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Article ; Online: Human Aldose Reductase Expression Prevents Atherosclerosis Regression in Diabetic Mice.

Yuan, Chujun / Hu, Jiyuan / Parathath, Saj / Grauer, Lisa / Cassella, Courtney Blachford / Bagdasarov, Svetlana / Goldberg, Ira J / Ramasamy, Ravichandran / Fisher, Edward A

Diabetes

2018 Volume 67, Issue 9, Page(s) 1880–1891

Abstract: Guidelines to reduce cardiovascular risk in diabetes include aggressive LDL lowering, but benefits are attenuated compared with those in patients without diabetes. Consistent with this, we have reported in mice that hyperglycemia impaired atherosclerosis ...

Abstract	Guidelines to reduce cardiovascular risk in diabetes include aggressive LDL lowering, but benefits are attenuated compared with those in patients without diabetes. Consistent with this, we have reported in mice that hyperglycemia impaired atherosclerosis regression. Aldose reductase (AR) is thought to contribute to clinical complications of diabetes by directing glucose into pathways producing inflammatory metabolites. Mice have low levels of AR, thus raising them to human levels would be a more clinically relevant model to study changes in diabetes under atherosclerosis regression conditions. Donor aortae from Western diet-fed
MeSH term(s)	Aldehyde Reductase/genetics ; Aldehyde Reductase/metabolism ; Animals ; Aorta/physiopathology ; Aorta/transplantation ; Atherosclerosis/immunology ; Atherosclerosis/metabolism ; Atherosclerosis/pathology ; Atherosclerosis/physiopathology ; Biomarkers/blood ; Biomarkers/metabolism ; Crosses, Genetic ; Diabetic Angiopathies/immunology ; Diabetic Angiopathies/metabolism ; Diabetic Angiopathies/pathology ; Diabetic Angiopathies/physiopathology ; Diet, Western/adverse effects ; Disease Models, Animal ; Disease Progression ; Gene Expression Regulation ; Humans ; Macrophages/immunology ; Macrophages/metabolism ; Macrophages/pathology ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Transgenic ; Oxidative Stress ; Plaque, Atherosclerotic/immunology ; Plaque, Atherosclerotic/metabolism ; Plaque, Atherosclerotic/pathology ; Plaque, Atherosclerotic/physiopathology ; Receptors, LDL/genetics ; Receptors, LDL/metabolism ; Species Specificity
Chemical Substances	Biomarkers ; Receptors, LDL ; Aldehyde Reductase (EC 1.1.1.21)
Language	English
Publishing date	2018-06-11
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	80085-5
ISSN	1939-327X ; 0012-1797
ISSN (online)	1939-327X
ISSN	0012-1797
DOI	10.2337/db18-0156
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Article ; Online: Hypoxia in murine atherosclerotic plaques and its adverse effects on macrophages.

Parathath, Saj / Yang, Yuan / Mick, Stephanie / Fisher, Edward A

Trends in cardiovascular medicine

2013 Volume 23, Issue 3, Page(s) 80–84

Abstract: Hypoxia has been found in the atherosclerotic plaques of larger mammals, including humans. Whether hypoxia occurs in the plaques of standard mouse models with atherosclerosis has been controversial, given their small size. In this review, we summarize ... ...

