Database : MEDLINE
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[PMID]: 24897618
[Au] Autor:Wysoczynski M; Hong KU; Moore JB
[Ad] Address:University of Louisville, Institute of Molecular Cardiology, Department of Medicine , Louisville, KY , USA.
[Ti] Title:Bone marrow cell therapies in ischemic cardiomyopathy.
[So] Source:Expert Opin Biol Ther;14(9):1229-32, 2014 Sep.
[Is] ISSN:1744-7682
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Decrements in ventricular function due to the permanent loss of contractile tissue remain problematic in patients with ischemic cardiomyopathy. For this reason, cell replacement therapy has received much popularity in recent years. Bone marrow is an abundant and accessible source of stem cells with regenerative potential. However, ischemic heart disease clinical trials based on bone marrow-derived stem cell (BMC) infusion have yielded discrepant results and marginal therapeutic benefits, making this modality's future uncertain. Further investigation of molecular and cellular characteristics critical for therapeutic efficacy and defining the mechanism(s) of BMC-mediated cardiac repair will be paramount for harnessing their full therapeutic potential.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1408
[Js] Journal subset:IM
[St] Status:In-Process
[do] DOI:10.1517/14712598.2014.925873

  2 / 311347 MEDLINE  
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[PMID]: 24955854
[Au] Autor:Yeh LC; Ford JJ; Lee JC; Adamo ML
[Ad] Address:Department of Biochemistry, The University of Texas Health Science Center at San Antonio, TX, United States....
[Ti] Title:Palmitate attenuates osteoblast differentiation of fetal rat calvarial cells.
[So] Source:Biochem Biophys Res Commun;450(1):777-81, 2014 Jul 18.
[Is] ISSN:1090-2104
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Aging is associated with the accumulation of ectopic lipid resulting in the inhibition of normal organ function, a phenomenon known as lipotoxicity. Within the bone marrow microenvironment, elevation in fatty acid levels may produce an increase in osteoclast activity and a decrease in osteoblast number and function, thus contributing to age-related osteoporosis. However, little is known about lipotoxic mechanisms in intramembraneous bone. Previously we reported that the long chain saturated fatty acid palmitate inhibited the expression of the osteogenic markers RUNX2 and osteocalcin in fetal rat calvarial cell (FRC) cultures. Moreover, the acetyl CoA carboxylase inhibitor TOFA blocked the inhibitory effect of palmitate on expression of these two markers. In the current study we have extended these observations to show that palmitate inhibits spontaneous mineralized bone formation in FRC cultures in association with reduced mRNA expression of RUNX2, alkaline phosphatase, osteocalcin, and bone sialoprotein and reduced alkaline phosphatase activity. The effects of palmitate on osteogenic marker expression were inhibited by TOFA. Palmitate also inhibited the mRNA expression of fatty acid synthase and PPARγ in FRC cultures, and as with osteogenic markers, this effect was inhibited by TOFA. Palmitate had no effect on FRC cell proliferation or apoptosis, but inhibited BMP-7-induced alkaline phosphatase activity. We conclude that palmitate accumulation may lead to lipotoxic effects on osteoblast differentiation and mineralization and that increases in fatty acid oxidation may help to prevent these lipotoxic effects.
[Mh] MeSH terms primary: Embryonic Stem Cells/cytology
Osteoblasts/cytology
Osteogenesis/physiology
Palmitates/administration & dosage
Skull/cytology
Skull/embryology
[Mh] MeSH terms secundary: Animals
Cell Differentiation/drug effects
Cell Differentiation/physiology
Cells, Cultured
Dose-Response Relationship, Drug
Embryonic Stem Cells/drug effects
Embryonic Stem Cells/physiology
Osteoblasts/drug effects
Osteoblasts/physiology
Osteogenesis/drug effects
Rats
Skull/drug effects
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Name of substance:0 (Palmitates)
[Em] Entry month:1409
[Js] Journal subset:IM
[Da] Date of entry for processing:140721
[St] Status:MEDLINE

  3 / 311347 MEDLINE  
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[PMID]: 24953693
[Au] Autor:Wang Y; Lu H; Huang Z; Lin H; Lei Z; Chen X; Tang M; Gao F; Dong M; Li R; Lin L
[Ad] Address:Cardiovascular Department, Liaocheng People's Hospital of Shandong University, Liaocheng, Shandong 252000, PR China; Cardiovascular Department, The Second Clinical Medical College of Fujian Medical University, Quanzhou, Fujian 362000, PR China....
