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CELL. A small room in a prison. See Dungeon.

A Law Dictionary, Adapted to the Constitution and Laws of the United States. By John Bouvier. Published 1856.
References in periodicals archive ?
To examine whether TREM-1 is involved in the regulation of TNF-[alpha] and IL-8 production in U937 foam cells, siRNA-mediated silencing of the TREM-1 gene was performed.
We used U937-derived macrophages because these cells are frequently used to develop foam cells after treatment with modified low density protein (Martens et al.
Our group has previously demonstrated that an Asp49 [sPLA.sub.2], named myotoxin-III (MT-III), isolated from Bothrops asper snake venom, activates inflammatory functions of macrophages, including formation of lipid droplets (LDs) and upregulation of perilipin 2 (PLIN2), a scaffold protein involved in LD assembly and macrophage differentiation into foam cells [5-7].
The present study is the first to demonstrate that combination therapy with SGLT2i and DPP-4i prevents macrophage foam cell formation in diabetic db/db mice.
However, accumulation of high levels of cholesteryl ester may lead to the formation of foam cells and, later, to atherogenesis.
Foam cell models derived from macrophages were established 48 h after adding 0.1 mg/1 EGb 761 with or without 40 mg/1 Ox-LDL into an RPMI 1640 medium of macrophages.
The earliest lesions of atherogenesis consist of arterial intimal accumulations of foam cells (primarily lipid-laden macrophages) and T lymphocytes intermixed with smooth muscle cells (7).
To determine whether teneligliptin regulated foam cell formation in macrophages ex vivo, we assessed the effect of teneligliptin on ox-LDL-induced foam cell formation in the peritoneal macrophages of the diabetic db/db mice and monocyte-derived macrophages differentiated by 7-day culture isolated from the T2D patients.
Paraoxonases 1, 2, and 3, oxidative stress, and macrophage foam cell formation during atherosclerosis development.
Although macrophage RCT is a very small part of RCT, the efficiency of cholesterol efflux from cholesterol-loaded macrophages and macrophage-derived foam cells to feces plays a key role in protecting against AS progression [8].
MCP-1 and its receptor play key roles in monocyte recruitment during foam cell and fatty streak formation in atherogenesis.
Liu et al., "Salusin-beta induces foam cell formation and monocyte adhesion in human vascular smooth muscle cells via miR155/NOX2/NFkappaB pathway," Scientific Reports, vol.