Netrin-1 inhibits leukocyte migration in vitro and in vivo Export

@article{citeulike:1631864, abstract = {Cell migration plays important roles in embryonic development and inflammation, and this process is highly regulated to ensure tissue homeostasis. A number of barriers exist to prevent the inappropriate migration of leukocytes into healthy peripheral tissues, including retention of these cells in the inactive state and maintenance of the integrity and charge of the vascular endothelium. However, active signals also are likely to exist that can repulse cells or abolish existing cell migration. One such paradigm exists in the developing nervous system, where neuronal migration is mediated by a balance between chemoattractive and chemorepulsive signals. The ability of the guidance molecule netrin-1 to repulse or abolish attraction of neuronal cells expressing the UNC5b receptor makes it an attractive candidate for the regulation of inflammatory cell migration. Here, we show that netrin-1 is expressed on vascular endothelium, where it is regulated by infection and inflammatory cytokines. The netrin-1 receptor UNC5b is strongly expressed by leukocytes, upon which netrin-1 acts as a potent inhibitor of migration to different chemotactic stimuli both in vivo and in vitro. These data suggest that endothelial expression of netrin-1 may inhibit basal cell migration into tissues and that its down-regulation with the onset of sepsis/inflammation may facilitate leukocyte recruitment. 10.1073/pnas.0506233102}, author = {Ly, Ngoc P. and Komatsuzaki, Katsumi and Fraser, Iain P. and Tseng, Anita A. and Prodhan, Parthak and Moore, Kathryn J. and Kinane, Bernard T.}, citeulike-article-id = {1631864}, citeulike-linkout-0 = {http://dx.doi.org/10.1073/pnas.0506233102}, citeulike-linkout-1 = {http://www.pnas.org/cgi/content/abstract/102/41/14729}, citeulike-linkout-2 = {http://view.ncbi.nlm.nih.gov/pubmed/16203981}, citeulike-linkout-3 = {http://www.hubmed.org/display.cgi?uids=16203981}, day = {11}, doi = {10.1073/pnas.0506233102}, journal = {Proceedings of the National Academy of Sciences}, keywords = {gene, ntn1}, month = {October}, number = {41}, pages = {14729--14734}, posted-at = {2007-09-07 15:47:47}, priority = {2}, title = {Netrin-1 inhibits leukocyte migration in vitro and in vivo}, url = {http://dx.doi.org/10.1073/pnas.0506233102}, volume = {102}, year = {2005} }

TY - JOUR ID - citeulike:1631864 L3 - citeulike-article-id:1631864 N2 - Cell migration plays important roles in embryonic development and inflammation, and this process is highly regulated to ensure tissue homeostasis. A number of barriers exist to prevent the inappropriate migration of leukocytes into healthy peripheral tissues, including retention of these cells in the inactive state and maintenance of the integrity and charge of the vascular endothelium. However, active signals also are likely to exist that can repulse cells or abolish existing cell migration. One such paradigm exists in the developing nervous system, where neuronal migration is mediated by a balance between chemoattractive and chemorepulsive signals. The ability of the guidance molecule netrin-1 to repulse or abolish attraction of neuronal cells expressing the UNC5b receptor makes it an attractive candidate for the regulation of inflammatory cell migration. Here, we show that netrin-1 is expressed on vascular endothelium, where it is regulated by infection and inflammatory cytokines. The netrin-1 receptor UNC5b is strongly expressed by leukocytes, upon which netrin-1 acts as a potent inhibitor of migration to different chemotactic stimuli both in vivo and in vitro. These data suggest that endothelial expression of netrin-1 may inhibit basal cell migration into tissues and that its down-regulation with the onset of sepsis/inflammation may facilitate leukocyte recruitment. 10.1073/pnas.0506233102 IS - 41 JF - Proceedings of the National Academy of Sciences EP - 14734 TI - Netrin-1 inhibits leukocyte migration in vitro and in vivo VL - 102 SP - 14729 KW - gene KW - ntn1 AU - Ly, Ngoc AU - Komatsuzaki, Katsumi AU - Fraser, Iain AU - Tseng, Anita AU - Prodhan, Parthak AU - Moore, Kathryn AU - Kinane, Bernard PY - 2005/10/11/ UR - http://dx.doi.org/10.1073/pnas.0506233102 ER -