TGF-β reduced binding of high-density lipoproteins in murine macrophages and macrophage-derived foam cells

Zuckerman, Steven H.; Panousis, Constantinos G.; Evans, Glenn F.

doi:10.1016/s0021-9150(00)00540-2

Cited by 21 publications

(13 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Conversely, we did observe an increase in the expression of the anti-inflammatory cytokine TGF-␤1. This antiinflammatory cytokine has been reported to down-regulate the expression of scavenger receptors and to hamper phagocytic function (2,59) and thus is consistent with the scavenger receptor gene expression observed here and with the persistence of PrP Sc in the spleen. Thus, the present data suggest that PrP Sc accumulation in the spleen down-regulates macrophage responses, and they provide in vivo evidence that PrP Sc is not inherently proinflammatory.…”

Section: Discussionsupporting

confidence: 88%

“…For absolute quantification of the SAA, ␣ 2 -AP, C3, and PTX3 transcripts, standard curves were made from in vitro transcripts of each gene, as previously optimized in our laboratory and described elsewhere (59). Acute-phase protein mRNA levels were thus expressed as numbers of copies per nanogram of total RNA (as determined by normalization with GAPDH).…”

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

Comparison of Inflammatory and Acute-Phase Responses in the Brain and Peripheral Organs of the ME7 Model of Prion Disease

Cunningham¹,

Wilcockson²,

Boche³

et al. 2005

J Virol

View full text Add to dashboard Cite

Chronic neurodegenerative diseases such as prion disease and Alzheimer's disease (AD) are reported to be associated with microglial activation and increased brain and serum cytokines and acute-phase proteins (APPs). Unlike AD, prion disease is also associated with a peripheral component in that the presumed causative agent, PrP Sc , also accumulates in the spleen and other lymphoreticular organs. It is unclear whether the reported systemic acute-phase response represents a systemic inflammatory response to prion disease or merely reflects central nervous system (CNS) inflammation. For this study, we investigated whether intracerebrally initiated prion disease (ME7 model) provokes splenic, hepatic, or brain inflammatory and acute-phase responses. We detected no significant elevation of proinflammatory cytokines or activation of macrophages in the spleens of these animals, despite clear PrP Sc deposition. Similarly, at 19 weeks we detected no significant elevation of transcripts for the APPs serum amyloid A, complement C3, pentraxin 3, and ␣ 2 -antiplasmin in the liver, despite CNS neurodegeneration and splenic PrP Sc deposition at this time. However, despite the low CNS expression levels of proinflammatory cytokines, there was robust expression of these APPs in degenerating brains. These findings suggest that PrP Sc is not a stimulus for splenic macrophages and that neither peripheral PrP Sc deposition nor CNS neurodegeneration is sufficient to produce a systemic acute-phase response. We also propose that serum cytokine and APP measurements are not useful during preclinical disease. Possible consequences of the clear chronic elevation of APPs in the CNS are discussed.

show abstract

Section: Discussionsupporting

confidence: 88%

Section: Methodsmentioning

confidence: 99%

Comparison of Inflammatory and Acute-Phase Responses in the Brain and Peripheral Organs of the ME7 Model of Prion Disease

Cunningham¹,

Wilcockson²,

Boche³

et al. 2005

J Virol

View full text Add to dashboard Cite

show abstract

“…41,42 It inhibits proliferation of smooth muscle cells and accelerates their differentiation. 22 Atherosclerosis is considered an inflammatory process, and the endothelial cells from atherosclerotic regions generally exhibit increased expression of adhesion molecules.…”

Section: Discussionmentioning

confidence: 99%

Transforming Growth Factor-β ₁ Modulates Oxidatively Modified LDL–Induced Expression of Adhesion Molecules

Chen

Saldeen

et al. 2001

Circulation Research

View full text Add to dashboard Cite

Abstract-Oxidatively modified LDL (ox-LDL) activates a lectin-like receptor, LOX-1, which results in the expression of adhesion molecules on endothelial surface. We investigated the regulation of the expression of transforming growth factor-␤ 1 (TGF-␤ 1 ) and its receptors by ox-LDL and the functional significance of this interaction with regard to adhesion molecule expression in human coronary artery endothelial cells (HCAECs

show abstract

“…This effect was independent of changes in the expression of SR-BI (111,112). Conversely, TGF-␤1 increased ABCA1 expression and cholesterol efflux (41,105,113), although the binding of HDL was decreased by this cytokine (85). Cytokines have many effects on macrophages with regard to intracellular cholesterol metabolism and its consequences on sterol efflux.…”

