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Next, the dynamic surface expression of CXCR4 CXCR7 on migrating monocytes was analyzed.

In response to CXCL12 and MIF but not to MCP-1, surface expression of CXCR7 on migrating monocytes is significantly enhanced as in platelets.

Additionally, MMP-14 has been shown to cluster at the lamellipodia of migrating monocytes, and inhibition of MMP-14 activity (either by neutralizing antibody or gene silencing) retards in vitro monocyte transmigration through activated endothelium.

Though, monocyte chemotactic protein MCP-1 induced a 3-fold higher transmigratory activity than spontaneously migrating monocytes.

Peripheral monocytes are precursors of osteoclasts which migrate towards the bone to differentiate into osteoclasts [ 3– 5].

Monocytes are recruited by chemokine gradients to migrate from circulation into tumour tissues where a further differentiation to TAMs or DCs takes place under the regulation of environmental signals of such as IL-6 [ 27].

The increased expression of CD54 and CD11b on naive monocytes is unlikely to influence chemotaxis as monocytes are triggered when migrating into a wound.

This oxidized LDL (oxLDL) initiates an inflammatory response, in which monocytes are recruited to sites of endothelial dysfunction, migrate into the subendothelial space, and subsequently differentiate into macrophages.

Subsequently, monocytes were placed to the upper wells of a chemotactic chamber (Neuroprobe) and migrated towards chemotactic growth factors which were added to the lower wells of the chamber.

Therefore, it is intriguing that hemozoin-laden monocytes are found only within the microvessel lumen and do not appear to have migrated through or beyond the vessel wall.

Monocytes are the first cells to attach to the endothelium and migrate into the underlying subendothelial space.