JAM-A mediates neutrophil transmigration in a stimulus-specific manner in vivo: evidence for sequential roles for JAM-A and PECAM-1 in neutrophil transmigration.
JAM-A mediates neutrophil transmigration in a stimulus-specific manner in vivo: evidence for sequential roles for JAM-A and PECAM-1 in neutrophil transmigration.
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JAM-A 在体内以刺激特异性方式介导中性粒细胞迁移：JAM-A 和 PECAM-1 在中性粒细胞迁移中顺序作用的证据。
DOI：
10.1182/blood-2006-09-047431
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发表时间：
2007
期刊：
影响因子：
20.3
通讯作者：
S. Nourshargh
中科院分区：
文献类型：
--
作者：
A. Woodfin;C. Reichel;A. Khandoga;M. Corada;M. Voisin;C. Scheiermann;D. Haskard;E. Dejana;F. Krombach;S. Nourshargh
连接粘附分子-A（Junctional adhesion molecule-A，JAM-A）是一种跨膜蛋白，在内皮细胞和上皮细胞的紧密连接处以及血小板和白细胞的表面上表达。使用JAM-A中和单克隆抗体（mAb）（BV-11）和JAM-A缺陷（敲除[KO]）小鼠，通过活体显微镜直接研究了JAM-A在体内白细胞迁移中的作用。在BV-11处理的野生型小鼠和JAM-A KO动物中，白细胞通过白细胞介素1 β（IL-1 β）或缺血/再灌注（I/R）损伤刺激的小鼠提睾肌小静脉的迁移（但不粘附）显著减少。相反，JAM-A阻断/基因缺失对白三烯B（4）（LTB（4））或血小板活化因子（PAF）引起的反应没有影响。此外，使用白细胞转移方法和内皮细胞JAM-A缺陷的小鼠，获得了内皮细胞JAM-A参与IL-1 β介导的白细胞迁移的证据。对JAM-A和PECAM-1（CD 31）之间的功能关系的研究确定，这些蛋白质的双重阻断/缺失不会导致比单独阻断/缺失任一分子所观察到的抑制作用更大的抑制作用。后者似乎是由于JAM-A和PECAM-1可以依次作用以介导体内白细胞通过微静脉壁的迁移。
Junctional adhesion molecule-A (JAM-A) is a transmembrane protein expressed at tight junctions of endothelial and epithelial cells and on the surface of platelets and leukocytes. The role of JAM-A in leukocyte transmigration in vivo was directly investigated by intravital microscopy using both a JAM-A-neutralizing monoclonal antibody (mAb) (BV-11) and JAM-A-deficient (knockout [KO]) mice. Leukocyte transmigration (but not adhesion) through mouse cremasteric venules as stimulated by interleukin 1beta (IL-1beta) or ischemia/reperfusion (I/R) injury was significantly reduced in wild-type mice treated with BV-11 and in JAM-A KO animals. In contrast, JAM-A blockade/genetic deletion had no effect on responses elicited by leukotriene B(4) (LTB(4)) or platelet-activating factor (PAF). Furthermore, using a leukocyte transfer method and mice deficient in endothelial-cell JAM-A, evidence was obtained for the involvement of endothelial-cell JAM-A in leukocyte transmigration mediated by IL-1beta. Investigation of the functional relationship between JAM-A and PECAM-1 (CD31) determined that dual blockade/deletion of these proteins does not lead to an inhibitory effect greater than that seen with blockade/deletion of either molecule alone. The latter appeared to be due to the fact that JAM-A and PECAM-1 can act sequentially to mediate leukocyte migration through venular walls in vivo.
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影响因子：
20.3
作者：
Khandoga, A;Kessler, JS;Krombach, F
通讯作者：
Krombach, F
DOI：
10.1084/jem.20060565
发表时间：
2006-07-10
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Wegmann F;Petri B;Khandoga AG;Moser C;Khandoga A;Volkery S;Li H;Nasdala I;Brandau O;Fässler R;Butz S;Krombach F;Vestweber D
通讯作者：
Vestweber D
影响因子：
4.4
作者：
Michael Loran Dustin;R. Rothlein;A. Bhan;C. Dinarello;T. Springer
通讯作者：
Michael Loran Dustin;R. Rothlein;A. Bhan;C. Dinarello;T. Springer
影响因子：
4.4
作者：
J. Pober;M. Gimbrone;L. Lapierre;D. Mendrick;W. Fiers;R. Rothlein;T. Springer
通讯作者：
J. Pober;M. Gimbrone;L. Lapierre;D. Mendrick;W. Fiers;R. Rothlein;T. Springer