[Ti] Title:Apolipoprotein E-knockout mice on high-fat diet show autoimmune injury on kidney and aorta.
[So] Source:Biochem Biophys Res Commun;450(1):788-93, 2014 Jul 18.
[Is] ISSN:1090-2104
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: Apolipoprotein E-knockout (ApoE(-/-)) mice is a classic model of atherosclerosis. We have found that ApoE(-/-) mice showed splenomegaly, higher titers of serum anti-nuclear antibody (ANA) and anti-dsDNA antibody compared with C57B6/L (B6) mice. However, whether ApoE(-/-) mice show autoimmune injury remains unclear. METHODS AND RESULTS: Six females and six males in each group, ApoE(-/)(-), Fas(-/-) and B6 mice, were used in this study. The titers of serum ANA, anti-dsDNA antibody and creatinine and urine protein were measured by ELISA after 4 months of high-fat diet. The spleen weight and the glomerular area were determined. The expressions of IgG, C3 and macrophage in kidney and atherosclerotic plaque were detected by immunostaining followed by morphometric analysis. Similar to the characteristics of Fas(-/-) mice, a model of systemic lupus erythematosus (SLE), ApoE(-/-) mice, especially female, displayed significant increases of spleen weight and glomerular area when compared to B6 mice. Also, elevated titers of serum ANA, anti-dsDNA antibody and creatinine and urine protein. Moreover, the expressions of IgG, C3 and macrophage in glomeruli and aortic plaques were found in ApoE(-/-) mice. In addition, the IgG and C3 expressions in glomeruli and plaques significantly increased (or a trend of increase) in female ApoE(-/-) mice compared with males. CONCLUSIONS: Apolipoprotein E-knockout mice on high-fat diet show autoimmune injury on kidney and aorta.
[Mh] MeSH terms primary: Aortitis/immunology
Apolipoproteins E/metabolism
Atherosclerosis/immunology
Autoimmune Diseases/immunology
Dietary Fats/immunology
Macrophages/immunology
Nephritis/immunology
[Mh] MeSH terms secundary: Animals
Aortitis/pathology
Apolipoproteins E/genetics
Atherosclerosis/pathology
Autoimmune Diseases/pathology
Cytokines/immunology
Female
Male
Mice
Mice, Inbred C57BL
Mice, Knockout
Nephritis/pathology
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (Apolipoproteins E); 0 (Cytokines); 0 (Dietary Fats)
[Em] Entry month:1409
[Js] Journal subset:IM
[Da] Date of entry for processing:140721
[St] Status:MEDLINE

  4 / 311347 MEDLINE  
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[PMID]: 24928385
[Au] Autor:Liu C; Ge B; He C; Zhang Y; Liu X; Liu K; Qian C; Zhang Y; Peng W; Guo X
[Ad] Address:Department of Cardiology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095 Jiefang Avenue, Wuhan 430030, PR China....
[Ti] Title:Mitofusin 2 decreases intracellular lipids in macrophages by regulating peroxisome proliferator-activated receptor-γ.
[So] Source:Biochem Biophys Res Commun;450(1):500-6, 2014 Jul 18.
[Is] ISSN:1090-2104
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Mitofusin 2 (Mfn2) inhibits atherosclerotic plaque formation, but the underlying mechanism remains elusive. This study aims to reveal how Mfn2 functions in the atherosclerosis. Mfn2 expression was found to be significantly reduced in arterial atherosclerotic lesions of both mice and human compared with healthy counterparts. Here, we observed that Mfn2 increased cellular cholesterol transporter expression in macrophages by upregulating peroxisome proliferator-activated receptor-γ, an effect achieved at least partially by inhibiting extracellular signal-regulated kinase1/2 (ERK1/2) and p38 mitogen-activated protein kinases (MAPKs) pathway. These findings provide insights into potential mechanisms of Mfn2-mediated alterations in cholesterol transporter expression, which may have significant implications for the treatment of atherosclerotic heart disease.
