release by Transmigrating Neutrophils Deactivates Endothelial-bound SDF-1{alpha} and Attenuates Subsequent T Lymphocyte Transendothelial Migration
J. Exp. Med.,
September 20, 2004;
200(6):
713 - 724.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
Y. Liu, S. K. Shaw, S. Ma, L. Yang, F. W. Luscinskas, and C. A. Parkos
Regulation of Leukocyte Transmigration: Cell Surface Interactions and Signaling Events
J. Immunol.,
January 1, 2004;
172(1):
7 - 13.
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
B. N. Stein, J. R. Gamble, S. M. Pitson, M. A. Vadas, and Y. Khew-Goodall
Activation of Endothelial Extracellular Signal-Regulated Kinase Is Essential for Neutrophil Transmigration: Potential Involvement of a Soluble Neutrophil Factor in Endothelial Activation
J. Immunol.,
December 1, 2003;
171(11):
6097 - 6104.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
B. Hermant, S. Bibert, E. Concord, B. Dublet, M. Weidenhaupt, T. Vernet, and D. Gulino-Debrac
Identification of Proteases Involved in the Proteolysis of Vascular Endothelium Cadherin during Neutrophil Transmigration
J. Biol. Chem.,
April 11, 2003;
278(16):
14002 - 14012.
[Abstract]
[Full Text]
[PDF]
|
 |
|
| |