Pressure Modulates Monocyte Migration

Abstract

Migration of monocytes into the subendothelial space of the aorta has been considered to be an important event in the development of atherosclerosis. Because hypertension is commonly associated with atherosclerosis, we studied the effect of applied pressure on the migration of monocytes. Direct applied pressure increased the migration (P < .001) of monocytes across a filter when compared with normal atmospheric pressure. The migration of monocytes was found to be directly related to the amount of the applied pressure. Amlodipine, a calcium channel blocker, attenuated the migration of monocytes under normal as well as increased pressure conditions in a dose-dependent manner. These studies provide a basis to speculate on the role of direct pressure in the migration of monocytes into the subendothelial space and the possibility that vasoactive agents may modulate the migration of monocytes independent of their pressure-lowering effect.

Effects of efonidipine on platelet and monocyte activation markers in hypertensive patients with and without type 2 diabetes mellitus

“…[44][45][46] Activated platelets stimulate the production of monocyte chemotactic protein-1 by monocytes through enhanced chemokine secretion and direct platelet-monocyte contact, which is mediated by expression of P-selection on the platelet surface. 47 Such a mechanism leading to enhanced expression of monocyte chemotactic protein-1 in leukocytes has recently been found in acute myocardial infarction patients.…”

Propofol inhibits pressure-stimulated macrophage phagocytosis via the GABAA receptor and dysregulation of p130cas phosphorylation

“…Recent reports suggest that mechanical stimuli, such as extracellular pressure and repetitive strain, may alter other aspects of macrophage functions (25,34). Pressure (40 -130 mmHg) increases monocyte migration in a dose-dependent manner and enhances scavenger receptor expression in macrophages (44,55); increased pressure (40 -90 mmHg) has been shown to increase aggregated IgG uptake in mouse macrophage J774.16 cells (34), and extracellular pressure modulates the release of proinflammatory cytokines from human monocytic cells (50). Mechanical strain augments matrix metalloproteinase (MMP)-1 and MMP-3, but not MMP-9, expression in PMA-treated human monocytes or macrophages (63).…”

The effect of cyclic pressure on human monocyte-derived macrophages in vitro

“…There has been increasing interest in the effect of cyclic mechanical strain on cells in the skeleton, with several methods of investigation being described 18,29,30 and fluid flow has also been postulated as an important mechanism in other types of cell including osteoblasts. 31,32 Various methods have also been used to investigate the effect of changes in pressure on cells, 16,20,21 but there have been few investigations of the effect of changes in cyclic pressure. KleinNulend et al 17 showed that cyclic pressure influenced the metabolism of chondrocytes in an organ culture; the pressure was applied using a pump from a storage vessel.…”

“…This prevented the strain effect which was found to cause detectable changes in chondrocytes with the system of Wright et al 16 They found that chondrocytes failed to respond to the levels of cyclic pressure applied in these experiments in the absence of strain. Mattana et al 19 and Singhal et al 20 have made several studies of the effect of applied pressure on macrophages. They showed that small applied pressures resulted in increases in uptake of IgG by macrophage-like cells but that cyclic strain caused a decrease.…”

“…15 Studies on chondrocytes and osteoblasts have shown that physical factors can cause changes in cellular function and it has been suggested that macrophages elsewhere in the body respond to physical stimuli. [16][17][18][19][20] Mattana et al 18,19 have found that strain and pressure have opposing effects on the uptake of the IgG complex. We have examined whether cyclic pressure could cause activation of human macrophages in vitro.…”