Abstract	Hypoxia has been found in the atherosclerotic plaques of larger mammals, including humans. Whether hypoxia occurs in the plaques of standard mouse models with atherosclerosis has been controversial, given their small size. In this review, we summarize the findings of a recent report demonstrating that direct evidence of hypoxia can indeed be found in the plaques of mice deficient in apolipoprotein E (apoE-/-mice). Furthermore, studies in vitro showed that hypoxia promoted lipid synthesis and reduced cholesterol efflux through the ABCA1 pathway, and that the transcription factor HIF-1α mediated many, but not all, of the effects. These results are discussed in the context of the literature and clinical practice.
MeSH term(s)	ATP Binding Cassette Transporter 1 ; ATP-Binding Cassette Transporters/metabolism ; Animals ; Apolipoproteins E/deficiency ; Apolipoproteins E/genetics ; Atherosclerosis/genetics ; Atherosclerosis/metabolism ; Atherosclerosis/pathology ; Cholesterol/metabolism ; Disease Models, Animal ; Humans ; Hypoxia/metabolism ; Hypoxia/pathology ; Hypoxia-Inducible Factor 1, alpha Subunit/metabolism ; Macrophages/metabolism ; Macrophages/pathology ; Mice ; Mice, Knockout ; Plaque, Atherosclerotic
Chemical Substances	ABCA1 protein, human ; ATP Binding Cassette Transporter 1 ; ATP-Binding Cassette Transporters ; Apolipoproteins E ; HIF1A protein, human ; Hif1a protein, mouse ; Hypoxia-Inducible Factor 1, alpha Subunit ; Cholesterol (97C5T2UQ7J)
Language	English
Publishing date	2013-02-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	1097434-9
ISSN	1873-2615 ; 1050-1738
ISSN (online)	1873-2615
ISSN	1050-1738
DOI	10.1016/j.tcm.2012.09.004
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Article: Nitric oxide mediates neurodegeneration and breakdown of the blood-brain barrier in tPA-dependent excitotoxic injury in mice.

Parathath, Susana R / Parathath, Saj / Tsirka, Stella E

Journal of cell science

2006 Volume 119, Issue Pt 2, Page(s) 339–349

Abstract: Stroke and many neurodegenerative diseases culminate in neuronal death through a mechanism known as excitotoxicity. Excitotoxicity proceeds through a complex signaling pathway that includes the participation of the serine protease tissue plasminogen ... ...

Abstract	Stroke and many neurodegenerative diseases culminate in neuronal death through a mechanism known as excitotoxicity. Excitotoxicity proceeds through a complex signaling pathway that includes the participation of the serine protease tissue plasminogen activator (tPA). tPA mediates neurotoxic effects on resident central nervous system cells as well alters blood-brain barrier (BBB) permeability, which further promotes neurodegeneration. Another signaling molecule that promotes neurodegeneration and BBB dysfunction is nitric oxide (NO), although its precise role in pathological progression remains unclear. We examine here the potentially interrelated roles of tPA, NO and peroxynitrite (ONOO-), which is the toxic metabolite of NO, in BBB breakdown and neurodegeneration following intrahippocampal injection of the glutamate analog kainite (KA). We find that NO and ONOO- production are linked to tPA-mediated excitotoxic injury, and demonstrate that NO provision suffices to restore the toxic effects of KA in tPA-deficient mice that are normally resistant to excitotoxicity. NO also promotes BBB breakdown and excitotoxicity. Interestingly, BBB breakdown in itself does not suffice to elicit neurodegeneration; a subsequent ONOO(-)-mediated event is required. In conclusion, NO and ONOO- function as downstream effectors of tPA-mediated excitotoxicity.
MeSH term(s)	Animals ; Blood-Brain Barrier/pathology ; Blood-Brain Barrier/physiology ; Excitatory Amino Acid Agonists/metabolism ; Hippocampus/cytology ; Hippocampus/metabolism ; Hippocampus/pathology ; Kainic Acid/administration & dosage ; Kainic Acid/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Neurons/cytology ; Neurons/metabolism ; Neurotoxins/administration & dosage ; Neurotoxins/metabolism ; Nitric Oxide/metabolism ; Nitric Oxide Donors/metabolism ; Nitric Oxide Synthase/antagonists & inhibitors ; Nitric Oxide Synthase/metabolism ; Nitroso Compounds/metabolism ; Peroxynitrous Acid/metabolism ; Signal Transduction/physiology ; Tissue Plasminogen Activator/genetics ; Tissue Plasminogen Activator/metabolism
Chemical Substances	Excitatory Amino Acid Agonists ; NOC 18 ; Neurotoxins ; Nitric Oxide Donors ; Nitroso Compounds ; Peroxynitrous Acid (14691-52-2) ; Nitric Oxide (31C4KY9ESH) ; Nitric Oxide Synthase (EC 1.14.13.39) ; Tissue Plasminogen Activator (EC 3.4.21.68) ; Kainic Acid (SIV03811UC)
Language	English
Publishing date	2006-01-15
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2993-2
ISSN	1477-9137 ; 0021-9533
ISSN (online)	1477-9137
ISSN	0021-9533
DOI	10.1242/jcs.02734
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Article ; Online: Rapid regression of atherosclerosis with MTP inhibitor treatment.

