Imhof, B. A. & Aurrand-Lions, M. Adhesion mechanisms regulating the migration of monocytes.
These data point to a role of MMP-14 during transendothelial migration of monocytes and T-cell attraction.
The migration of monocytes in vitro elicited by N-formyl-methionyl-leucyl-phenylalanine was potently inhibited by fasudil and its active metabolite, hydroxyfasudil.
The material eluted from Sepharose-bound anti-p15E antibodies was devoid of chemotactic and polarizing activity and suppressed the polarization and migration of monocytes in response to chemoattractants.
Moreover, the unchanged levels of Erk1/2, JNK, and p38 did not provide the molecular basis for the adhesion and migration of monocytes [46].
IL-8/CXCL8 is a proinflammatory cytokine that is produced by endothelial cells, monocytes, and vascular smooth muscle cells, and plays an important role in the migration of monocytes into the subendothelial space[30].
They secrete cytokines that act on the bone marrow to stimulate the production of monocytes and neutrophils, and they secrete some of the cytokines that are responsible for the migration of monocytes and neutrophils out of the bloodstream.
The lack of FLNa not only disrupts receptor internalization but also the migration of monocytes on a chemokine gradient.
It was hypothesized that these treatments ultimately affect migration of monocytes and/or retention of macrophages [21].
Endometrial CD14+ cells may themselves promote migration of monocytes and other leukocytes into the endometrium as indicated by upregulation of CXCL14 and chemokines CCL8, CCL22 and CCL24.
It is well known that MCP-1 promotes migration of monocytes [26] and this mechanism has also been proposed for bladder inflammation [27].
