The phenotype of macrophages which are not transformed into foam cells in atherogenesis

Нагорнев, В. А.; Мальцева, С.В.

doi:10.1016/0021-9150(95)05726-9

Cited by 9 publications

(6 citation statements)

References 5 publications

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“…Interestingly, low uptake of modified LDL by HARM cells is associated with increased TNF-␣ release in response to hypoxia. A similar phenotype (macrophages that are not transformed into foam cells) has been observed in human atherosclerotic lesions (14). The production of IL-1␣, IL-1␤, and TNF-␣ was associated only with the macrophages that were not transformed into foam cells.…”

Section: Discussionmentioning

confidence: 52%

“…Previous studies have shown that heterogeneous populations of macrophages are recruited to inflammatory sites (14,18). A small population of macrophages that are not transformed into foam cells is observed in atherosclerotic lesions (14). Additionally, Tidball and St. Pierre (18) demonstrated that ED1 or ED2 antigen-expressing macrophages are specifically recruited to muscle inflammatory sites and cleared through apoptosis during the resolution of inflammation.…”

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Inflammatory mediators are perpetuated in macrophages resistant to apoptosis induced by hypoxia

Yun

McCormick

Villabona

et al. 1997

Proc. Natl. Acad. Sci. U.S.A.

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A hypoxic͞anoxic microenvironment has been proposed to exist within a vascular lesion due to intimal or medial cell proliferation in vascular diseases. Here, we examined whether hypoxia alters macrophage function by exposing murine macrophage-like RAW 264.7 (RAW) cells to hypoxia (2% O 2 ). When cells were exposed to hypoxia, a significant number of RAW cells underwent apoptosis. Additionally, small subpopulations of RAW cells were resistant to hypoxia-induced apoptosis. Through repeated cycles of hypoxia exposure, hypoxia-induced apoptosis-resistant macrophages (HARMs) were selected; HARM cells demonstrate >70% resistance to hypoxia-induced apoptosis, as compared with the parental RAW cells. When heat shock protein (HSP) expression was examined after hypoxia, we observed a significant decrease in constitutive heat shock protein 70 (HSC 70) in RAW cells, but not in HARMs, as compared with the control normoxic condition (21% O 2 ). In contrast, the expression level of glucose-regulated protein 78 (GRP 78) in RAW and HARM cells after hypoxia treatment was not altered, suggesting that HSC 70 and not GRP 78 may play a role in protection against hypoxia-induced apoptosis. When tumor necrosis factor ␣ (TNF-␣) production was examined after hypoxic treatment, a significant increase in TNF-␣ production in HARM but decrease in RAW was observed, as compared with cells cultured in normoxic conditions. HARM cells also exhibit a much lower level of modified-LDL uptake than do RAW cells, suggesting that HARMs may not transform into foam cells. These results suggest that a selective population of macrophages may adapt to potentially pathological hypoxic conditions by overcoming the apoptotic signal.

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Section: Discussionmentioning

confidence: 52%

Section: Discussionmentioning

confidence: 99%

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Inflammatory mediators are perpetuated in macrophages resistant to apoptosis induced by hypoxia

Yun

McCormick

Villabona

et al. 1997

Proc. Natl. Acad. Sci. U.S.A.

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“…The role of this subpopulation in atherogenesis is not clear. It might, however, correspond to a macrophage subset identified by Nagornev and Maltesva in both the superficial and deep layers of human plaques [43]. These cells are devoid of lipid vacuoles and apparently do not form foam cells.…”

Section: Discussionmentioning

confidence: 99%

Apoptosis induced by oxidized low density lipoprotein in human monocyte‐derived macrophages involves CD36 and activation of caspase‐3

Wintergerst¹,

Jelk²,

Rahner

et al. 2000

European Journal of Biochemistry

102

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Macrophage death may play a crucial role in the progression of atherosclerotic lesions. Here we present evidence that CD36 is involved in oxidized LDL (OxLDL)-induced apoptosis in human monocyte-derived macrophages. Anti-CD36 mAb SMO and OKM-5 reduced the number of apoptotic cells in OxLDL-treated macrophages by more than 94%, but they did not block ceramide-triggered apoptosis. Thrombospondin inhibited the induction of apoptosis by OxLDL in a dose-dependent manner with an IC 50 of 10±30 mm. OxLDL did not induce apoptosis in CD36-negative macrophages, demonstrating the essential role of this scavenger receptor in OxLDL-triggered programmed cell death. Neither anti-CD36 Ig nor thrombospondin triggered programmed cell death suggesting that binding to CD36 alone is not sufficient to initiate apoptosis. However, inhibitors of OxLDL-induced apoptosis did not block the uptake of 3 H-labeled OxLDL. In contrast, acetylated LDL and polyinosinic acid, ligands of scavenger receptor A (SRA), inhibited uptake of 3 H-labeled OxLDL by 65 and 49%, respectively, but did not block OxLDL-induced apoptosis, indicating that SRA is not involved in this process. OxLDL also stimulated caspase-3 activity in human macrophages. Activation of caspase-3 was blocked by anti-CD36 Ig and the caspase-3 inhibitor Z-DEVD-FMK. These results suggest that binding of OxLDL to CD36 initiates a yet unknown OxLDL-specific signaling event, which leads to the rapid activation of caspase-3 resulting in apoptosis of human macrophages. Our data demonstrate a novel role for CD36 in macrophage biology with likely consequences for the development of atherosclerotic lesions.

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“…[6] показали, что популяция макрофагов в сосудистой стенке не является однородной. Были выделены и описаны 3 популяции макрофагов, включающихся в атерогенез [7].…”

Section: клинические семинары §unclassified

Macrophages and Their Role in Destabilization of an Atherosclerotic Plaque

2019

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The modern data on structure and the functional activity of macrophages are presented in the review. It is shown that they are the nonhomogeneous cell population. Two of their main subpopulations are presented as M1 and M2 phenotypes which perform opposite functions at inflammation development. The main attention in the review is paid to a role of macrophages in pathogenesis of atherosclerosis and, first, in formation of unstable atherosclerotic plaques which are the cause of the most severe complications of the disease. It is shown that main subpopulations of macrophages play different roles in formation of unstable and stable atherosclerotic plaques. Macrophages of M1 phenotype in the vascular wall carry out pro-atherogenic role and influence destabilization of an atherosclerotic plaque, while M2 macrophages perform atheroprotective function.

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The phenotype of macrophages which are not transformed into foam cells in atherogenesis

Cited by 9 publications

References 5 publications

Inflammatory mediators are perpetuated in macrophages resistant to apoptosis induced by hypoxia

Inflammatory mediators are perpetuated in macrophages resistant to apoptosis induced by hypoxia

Apoptosis induced by oxidized low density lipoprotein in human monocyte‐derived macrophages involves CD36 and activation of caspase‐3

Macrophages and Their Role in Destabilization of an Atherosclerotic Plaque

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