Hewing, Bernd / Parathath, Saj / Mai, Christina K / Fiel, M Isabel / Guo, Liang / Fisher, Edward A

Atherosclerosis

2013 Volume 227, Issue 1, Page(s) 125–129

Abstract: Objective: Regression of atherosclerosis is a vital treatment goal of atherosclerotic vascular disease. Inhibitors of the microsomal triglyceride transfer protein (MTP) have been shown to reduce apolipoprotein B (apoB)-containing lipoproteins in animals ...

Abstract	Objective: Regression of atherosclerosis is a vital treatment goal of atherosclerotic vascular disease. Inhibitors of the microsomal triglyceride transfer protein (MTP) have been shown to reduce apolipoprotein B (apoB)-containing lipoproteins in animals and humans effectively. Therefore, the major aim of our study is to evaluate the effect of MTP inhibition on atherosclerotic plaque regression. Methods: LDL-receptor-deficient (LDLr(-/-)) mice were fed a Western diet for 16 weeks and then harvested for baseline (n = 8), switched to chow diet (n = 8) or chow diet containing MTP inhibitor (BMS 212122; n = 8) for 2 weeks before harvesting. Results: Treatment with MTP inhibitor led to rapid reduction in plasma lipid levels, which were accompanied by a significant decrease in lipid content and monocyte-derived (CD68+) cells in atherosclerotic plaques compared to baseline and chow diet control groups. MTP inhibitor-treated mice had increased collagen content, a marker associated with increased stability in human plaques. Furthermore, plaques of these mice showed a significant decrease in tissue factor and pro-inflammatory M1 macrophage marker monocyte chemoattractant protein-1 (MCP-I) and an increase in anti-inflammatory M2 macrophage markers arginase-I and mannose receptor 1 compared to mice in the baseline group. Conclusion: Reversal of hyperlipidemia in atherosclerotic mice by inhibition of MTP leads to rapid and beneficial changes in the composition and inflammatory state of the plaque.
MeSH term(s)	Animals ; Apolipoproteins B/metabolism ; Atherosclerosis/drug therapy ; Benzimidazoles/therapeutic use ; Carrier Proteins/antagonists & inhibitors ; Fluorenes/therapeutic use ; Mice ; Plaque, Atherosclerotic/drug therapy ; Plaque, Atherosclerotic/pathology
Chemical Substances	9-(4-(2,5-dimethyl-4-(((4'-(trifluoromethyl)(1,1'-biphenyl)-2-yl)carbonyl)amino)-1H-benzimidazol-1-yl)butyl)-N-(2,2,2-trifluoroethyl)-9H-fluorene-9-carboxamide ; Apolipoproteins B ; Benzimidazoles ; Carrier Proteins ; Fluorenes ; microsomal triglyceride transfer protein
Language	English
Publishing date	2013-01-01
Publishing country	Ireland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80061-2
ISSN	1879-1484 ; 0021-9150
ISSN (online)	1879-1484
ISSN	0021-9150
DOI	10.1016/j.atherosclerosis.2012.12.026
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Zs.A 226: Show issues

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Article: Nitric oxide mediates neurodegeneration and breakdown of the blood-brain barrier in tPA-dependent excitotoxic injury in mice

