Apolipoprotein E restricts interleukin-dependent T lymphocyte proliferation at the G1A/G1B boundary

Mistry, Meenakshi J.; Clay, Moira A.; Kelly, Michael E.; Steiner, Meredith A.; Harmony, Judith A.K.

doi:10.1016/0008-8749(95)80004-3

Cited by 57 publications

(33 citation statements)

References 59 publications

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“…For example, the suppressive effect of apoE on steroidogenesis in adrenals and ovaries is mediated through inhibition of cyclic AMP signaling mechanisms (47)(48)(49). In contrast, apoE has no effect on cyclic AMP pathway in lymphocytes, but its inhibition of lymphocyte proliferation was shown to be mediated by suppression of other early cell signaling events that lead to cell arrest at the G1a/G1b boundary (55)(56)(57). The mechanism for apoE inhibition of smooth muscle cell proliferation and migration reported herein is different from the apoE effect on lymphocyte proliferation.…”

Section: Figcontrasting

confidence: 42%

Apolipoprotein E Inhibits Platelet-derived Growth Factor-induced Vascular Smooth Muscle Cell Migration and Proliferation by Suppressing Signal Transduction and Preventing Cell Entry to G1 Phase

Ishigami

Swertfeger

Granholm

et al. 1998

Journal of Biological Chemistry

132

110

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The anti-atherogenic effects of apolipoprotein (apo) E have been attributed to its ability to reduce plasma cholesterol level and to limit foam cell formation. The purpose of this study was to ascertain if apoE also may have cytostatic functions that could attenuate vascular occlusive diseases. Purified apoE inhibited smooth muscle cell migration directed to platelet-derived growth factor (PDGF) or oxidized LDL (oxLDL) (p < 0.0001). The purified apoE also suppressed PDGF-and oxLDL-induced smooth muscle cell proliferation (p < 0.001). These apoE inhibitory effects were not because of suppression of PDGF binding to its receptors on the smooth muscle cells, but was correlated with a significant reduction in agonist-stimulated mitogen-activated protein kinase activity (p < 0.01). ApoE also inhibited PDGF-induced cyclin D1 mRNA expression, suggesting that the apoE effect was mediated by growth arrest at the G 0 to G 1 phase. Taken together, these results suggest that apoE has cytostatic functions in the vessel wall and may protect against vascular diseases through inhibition of cell signaling events associated with growth factor-induced smooth muscle cell migration and proliferation.

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Section: Figcontrasting

confidence: 42%

Apolipoprotein E Inhibits Platelet-derived Growth Factor-induced Vascular Smooth Muscle Cell Migration and Proliferation by Suppressing Signal Transduction and Preventing Cell Entry to G1 Phase

Ishigami

Swertfeger

Granholm

et al. 1998

Journal of Biological Chemistry

132

110

View full text Add to dashboard Cite

show abstract

“…These include the role of ApoE in lipid metabolism (as described above), intracellular lipid redistribution (281,448), atherogenesis (75, 463, 549), neurobiology (nerve regeneration, association of the ApoE4 serotype with neuropathologic lesions in Alzheimer's disease) (342,580), and immunomodulation (inhibition of proliferation of peripheral blood mononuclear cells and lymphocyte activation; inhibition of TNF secretion by glial cells) (20,228,299,364,399,417).…”

Section: Apolipoprotein Ementioning

confidence: 99%

Receptors, Mediators, and Mechanisms Involved in Bacterial Sepsis and Septic Shock

2003

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Bacterial sepsis and septic shock result from the overproduction of inflammatory mediators as a consequence of the interaction of the immune system with bacteria and bacterial wall constituents in the body. Bacterial cell wall constituents such as lipopolysaccharide, peptidoglycans, and lipoteichoic acid are particularly responsible for the deleterious effects of bacteria. These constituents interact in the body with a large number of proteins and receptors, and this interaction determines the eventual inflammatory effect of the compounds. Within the circulation bacterial constituents interact with proteins such as plasma lipoproteins and lipopolysaccharide binding protein. The interaction of the bacterial constituents with receptors on the surface of mononuclear cells is mainly responsible for the induction of proinflammatory mediators by the bacterial constituents. The role of individual receptors such as the toll-like receptors and CD14 in the induction of proinflammatory cytokines and adhesion molecules is discussed in detail. In addition, the roles of a number of other receptors that bind bacterial compounds such as scavenger receptors and their modulating role in inflammation are described. Finally, the therapies for the treatment of bacterial sepsis and septic shock are discussed in relation to the action of the aforementioned receptors and proteins

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“…[49][50][51][52][53][54][55][56][57][58][59] Cancer breast, prostate, colorectal, lung, endometrial cancers, etc. [10,11] Cardiovascular diseases atherosclerosis, coronary heart disease, congestive heart failure, hypertension, diabetes, etc.…”

Section: Functionsmentioning

confidence: 99%

“…Interestingly, apolipoprotein E (apoE), a plasma protein closely associated with a variety of human diseases including Alzheimer's disease [47] , MS [48] , etc., resembles vitamin D in many aspects regarding the immunomodulatory roles [49,50] .…”

Section: Functionsmentioning

confidence: 99%

维生素d 在免疫反应和自身免疫性疾病特别是多发性硬化中的作用

Zhang

2010

Neurosci. Bull.

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Apolipoprotein E restricts interleukin-dependent T lymphocyte proliferation at the G1A/G1B boundary

Cited by 57 publications

References 59 publications

Apolipoprotein E Inhibits Platelet-derived Growth Factor-induced Vascular Smooth Muscle Cell Migration and Proliferation by Suppressing Signal Transduction and Preventing Cell Entry to G1 Phase

Apolipoprotein E Inhibits Platelet-derived Growth Factor-induced Vascular Smooth Muscle Cell Migration and Proliferation by Suppressing Signal Transduction and Preventing Cell Entry to G1 Phase

Receptors, Mediators, and Mechanisms Involved in Bacterial Sepsis and Septic Shock

维生素d 在免疫反应和自身免疫性疾病特别是多发性硬化中的作用

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