[Mh] MeSH terms primary: GTP Phosphohydrolases/metabolism
Lipid Metabolism/physiology
MAP Kinase Signaling System/physiology
Macrophages/metabolism
Membrane Transport Proteins/metabolism
Mitochondrial Proteins/metabolism
PPAR gamma/metabolism
[Mh] MeSH terms secundary: Cell Line
Gene Expression Regulation/physiology
Humans
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (Membrane Transport Proteins); 0 (Mitochondrial Proteins); 0 (PPAR gamma); EC 3.6.1.- (GTP Phosphohydrolases); EC 3.6.1.- (MFN2 protein, human)
[Em] Entry month:1409
[Js] Journal subset:IM
[Da] Date of entry for processing:140721
[St] Status:MEDLINE

  5 / 311347 MEDLINE  
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[PMID]: 24878532
[Au] Autor:Curtis BM; Leix KA; Ji Y; Glaves RS; Ash DE; Mohanty DK
[Ad] Address:Department of Chemistry, Central Michigan University, Mount Pleasant, MI 48859, USA....
[Ti] Title:Slow and sustained nitric oxide releasing compounds inhibit multipotent vascular stem cell proliferation and differentiation without causing cell death.
[So] Source:Biochem Biophys Res Commun;450(1):208-12, 2014 Jul 18.
[Is] ISSN:1090-2104
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Atherosclerosis is the leading cause of cerebral and myocardial infarction. It is believed that neointimal growth common in the later stages of atherosclerosis is a result of vascular smooth muscle cell (SMC) de-differentiation in response to endothelial injury. However, the claims of the SMC de-differentiation theory have not been substantiated by monitoring the fate of mature SMCs in response to such injuries. A recent study suggests that atherosclerosis is a consequence of multipotent vascular stem cell (MVSC) differentiation. Nitric oxide (NO) is a well-known mediator against atherosclerosis, in part because of its inhibitory effect on SMC proliferation. Using three different NO-donors, we have investigated the effects of NO on MVSC proliferation. Results indicate that NO inhibits MVSC proliferation in a concentration dependent manner. A slow and sustained delivery of NO proved to inhibit proliferation without causing cell death. On the other hand, larger, single-burst NO concentrations, inhibits proliferation, with concurrent significant cell death. Furthermore, our results indicate that endogenously produced NO inhibits MVSC differentiation to mesenchymal-like stem cells (MSCs) and subsequently to SMC as well.
[Mh] MeSH terms primary: Mesenchymal Stromal Cells/cytology
Mesenchymal Stromal Cells/physiology
Multipotent Stem Cells/cytology
Multipotent Stem Cells/physiology
Myocytes, Smooth Muscle/cytology
Myocytes, Smooth Muscle/physiology
Nitric Oxide Donors/administration & dosage
[Mh] MeSH terms secundary: Animals
Apoptosis/drug effects
Apoptosis/physiology
Cell Differentiation/drug effects
Cell Proliferation/drug effects
Cells, Cultured
Delayed-Action Preparations/administration & dosage
Mesenchymal Stromal Cells/drug effects
Multipotent Stem Cells/drug effects
Myocytes, Smooth Muscle/drug effects
Oxidative Stress/drug effects
Oxidative Stress/physiology
Rats
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Name of substance:0 (Delayed-Action Preparations); 0 (Nitric Oxide Donors)
[Em] Entry month:1409
[Js] Journal subset:IM
[Da] Date of entry for processing:140721
[St] Status:MEDLINE

  6 / 311347 MEDLINE  
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[PMID]: 24866239
[Au] Autor:Kim SH; Kothari S; Patel AB; Bielicki JK; Narayanaswami V
[Ad] Address:Department of Chemistry & Biochemistry, California State University Long Beach, Long Beach, CA 90840, USA....