Parathath, Susana R / Parathath, Saj / Tsirka, Stella E

Journal of cell science. 2006 Jan. 15, v. 119, no. 2

2006

Abstract	Stroke and many neurodegenerative diseases culminate in neuronal death through a mechanism known as excitotoxicity. Excitotoxicity proceeds through a complex signaling pathway that includes the participation of the serine protease tissue plasminogen activator (tPA). tPA mediates neurotoxic effects on resident central nervous system cells as well alters blood-brain barrier (BBB) permeability, which further promotes neurodegeneration. Another signaling molecule that promotes neurodegeneration and BBB dysfunction is nitric oxide (NO), although its precise role in pathological progression remains unclear. We examine here the potentially interrelated roles of tPA, NO and peroxynitrite (ONOO⁻), which is the toxic metabolite of NO, in BBB breakdown and neurodegeneration following intrahippocampal injection of the glutamate analog kainite (KA). We find that NO and ONOO⁻ production are linked to tPA-mediated excitotoxic injury, and demonstrate that NO provision suffices to restore the toxic effects of KA in tPA-deficient mice that are normally resistant to excitotoxicity. NO also promotes BBB breakdown and excitotoxicity. Interestingly, BBB breakdown in itself does not suffice to elicit neurodegeneration; a subsequent ONOO⁻-mediated event is required. In conclusion, NO and ONOO⁻ function as downstream effectors of tPA-mediated excitotoxicity.
Language	English
Dates of publication	2006-0115
Size	p. 339-349.
Document type	Article
ZDB-ID	2993-2
ISSN	1477-9137 ; 0021-9533
ISSN (online)	1477-9137
ISSN	0021-9533
Database	NAL-Catalogue (AGRICOLA)

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Article: Rapid regression of atherosclerosis with MTP inhibitor treatment

Hewing, Bernd / Parathath, Saj / Mai, Christina K / Fiel, M. Isabel / Guo, Liang / Fisher, Edward A

Atherosclerosis. 2013 Mar., v. 227, no. 1

2013

Abstract: OBJECTIVE: Regression of atherosclerosis is a vital treatment goal of atherosclerotic vascular disease. Inhibitors of the microsomal triglyceride transfer protein (MTP) have been shown to reduce apolipoprotein B (apoB)-containing lipoproteins in animals ... ...

Abstract	OBJECTIVE: Regression of atherosclerosis is a vital treatment goal of atherosclerotic vascular disease. Inhibitors of the microsomal triglyceride transfer protein (MTP) have been shown to reduce apolipoprotein B (apoB)-containing lipoproteins in animals and humans effectively. Therefore, the major aim of our study is to evaluate the effect of MTP inhibition on atherosclerotic plaque regression. METHODS: LDL-receptor-deficient (LDLr⁻/⁻) mice were fed a Western diet for 16 weeks and then harvested for baseline (n = 8), switched to chow diet (n = 8) or chow diet containing MTP inhibitor (BMS 212122; n = 8) for 2 weeks before harvesting. RESULTS: Treatment with MTP inhibitor led to rapid reduction in plasma lipid levels, which were accompanied by a significant decrease in lipid content and monocyte-derived (CD68+) cells in atherosclerotic plaques compared to baseline and chow diet control groups. MTP inhibitor-treated mice had increased collagen content, a marker associated with increased stability in human plaques. Furthermore, plaques of these mice showed a significant decrease in tissue factor and pro-inflammatory M1 macrophage marker monocyte chemoattractant protein-1 (MCP-I) and an increase in anti-inflammatory M2 macrophage markers arginase-I and mannose receptor 1 compared to mice in the baseline group. CONCLUSION: Reversal of hyperlipidemia in atherosclerotic mice by inhibition of MTP leads to rapid and beneficial changes in the composition and inflammatory state of the plaque.
Keywords	Western diets ; apolipoprotein B ; atherosclerosis ; blood lipids ; chemokines ; collagen ; harvesting ; humans ; hyperlipidemia ; lipid content ; macrophages ; mannose ; mice ; triacylglycerols
Language	English
Dates of publication	2013-03
Size	p. 125-129.
Publishing place	Elsevier Ireland Ltd
Document type	Article
ZDB-ID	80061-2
ISSN	1879-1484 ; 0021-9150
ISSN (online)	1879-1484
ISSN	0021-9150
DOI	10.1016/j.atherosclerosis.2012.12.026
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Article ; Online: Diabetes adversely affects macrophages during atherosclerotic plaque regression in mice.

Parathath, Saj / Grauer, Lisa / Huang, Li-Shin / Sanson, Marie / Distel, Emilie / Goldberg, Ira J / Fisher, Edward A

Diabetes

2011 Volume 60, Issue 6, Page(s) 1759–1769

Abstract: Objective: Patients with diabetes have increased cardiovascular risk. Atherosclerosis in these patients is often associated with increased plaque macrophages and dyslipidemia. We hypothesized that diabetic atherosclerosis involves processes that impair ... ...