Section: Cytokine Regulation Of Intracellular Lipid Distribution and mentioning

confidence: 99%

“…The expression of CD36 on macrophages is increased by IL-4 and M-CSF (80,81). The effects of IFN-␥ and TGF-␤ on CD36 expression in macrophages have been inconsistent (81)(82)(83)(84)(85).…”

Section: Cytokine Regulation Of Lipoprotein Entry Into Macrophagesmentioning

confidence: 99%

Thematic review series: The Immune System and Atherogenesis. Cytokine regulation of macrophage functions in atherogenesis

Daugherty

Webb

Rateri

et al. 2005

Journal of Lipid Research

View full text Add to dashboard Cite

This review will focus on the role of cytokines in the behavior of macrophages, a prominent cell type of atherosclerotic lesions. Once these macrophages have immigrated into the vessel wall, they propagate the development of atherosclerosis by modifying lipoproteins, accumulating intracellular lipids, remodeling the extracellular environment, and promoting local coagulation. The numerous cytokines that have been detected in atherosclerosis, combined with the expression of large numbers of cytokine receptors on macrophages, are consistent with this axis being an important contributor to lesion development. Given the vast literature on cytokine-macrophage interactions, this review will be selective, with an emphasis on the major cytokines that have been detected in atherosclerotic lesions and their effects on properties that are relevant to lesion formation and maturation. There will be an emphasis on the role of cytokines in regulating lipid metabolism by macrophages. We will provide an overview of the major findings in cell culture and then put these in the context of in vivo studies. As noted in Getz's overview (1), lesions contain large numbers of cytokines that can be derived from several cell types. These cytokines may affect the function of many cell types in atherogenesis. The effects of cytokines on endothelial and smooth muscle cells are discussed in Raines and Ferri's contribution to this series (2). The purpose of this review is to focus on the effects of cytokines on macrophages in the evolution of atherosclerotic lesions. This is a vast literature that has necessitated some selectivity in the areas that can be covered. Given the subject area of this journal, we have elected to focus particular attention on the effect of cytokines on lipid metabolism in macrophages. MACROPHAGE FUNCTIONS IN ATHEROSCLEROTIC LESIONSMacrophages are hypothesized to be attracted to the subendothelial space to remove noxious materials deposited at atherosclerosis-prone regions of arteries. The precise chemical identity of the substance that attracts macrophages has not been unequivocally defined, although many candidate molecules are components of modified lipoproteins (3, 4). However, the function of infiltrating cells becomes subverted and leads to their retention within the subendothelial space. In this region, it is proposed that macrophages modify adjacent lipoproteins while also providing major mechanisms of removal for modified materials from the extracellular environment. The combination of lipoprotein modification and uptake leads to macrophages becoming engorged with lipids and resulting in a morphology that is given the descriptive name of "foam cells." Lipid engorgement causes pronounced cellular hypertrophy, with the cell diameter being Ͼ 10 times that of the originating monocyte. Probably as a result of the immense size increase, lipid-laden macrophages are chronically entrapped in the subendothelial space. Trapped macrophages can then invoke processes that perpetuate the continual recruitment of monoc...

show abstract

TGF-β reduced binding of high-density lipoproteins in murine macrophages and macrophage-derived foam cells

Cited by 21 publications

References 34 publications

Comparison of Inflammatory and Acute-Phase Responses in the Brain and Peripheral Organs of the ME7 Model of Prion Disease

Comparison of Inflammatory and Acute-Phase Responses in the Brain and Peripheral Organs of the ME7 Model of Prion Disease

Transforming Growth Factor-β ₁ Modulates Oxidatively Modified LDL–Induced Expression of Adhesion Molecules

Thematic review series: The Immune System and Atherogenesis. Cytokine regulation of macrophage functions in atherogenesis

Contact Info

Product

Resources

About

TGF-β reduced binding of high-density lipoproteins in murine macrophages and macrophage-derived foam cells

Cited by 21 publications

References 34 publications

Comparison of Inflammatory and Acute-Phase Responses in the Brain and Peripheral Organs of the ME7 Model of Prion Disease

Comparison of Inflammatory and Acute-Phase Responses in the Brain and Peripheral Organs of the ME7 Model of Prion Disease

Transforming Growth Factor-β 1 Modulates Oxidatively Modified LDL–Induced Expression of Adhesion Molecules

Thematic review series: The Immune System and Atherogenesis. Cytokine regulation of macrophage functions in atherogenesis

Contact Info

Product

Resources

About

Transforming Growth Factor-β ₁ Modulates Oxidatively Modified LDL–Induced Expression of Adhesion Molecules