[Ti] Title:A pyrene based fluorescence approach to study conformation of apolipoprotein E3 in macrophage-generated nascent high density lipoprotein.
[So] Source:Biochem Biophys Res Commun;450(1):124-8, 2014 Jul 18.
[Is] ISSN:1090-2104
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Apolipoprotein E3 (apoE3) is an anti-atherogenic apolipoprotein with the ability to exist in lipid-free and lipoprotein-associated states. During atherosclerosis, its function in promoting cholesterol efflux from macrophages via the ATP-binding cassette transporter A1 (ABCA1) takes a prominent role, leading to generation of nascent high density lipoprotein (nHDL) particles. The objective of this study is to understand the conformation adopted by apoE3 in macrophage-generated nHDL using a fluorescence spectroscopic approach involving pyrene. Pyrene-labeled recombinant human apoE3 displayed a robust ability to stimulate ABCA1-mediated cholesterol efflux from cholesterol-loaded J774 macrophages (which do not express apoE), comparable to that elicited by unlabeled apoE3. The nHDL recovered from the conditioned medium revealed the presence of apoE3 by immunoblot analysis. A heterogeneous population of nHDL bearing exogenously added apoE3 was generated with particle size varying from ∼12 to ∼19 nm in diameter, corresponding to molecular mass of ∼450 to ∼700 kDa. The lipid: apoE3 ratio varied from ∼60:1 to 10:1. A significant extent of pyrene excimer emission was noted in nHDL, indicative of spatial proximity between Cys112 on neighboring apoE3 molecules similar to that noted in reconstituted HDL. Cross-linking analysis using Cys-specific cross-linkers revealed the predominant presence of dimers. Taken together the data indicate a double belt arrangement of apoE molecules on nHDL. A similar organization of the C-terminal tail of apoE on nHDL was noted when pyrene-apoEA277C(201-299) was used as the cholesterol acceptor. These studies open up the possibility of using exogenously labeled apoE3 to generate nHDL for structural and conformational analysis.
[Mh] MeSH terms primary: Apolipoprotein E3/chemistry
Apolipoprotein E3/metabolism
High-Density Lipoproteins, Pre-beta/chemistry
High-Density Lipoproteins, Pre-beta/metabolism
Macrophages/metabolism
Pyrenes/chemistry
Spectrometry, Fluorescence/methods
[Mh] MeSH terms secundary: Animals
Cell Line
Humans
Mice
Microscopy, Fluorescence/methods
Protein Conformation
Pyrenes/metabolism
Staining and Labeling
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (Apolipoprotein E3); 0 (High-Density Lipoproteins, Pre-beta); 0 (Pyrenes); 9E0T7WFW93 (pyrene)
[Em] Entry month:1409
[Js] Journal subset:IM
[Da] Date of entry for processing:140721
[St] Status:MEDLINE

  7 / 311347 MEDLINE  
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[PMID]: 24866235
[Au] Autor:Choi B; Kang SS; Kang SW; Min BH; Lee EJ; Song DH; Kim SM; Song Y; Yoon SY; Chang EJ
[Ad] Address:Department of Biomedical Sciences, University of Ulsan College of Medicine, Asan Medical Center, Seoul 138-736, Republic of Korea....
[Ti] Title:Secretory clusterin inhibits osteoclastogenesis by attenuating M-CSF-dependent osteoclast precursor cell proliferation.
[So] Source:Biochem Biophys Res Commun;450(1):105-9, 2014 Jul 18.