Abstract	Objective: Patients with diabetes have increased cardiovascular risk. Atherosclerosis in these patients is often associated with increased plaque macrophages and dyslipidemia. We hypothesized that diabetic atherosclerosis involves processes that impair favorable effects of lipid reduction on plaque macrophages. Research design and methods: Reversa mice are LDL receptor-deficient mice that develop atherosclerosis. Their elevated plasma LDL levels are lowered after conditional knockout of the gene encoding microsomal triglyceride transfer protein. We examined the morphologic and molecular changes in atherosclerotic plaques in control and streptozotocin-induced diabetic Reversa mice after LDL lowering. Bone marrow-derived macrophages were also used to study changes mediated by hyperglycemia. Results: Reversa mice were fed a western diet for 16 weeks to develop plaques (baseline). Four weeks after lipid normalization, control (nondiabetic) mice had reduced plasma cholesterol (-77%), plaque cholesterol (-53%), and plaque cells positive for macrophage marker CD68+ (-73%), but increased plaque collagen (+116%) compared with baseline mice. Diabetic mice had similarly reduced plasma cholesterol, but collagen content increased by only 34% compared with baseline; compared with control mice, there were lower reductions in plaque cholesterol (-30%) and CD68+ cells (-41%). Diabetic (vs. control) plaque CD68+ cells also exhibited more oxidant stress and inflammatory gene expression and less polarization toward the anti-inflammatory M2 macrophage state. Many of the findings in vivo were recapitulated by hyperglycemia in mouse bone marrow-derived macrophages. Conclusions: Diabetes hindered plaque regression in atherosclerotic mice (based on CD68+ plaque content) and favorable changes in plaque macrophage characteristics after the reduction of elevated plasma LDL.
MeSH term(s)	Animals ; Antigens, CD/metabolism ; Antigens, Differentiation, Myelomonocytic/metabolism ; Cells, Cultured ; Cholesterol/blood ; Cholesterol/metabolism ; Collagen/blood ; Collagen/metabolism ; Diabetes Mellitus, Experimental/metabolism ; Diabetes Mellitus, Experimental/physiopathology ; Diet, Atherogenic ; Macrophages/metabolism ; Mice ; Mice, Knockout ; Oxidative Stress/genetics ; Oxidative Stress/physiology ; Plaque, Atherosclerotic ; Polymerase Chain Reaction ; Receptors, LDL/deficiency ; Receptors, LDL/genetics
Chemical Substances	Antigens, CD ; Antigens, Differentiation, Myelomonocytic ; CD68 antigen, human ; Receptors, LDL ; Collagen (9007-34-5) ; Cholesterol (97C5T2UQ7J)
Language	English
Publishing date	2011-05-11
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	80085-5
ISSN	1939-327X ; 0012-1797
ISSN (online)	1939-327X
ISSN	0012-1797
DOI	10.2337/db10-0778
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Uh III Zs.175: Show issues

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Article ; Online: Cholesterol 27-hydroxylase but not apolipoprotein apoE contributes to A2A adenosine receptor stimulated reverse cholesterol transport.

Bingham, Taiese Crystal / Parathath, Saj / Tian, Heather / Reiss, Allison / Chan, Edwin / Fisher, Edward A / Cronstein, Bruce N

Inflammation

2011 Volume 35, Issue 1, Page(s) 49–57

Abstract: Movement of free cholesterol between the cellular compartment and acceptor is governed by cholesterol gradients that are determined by several enzymes and reverse cholesterol transport proteins. We have previously demonstrated that adenosine A(2A) ... ...

