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© Research
Publication : Journal of leukocyte biology

RhoA activation promotes transendothelial migration of monocytes via ROCK

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in Journal of leukocyte biology - 21 Nov 2003

Honing H, van den Berg TK, van der Pol SM, Dijkstra CD, van der Kammen RA, Collard JG, de Vries HE

Link to Pubmed [PMID] – 14634067

J. Leukoc. Biol. 2004 Mar;75(3):523-8

Monocyte infiltration into inflamed tissue requires the initial arrest of the cells on the endothelium followed by firm adhesion and their subsequent migration. Migration of monocytes and other leukocytes is believed to involve a coordinated remodeling of the actin cytoskeleton. The small GTPases RhoA, Rac1, and Cdc42 are critical regulators of actin reorganization. In this study, we have investigated the role of Rho-like GTPases RhoA, Rac1, and Cdc42 in the adhesion and migration of monocytes across brain endothelial cells by expressing their constitutively active or dominant-negative constructs in NR8383 rat monocytic cells. Monocytes expressing the active form of Cdc42 show a reduced migration, whereas Rac1 expression did not affect adhesion or migration. In contrast, expression of the active form of RhoA in monocytes leads to a dramatic increase in their adhesion and migration across endothelial cells. The effect of RhoA was found to be mediated by its down-stream effector Rho kinase (ROCK), as pretreatment with the selective ROCK inhibitor Y-27632 prevented this enhanced adhesion and migration. These results demonstrate that RhoA activation in monocytes is sufficient to enhance adhesion and migration across monolayers of endothelial cells.

https://www.ncbi.nlm.nih.gov/pubmed/14634067