[Is] ISSN:1090-2104
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Secretory clusterin (sCLU)/apolipoprotein J is a multifunctional glycoprotein that is ubiquitously expressed in various tissues. Reduced sCLU in the joints of patients with bone erosive disease is associated with disease activity; however, its exact role has yet to be elucidated. Here, we report that CLU is expressed and secreted during osteoclastogenesis in mouse bone marrow-derived macrophages (BMMs) that are treated with receptor activator of nuclear factor kappa-B ligand (RANKL) and macrophage colony-stimulating factor (M-CSF). CLU-deficient BMMs obtained from CLU(-/-) mice exhibited no significant alterations in OC differentiation in comparison with BMMs obtained from wild-type mice. In contrast, exogenous sCLU treatment significantly inhibited OC formation in both BMMs and OC precursor cultures. The inhibitory effect of sCLU was more prominent in BMMs than OC precursor cultures. Interestingly, treating BMMs with sCLU decreased the proliferative effects elicited by M-CSF and suppressed M-CSF-induced ERK activation of OC precursor cells without causing apoptotic cell death. This study provides the first evidence that sCLU reduces OC formation by inhibiting the actions of M-CSF, thereby suggesting its protective role in bone erosion.
[Mh] MeSH terms primary: Clusterin/secretion
Macrophage Colony-Stimulating Factor/metabolism
Macrophages/physiology
Osteoclasts/cytology
Osteoclasts/physiology
Stem Cells/cytology
Stem Cells/physiology
[Mh] MeSH terms secundary: Animals
Cell Differentiation
Cell Proliferation
Cells, Cultured
Macrophage Activation/physiology
Mice
Mice, Inbred C57BL
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (Clu protein, mouse); 0 (Clusterin); 81627-83-0 (Macrophage Colony-Stimulating Factor)
[Em] Entry month:1409
[Js] Journal subset:IM
[Da] Date of entry for processing:140721
[St] Status:MEDLINE

  8 / 311347 MEDLINE  
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[PMID]: 24950468
[Au] Autor:Ouyang Z; Zhai Z; Li H; Liu X; Qu X; Li X; Fan Q; Tang T; Qin A; Dai K
[Ad] Address:Department of Orthopaedics, Shanghai Key Laboratory of Orthopaedic Implant, Shanghai Ninth People's Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200011, China; Department of Orthopaedics, Hunan Cancer Hospital and The Affiliated Cancer Hospital of Xiangya School of Medicine, C...
[Ti] Title:Hypericin suppresses osteoclast formation and wear particle-induced osteolysis via modulating ERK signalling pathway.
[So] Source:Biochem Pharmacol;90(3):276-87, 2014 Aug 1.
[Is] ISSN:1873-2968
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Osteoclast-induced bone resorption and wear-particle-induced osteolysis leads to prosthetic loosening, one of the most common causes of joint implant failure, resulting in revision surgery. Thus, inhibition of osteoclastic bone resorption, which further prevents wear particle-induced osteolysis, is a potential treatment strategy for prosthetic loosening. Here, we examined the therapeutic effect of hypericin (HP), which was photosensitive, on osteoclastogenesis and wear particle-induced osteolysis in the absence of visible light. HP inhibited RANKL-induced osteoclast differentiation in bone marrow macrophages (BMMs) and RAW264.7 cell line without any evidence of cytotoxicity. The bone-resorbing activity of mature osteoclasts was significantly inhibited by HP. As HP has been previously reported to inhibit signalling pathway such as ERK and NF-κB in other cells, which is also important in osteoclast differentiation. We thus examined the molecular mechanism and showed that HP significantly inhibited the ERK/mitogen-activated protein kinase (MAPK) signalling pathway without affecting nuclear factor kappaB (NF-κB), c-Jun N-terminal kinase (JNK) and p38 signalling in RANKL-stimulated BMMs. Further in vivo studies revealed HP attenuated osteoclast formation and subsequently prevented wear particle-induced bone erosion. Taken together, the results suggest that HP inhibits RANKL-mediated osteoclastogenesis via affecting ERK signalling in vitro and suppresses wear particle-induced osteolysis in vivo. We therefore conclude that HP may be an innovative and safe alternative treatment for osteoclast-related prosthetic loosening.