Abstract	Movement of free cholesterol between the cellular compartment and acceptor is governed by cholesterol gradients that are determined by several enzymes and reverse cholesterol transport proteins. We have previously demonstrated that adenosine A(2A) receptors inhibit foam cell formation and stimulate production of cholesterol 27-hydroxylase (CYP27A1), an enzyme involved in the conversion of cholesterol to oxysterols. We therefore asked whether the effect of adenosine A(2A) receptors on foam cell formation in vitro is mediated by CYP27A1 or apoE, a carrier for cholesterol in the serum. We found that specific lentiviral siRNA infection markedly reduced apoE or 27-hydroxylase mRNA in THP-1 cells. Despite diminished apoE expression (p < 0.0002, interferon-gamma (IFNγ) CGS vs. IFNγ alone, n=4), CGS-21680, an adenosine A(2A) receptor agonist, inhibits foam cell formation. In contrast, CGS-21680 had no effect on reducing foam cell formation in CYP27A1 KD cells (4 ± 2%; p<0.5113, inhibition vs. IFNγ alone, n=4). Previously, we reported the A(2A) agonist CGS-21680 increases apoAI-mediated cholesterol efflux nearly twofold in wild-type macrophages. Adenosine receptor activation had no effect on cholesterol efflux in CYP27A1 KD cells but reduced efflux in apoE KD cells. These results demonstrate that adenosine A(2A) receptor occupancy diminishes foam cell formation by increasing expression and function of CYP27A1.
MeSH term(s)	ATP Binding Cassette Transporter 1 ; ATP-Binding Cassette Transporters/metabolism ; Adenosine/analogs & derivatives ; Adenosine/pharmacology ; Adenosine A2 Receptor Agonists/pharmacology ; Apolipoproteins E/metabolism ; Biological Transport ; Cell Line, Tumor ; Cholestanetriol 26-Monooxygenase/genetics ; Cholestanetriol 26-Monooxygenase/metabolism ; Cholesterol/metabolism ; Foam Cells/cytology ; Foam Cells/drug effects ; Foam Cells/metabolism ; Humans ; Macrophages/cytology ; Macrophages/metabolism ; Phenethylamines/pharmacology ; RNA Interference ; RNA, Messenger/biosynthesis ; RNA, Small Interfering ; Receptor, Adenosine A2A/genetics ; Receptor, Adenosine A2A/metabolism
Chemical Substances	ATP Binding Cassette Transporter 1 ; ATP-Binding Cassette Transporters ; Adenosine A2 Receptor Agonists ; Apolipoproteins E ; Phenethylamines ; RNA, Messenger ; RNA, Small Interfering ; Receptor, Adenosine A2A ; 2-(4-(2-carboxyethyl)phenethylamino)-5'-N-ethylcarboxamidoadenosine (120225-54-9) ; Cholesterol (97C5T2UQ7J) ; CYP27A1 protein, human (EC 1.14.15.15) ; Cholestanetriol 26-Monooxygenase (EC 1.14.15.15) ; Adenosine (K72T3FS567)
Language	English
Publishing date	2011-01-22
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	434408-x
ISSN	1573-2576 ; 0360-3997
ISSN (online)	1573-2576
ISSN	0360-3997
DOI	10.1007/s10753-010-9288-y
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Article ; Online: miR33 inhibition overcomes deleterious effects of diabetes mellitus on atherosclerosis plaque regression in mice.

Distel, Emilie / Barrett, Tessa J / Chung, Kellie / Girgis, Natasha M / Parathath, Saj / Essau, Christine C / Murphy, Andrew J / Moore, Kathryn J / Fisher, Edward A

Circulation research

2014 Volume 115, Issue 9, Page(s) 759–769

Abstract: Rationale: Diabetes mellitus increases cardiovascular disease risk in humans and remains elevated despite cholesterol-lowering therapy with statins. Consistent with this, in mouse models, diabetes mellitus impairs atherosclerosis plaque regression after ...

Abstract	Rationale: Diabetes mellitus increases cardiovascular disease risk in humans and remains elevated despite cholesterol-lowering therapy with statins. Consistent with this, in mouse models, diabetes mellitus impairs atherosclerosis plaque regression after aggressive cholesterol lowering. MicroRNA 33 (miR33) is a key negative regulator of the reverse cholesterol transport factors, ATP-binding cassette transporter A1 and high-density lipoprotein, which suggested that its inhibition may overcome this impairment. Objective: To assess the effects of miR33 inhibition on atherosclerosis regression in diabetic mice. Methods and results: Reversa mice, which are deficient in the low-density lipoprotein receptor and in which hypercholesterolemia is reversed by conditional inactivation of the microsomal triglyceride transfer protein gene, were placed on an atherogenic diet for 16 weeks, then either made diabetic by streptozotocin injection or kept normoglycemic. Lipid-lowering was induced by microsomal triglyceride transfer protein gene inactivation, and mice were treated with anti-miR33 or control oligonucleotides. Although regression was impaired in diabetic mice treated with control oligonucleotides, anti-miR33 treatment decreased plaque macrophage content and inflammatory gene expression in these mice. The decreased macrophage content in anti-miR33 treated diabetic mice was associated with a blunting of hyperglycemia-induced monocytosis and reduced monocyte recruitment to the plaque, which was traced to an inhibition of the proliferation of bone marrow monocyte precursors associated with the upregulation of their Abca1. Conclusions: miR33 inhibition overcomes deleterious effects of diabetes mellitus in atherosclerosis regression in mice, which suggests a therapeutic strategy in diabetic patients, who remain at elevated cardiovascular disease risk, despite plasma cholesterol lowering.
MeSH term(s)	ATP Binding Cassette Transporter 1/genetics ; ATP Binding Cassette Transporter 1/metabolism ; ATP Binding Cassette Transporter, Subfamily G, Member 1 ; ATP-Binding Cassette Transporters/genetics ; ATP-Binding Cassette Transporters/metabolism ; Animals ; Aortic Diseases/blood ; Aortic Diseases/etiology ; Aortic Diseases/genetics ; Aortic Diseases/pathology ; Aortic Diseases/prevention & control ; Atherosclerosis/blood ; Atherosclerosis/etiology ; Atherosclerosis/genetics ; Atherosclerosis/pathology ; Atherosclerosis/prevention & control ; Carrier Proteins/genetics ; Carrier Proteins/metabolism ; Diabetes Mellitus, Experimental/blood ; Diabetes Mellitus, Experimental/complications ; Diabetes Mellitus, Experimental/genetics ; Diabetes Mellitus, Experimental/therapy ; Diabetic Angiopathies/blood ; Diabetic Angiopathies/etiology ; Diabetic Angiopathies/genetics ; Diabetic Angiopathies/pathology ; Diabetic Angiopathies/prevention & control ; Diet, Western ; Disease Progression ; Gene Silencing ; Inflammation Mediators/metabolism ; Lipids/blood ; Lipoproteins/genetics ; Lipoproteins/metabolism ; Liver/metabolism ; Macrophages/metabolism ; Mice, Inbred C57BL ; MicroRNAs/antagonists & inhibitors ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Oligonucleotides, Antisense/administration & dosage ; Plaque, Atherosclerotic ; Receptors, LDL/deficiency ; Receptors, LDL/genetics ; Stem Cells/metabolism ; Time Factors
Chemical Substances	ABCA1 protein, mouse ; ABCG1 protein, mouse ; ATP Binding Cassette Transporter 1 ; ATP Binding Cassette Transporter, Subfamily G, Member 1 ; ATP-Binding Cassette Transporters ; Carrier Proteins ; Inflammation Mediators ; Lipids ; Lipoproteins ; MicroRNAs ; Mirn33 microRNA, mouse ; Oligonucleotides, Antisense ; Receptors, LDL ; microsomal triglyceride transfer protein
Language	English
Publishing date	2014-09-08
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80100-8
ISSN	1524-4571 ; 0009-7330 ; 0931-6876
ISSN (online)	1524-4571
ISSN	0009-7330 ; 0931-6876
DOI	10.1161/CIRCRESAHA.115.304164
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Article ; Online: A2A adenosine receptor stimulation decreases foam cell formation by enhancing ABCA1-dependent cholesterol efflux.

Bingham, Taiese Crystal / Fisher, Edward A / Parathath, Saj / Reiss, Allison B / Chan, Edwin S / Cronstein, Bruce N

Journal of leukocyte biology

2010 Volume 87, Issue 4, Page(s) 683–690

Abstract: Immune and inflammatory cells play a critical role in the pathogenesis of atherosclerotic plaques. We have demonstrated that A2ARs inhibit foam cell formation and stimulate production of ABCA1, the primary transporter of lipoproteins. We asked whether ... ...