[Mh] MeSH terms primary: Bone Density Conservation Agents/therapeutic use
Disease Models, Animal
MAP Kinase Signaling System/drug effects
Osteoclasts/drug effects
Osteolysis/drug therapy
Perylene/analogs & derivatives
Prosthesis Failure/adverse effects
[Mh] MeSH terms secundary: Animals
Bone Density Conservation Agents/administration & dosage
Bone Density Conservation Agents/adverse effects
Bone Density Conservation Agents/pharmacology
Cell Line, Transformed
Cell Survival/drug effects
Cell Transdifferentiation/drug effects
Cells, Cultured
Dose-Response Relationship, Drug
Gene Expression Regulation/drug effects
Macrophages/cytology
Macrophages/drug effects
Macrophages/pathology
Male
Mice
Mice, Inbred C57BL
Osteoclasts/pathology
Osteolysis/etiology
Osteolysis/pathology
Perylene/administration & dosage
Perylene/adverse effects
Perylene/pharmacology
Perylene/therapeutic use
RANK Ligand/antagonists & inhibitors
RANK Ligand/genetics
RANK Ligand/metabolism
RANK Ligand/pharmacology
Random Allocation
Recombinant Proteins/chemistry
Recombinant Proteins/metabolism
Recombinant Proteins/pharmacology
Skull
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (Bone Density Conservation Agents); 0 (RANK Ligand); 0 (Recombinant Proteins); 0 (Tnfsf11 protein, mouse); 5QD5427UN7 (Perylene); 7V2F1075HD (hypericin)
[Em] Entry month:1409
[Js] Journal subset:IM
[Da] Date of entry for processing:140708
[St] Status:MEDLINE

  9 / 311347 MEDLINE  
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[PMID]: 24875449
[Au] Autor:Qian L; Li X; Fang R; Wang Z; Xu Y; Zhang H; Bai H; Yang Q; Zhu X; Ben J; Xu Y; Chen Q
[Ad] Address:Atherosclerosis Research Center, Key Laboratory of Cardiovascular Disease and Molecular Intervention, Nanjing Medical University, Nanjing 210029, People's Republic of China; Department of Cardiology, Affiliated Wuxi People's Hospital of Nanjing Medical University, Wuxi 214023, People's Republic of C...
[Ti] Title:Class A scavenger receptor deficiency augments angiotensin II-induced vascular remodeling.
[So] Source:Biochem Pharmacol;90(3):254-64, 2014 Aug 1.
[Is] ISSN:1873-2968
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Class A scavenger receptor (SR-A) is a multifunctional molecule that participates in macrophage-mediated inflammation. Here we evaluated the role of SR-A in angiotensin II (Ang II)-induced hypertensive vascular remodeling. Chronic infusion of Ang II leads to an increased systolic blood pressure both in SR-A knockout (SR-A(-/-)) and wild type (SR-A(+/+)) mice with no significant difference between these two groups. SR-A(-/-) hypertensive mice, however, exhibited a marked augmentation of arterial wall thickening and vascular cell proliferation compared with SR-A(+/+) hypertensive mice. M1 macrophage markers were increased whereas M2 macrophage markers were decreased in vascular tissues of SR-A(-/-) mice. Co-culture experiments revealed that more pro-inflammatory cytokines like TNF-α were produced by SR-A(-/-) peritoneal macrophages leading to a stronger proliferation of primary vascular smooth muscle cells in vitro. In addition, SR-A(-/-) macrophages were more prone to lipopolysaccharide-induced M1 differentiation while resisting interleukin-4-induced M2 differentiation. Importantly, transplantation of SR-A(-/-) bone marrow into SR-A(+/+) mice significantly augmented Ang II-induced vascular remodeling. These results show that SR-A is critical for Ang II-induced vascular remodeling by regulating macrophage polarization. Therefore, SR-A may be a useful therapeutic target for the intervention of hypertensive vascular remodeling.