Abstract	Immune and inflammatory cells play a critical role in the pathogenesis of atherosclerotic plaques. We have demonstrated that A2ARs inhibit foam cell formation and stimulate production of ABCA1, the primary transporter of lipoproteins. We asked whether the effects of A2ARs on foam cell formation in vitro are mediated by transporters involved in reverse cholesterol transport, ABCA1 and ABCG1. Foam cells were generated from THP-1 cells by incubation with 100 nM PMA for 2 days and incubated with acLDL (50 microg/mL) plus IFN-gamma (500 U/mL) +/- A2AR agonist CGS-21680 (1 microM). Radiolabeled cholesterol (0.2 microCi/ml) was added to cells, and efflux was measured using a liquid scintillation counter. Lentiviral siRNA infection markedly reduces ABCA1 or ABCG1 mRNA in THP-1 cells. Despite diminished ABCG1 expression (KD), CGS-21680 inhibits foam cell formation (81+5% inhibition; P<0.0001 vs. IFN-gamma alone; n=3) but has no effect on foam cell formation in ABCA1 KD cells (5+3% inhibition; P<0.85 vs. IFN-gamma alone; n=3). The A2A agonist increases apoA-I-mediated cholesterol efflux nearly twofold in THP-1-derived macrophages (from 9.5% to 17.5+2.5% [3H]-cholesterol efflux; P<0.0090 vs. control; n=3) but not in ABCA1 KD cells. Activation of Epac, a signaling molecule downstream of the A2AR, increased ABCA1 (23+5%; P<0.0007 vs. control; n=3) and phospho-ABCA1 (13+5%; P<0.0003 vs. control; n=3) protein. These results demonstrate that A2AR occupancy diminishes foam cell formation by stimulating increased reverse cholesterol transport via ABCA1.
MeSH term(s)	ATP Binding Cassette Transporter 1 ; ATP Binding Cassette Transporter, Subfamily G, Member 1 ; ATP-Binding Cassette Transporters/metabolism ; Adenosine/analogs & derivatives ; Adenosine/pharmacology ; Adenosine A2 Receptor Agonists ; Antihypertensive Agents/pharmacology ; Antiviral Agents/pharmacology ; Apolipoprotein A-I/pharmacology ; Biological Transport/drug effects ; Carcinogens/pharmacology ; Cell Differentiation/drug effects ; Cell Line ; Cholesterol/metabolism ; Foam Cells/metabolism ; Gene Expression Regulation/drug effects ; Guanine Nucleotide Exchange Factors/metabolism ; Humans ; Interferon-gamma/pharmacology ; Lipoproteins, LDL/pharmacology ; Phenethylamines/pharmacology ; RNA, Messenger/biosynthesis ; Receptor, Adenosine A2A/metabolism ; Signal Transduction/drug effects ; Tetradecanoylphorbol Acetate/pharmacology
Chemical Substances	ABCA1 protein, human ; ABCG1 protein, human ; ATP Binding Cassette Transporter 1 ; ATP Binding Cassette Transporter, Subfamily G, Member 1 ; ATP-Binding Cassette Transporters ; Adenosine A2 Receptor Agonists ; Antihypertensive Agents ; Antiviral Agents ; Apolipoprotein A-I ; Carcinogens ; Guanine Nucleotide Exchange Factors ; Lipoproteins, LDL ; Phenethylamines ; RAPGEF3 protein, human ; RNA, Messenger ; Receptor, Adenosine A2A ; acetyl-LDL ; 2-(4-(2-carboxyethyl)phenethylamino)-5'-N-ethylcarboxamidoadenosine (120225-54-9) ; Interferon-gamma (82115-62-6) ; Cholesterol (97C5T2UQ7J) ; Adenosine (K72T3FS567) ; Tetradecanoylphorbol Acetate (NI40JAQ945)
Language	English
Publishing date	2010-01-20
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	605722-6
ISSN	1938-3673 ; 0741-5400
ISSN (online)	1938-3673
ISSN	0741-5400
DOI	10.1189/jlb.0709513
Database	MEDical Literature Analysis and Retrieval System OnLINE

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