[Mh] MeSH terms primary: Blood Vessels/pathology
Disease Models, Animal
Hypertension/physiopathology
Macrophages/pathology
Neovascularization, Pathologic/etiology
Scavenger Receptors, Class A/metabolism
[Mh] MeSH terms secundary: Angiotensin II/administration & dosage
Angiotensin II/adverse effects
Animals
Aorta, Thoracic/cytology
Aorta, Thoracic/immunology
Aorta, Thoracic/metabolism
Aorta, Thoracic/pathology
Blood Vessels/immunology
Blood Vessels/metabolism
Cell Proliferation
Cell Transdifferentiation
Cells, Cultured
Coculture Techniques
Crosses, Genetic
Infusions, Intravenous
Macrophages/cytology
Macrophages/immunology
Macrophages/metabolism
Male
Mice
Mice, 129 Strain
Mice, Inbred ICR
Mice, Knockout
Muscle, Smooth, Vascular/cytology
Muscle, Smooth, Vascular/immunology
Muscle, Smooth, Vascular/metabolism
Muscle, Smooth, Vascular/pathology
Neovascularization, Pathologic/immunology
Neovascularization, Pathologic/metabolism
Neovascularization, Pathologic/pathology
Scavenger Receptors, Class A/deficiency
Scavenger Receptors, Class A/genetics
Transplantation Chimera/immunology
Transplantation Chimera/metabolism
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (Msr1 protein, mouse); 0 (Scavenger Receptors, Class A); 11128-99-7 (Angiotensin II)
[Em] Entry month:1409
[Js] Journal subset:IM
[Da] Date of entry for processing:140708
[St] Status:MEDLINE

  10 / 311347 MEDLINE  
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[PMID]: 24166283
[Au] Autor:Tu C; Ng TS; Jacobs RE; Louie AY
[Ad] Address:Department of Biomedical Engineering, University of California, Davis, Davis, CA, 95616, USA.
[Ti] Title:Multimodality PET/MRI agents targeted to activated macrophages.
[So] Source:J Biol Inorg Chem;19(2):247-58, 2014 Feb.
[Is] ISSN:1432-1327
[Cp] Country of publication:Germany
[La] Language:eng
[Ab] Abstract:The recent emergence of multimodality imaging, particularly the combination of PET and MRI, has led to excitement over the prospect of improving detection of disease. Iron oxide nanoparticles have become a popular platform for the fabrication of PET/MRI probes owing to their advantages of high MRI detection sensitivity, biocompatibility, and biodegradability. In this article, we report the synthesis of dextran-coated iron oxide nanoparticles (DIO) labeled with the positron emitter (64)Cu to generate a PET/MRI probe, and modified with maleic anhydride to increase the negative surface charge. The modified nanoparticulate PET/MRI probe (MDIO-(64)Cu-DOTA) bears repetitive anionic charges on the surface that facilitate recognition by scavenger receptor type A (SR-A), a ligand receptor found on activated macrophages but not on normal vessel walls. MDIO-(64)Cu-DOTA has an average iron oxide core size of 7-8 nm, an average hydrodynamic diameter of 62.7 nm, an r1 relaxivity of 16.8 mM(-1) s(-1), and an r 2 relaxivity of 83.9 mM(-1) s(-1) (37 C, 1.4 T). Cell studies confirmed that the probe was nontoxic and was specifically taken up by macrophages via SR-A. In comparison with the nonmodified analog, the accumulation of MDIO in macrophages was substantially improved. These characteristics demonstrate the promise of MDIO-(64)Cu-DOTA for identification of vulnerable atherosclerotic plaques via the targeting of macrophages.
[Mh] MeSH terms primary: Ferric Compounds/chemistry
Ferric Compounds/diagnostic use
Macrophage Activation
Macrophages/metabolism
Magnetic Resonance Imaging/methods
Positron-Emission Tomography/methods
[Mh] MeSH terms secundary: Animals
Cell Line
Copper Radioisotopes/diagnostic use
Dextrans/chemistry
Ferric Compounds/metabolism
Ferric Compounds/toxicity
Macrophages/cytology
Nanoparticles/chemistry
Particle Size
Rats
Surface Properties
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (Copper Radioisotopes); 0 (Ferric Compounds); 1309-37-1 (ferric oxide); K3R6ZDH4DU (Dextrans)
[Em] Entry month:1409
[Js] Journal subset:IM
[Da] Date of entry for processing:140127
[St] Status:MEDLINE
[do] DOI:10.1007/s00775-013-1054-9


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