Database : MEDLINE Search on : foam and cells [Words] References found : 5063 [refine] Displaying: 1 .. 10   in format [Detailed]

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[PMID]: 23668229 [Au] Autor: Woollard KJ [Ad] Address: Division of Immunology & Inflammation, Department of Medicine, Imperial College London, Hammersmith Campus, Du Cane Road, London W12 0NN, U.K. [Ti] Title: Immunological aspects of atherosclerosis. [So] Source: Clin Sci (Lond);125(5):221-35, 2013 Sep 1. [Is] ISSN: 1470-8736 [Cp] Country of publication: England [La] Language: eng [Ab] Abstract: Cardiovascular disease is the leading cause of death in several countries. The underlying process is atherosclerosis, a slowly progressing chronic disorder that can lead to intravascular thrombosis. There is overwhelming evidence for the underlying importance of our immune system in atherosclerosis. Monocytes, which comprise part of the innate immune system, can be recruited to inflamed endothelium and this recruitment has been shown to be proportional to the extent of atherosclerotic disease. Monocytes undergo migration into the vasculature, they differentiate into macrophage phenotypes, which are highly phagocytic and can scavenge modified lipids, leading to foam cell formation and development of the lipid-rich atheroma core. This increased influx leads to a highly inflammatory environment and along with other immune cells can increase the risk in the development of the unstable atherosclerotic plaque phenotype. The present review provides an overview and description of the immunological aspect of innate and adaptive immune cell subsets in atherosclerosis, by defining their interaction with the vascular environment, modified lipids and other cellular exchanges. There is a particular focus on monocytes and macrophages, but shorter descriptions of dendritic cells, lymphocyte populations, neutrophils, mast cells and platelets are also included. [Pt] Publication type: JOURNAL ARTICLE [Em] Entry month: 1305 [Js] Journal subset: IM [St] Status: In-Data-Review [do] DOI: 10.1042/CS20120576

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[PMID]: 23583194 [Au] Autor: Cai Y; Li JD; Yan C [Ad] Address: Aab Cardiovascular Research Institute, Department of Medicine, University of Rochester, 601 Elmwood Ave, Rochester, NY 14642, USA. [Ti] Title: Vinpocetine attenuates lipid accumulation and atherosclerosis formation. [So] Source: Biochem Biophys Res Commun;434(3):439-43, 2013 May 10. [Is] ISSN: 1090-2104 [Cp] Country of publication: United States [La] Language: eng [Ab] Abstract: Atherosclerosis, the major cause of myocardial infarction and stroke, is a chronic arterial disease characterized by lipid deposition and inflammation in the vessel wall. Cholesterol, in low-density lipoprotein (LDL), plays a critical role in the pathogenesis of atherosclerosis. Vinpocetine, a derivative of the alkaloid vincamine, has long been used as a cerebral blood flow enhancer for treating cognitive impairment. Recent study indicated that vinpocetine is a potent anti-inflammatory agent. However, its role in the pathogenesis of atherosclerosis remains unexplored. In the present study, we show that vinpocetine significantly reduced atherosclerotic lesion formation in ApoE knockout mice fed with a high-fat diet. In cultured murine macrophage RAW264.7 cells, vinpocetine markedly attenuated oxidized LDL (ox-LDL) uptake and foam cell formation. Moreover, vinpocetine greatly blocked the induction of ox-LDL receptor 1 (LOX-1) in cultured macrophages as well as in the LOX-1 level in atherosclerotic lesions. Taken together, our data reveal a novel role of vinpocetine in reduction of pathogenesis of atherosclerosis, at least partially through suppressing LOX-1 signaling pathway. Given the excellent safety profile of vinpocetine, this study suggests vinpocetine may be a therapeutic candidate for treating atherosclerosis. [Pt] Publication type: JOURNAL ARTICLE [Em] Entry month: 1305 [Js] Journal subset: IM [St] Status: In-Data-Review

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[PMID]: 23658787 [Au] Autor: Chai JT; Digby JE; Ruparelia N; Jefferson A; Handa A; Choudhury RP [Ad] Address: Division of Cardiovascular Medicine, University of Oxford, Oxford, United Kingdom. [Ti] Title: Nicotinic Acid Receptor GPR109A Is Down-Regulated in Human Macrophage-Derived Foam Cells. [So] Source: PLoS One;8(5):e62934, 2013. [Is] ISSN: 1932-6203 [Cp] Country of publication: United States [La] Language: eng [Ab] Abstract: Nicotinic acid (NA) regresses atherosclerosis in human imaging studies and reduces atherosclerosis in mice, mediated by myeloid cells, independent of lipoproteins. Since GPR109A is expressed by human monocytes, we hypothesized that NA may drive cholesterol efflux from foam cells. In THP-1 cells NA suppressed LPS-induced mRNA transcription of MCP-1 by 76.6±12.2% (P<0.01) and TNFα by 56.1±11.5% (P<0.01), yet restored LPS-induced suppression of PPARγ transcription by 536.5±46.4% (P<0.001) and its downstream effector CD36 by 116.8±19.8% (P<0.01). Whilst direct PPARγ-agonism promoted cholesterol efflux from THP-1 derived foam cells by 37.7±3.1% (P<0.01) and stimulated transcription of LXRα by 87.9±9.5% (P<0.001) and ABCG1 by 101.2±15.5% (P<0.01), NA showed no effect in foam cells on either cholesterol efflux or key RCT genes transcription. Upon foam cell induction, NA lost its effect on PPARγ and cAMP pathways, since its receptor, GPR109A, was down-regulated by foam cell transformation. This observation was confirmed in explanted human carotid plaques. In conclusion, despite NA's anti-inflammatory effect on human macrophages, it has no effect on foam cells in reverse cholesterol transport; due to GPR109A down-regulation. [Pt] Publication type: JOURNAL ARTICLE [Em] Entry month: 1305 [Js] Journal subset: IM [St] Status: In-Data-Review [do] DOI: 10.1371/journal.pone.0062934

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[PMID]: 22928784 [Au] Autor: Gonçalves MS; Fabris BA; Brinholi FF; Bortolasci CC; Watanabe MA; Oliveira KB; Delfino VD; Lavado EL; Barbosa DS [Ad] Address: Histocompatibility Laboratory, State University of Londrina, Londrina, PR, Brazil. [Ti] Title: Increased oxidative stress in foam cells obtained from hemodialysis patients. [So] Source: Hemodial Int;17(2):266-74, 2013 Apr. [Is] ISSN: 1542-4758 [Cp] Country of publication: Canada [La] Language: eng [Ab] Abstract: Premature atherosclerosis represents the main cause of mortality among end-stage renal disease patients (ESRD). Increased inflammation and oxidative stress are involved in initiation and progression of the atherosclerotic plaque. As foam cells are capable of producing significant amounts of inflammatory mediators and free radicals, we hypothesized that foam cells from uremic patients could produce more inflammation and oxidative stress than foam cells from normal people and be, somehow, involved in the accelerated atherosclerosis of uremia. To test this hypothesis, the levels of a few markers of inflammation and oxidative stress: Tumor necrosis factor-α, inducible nitric oxide synthase, malondialdehyde, nitric oxide by-products were measured in the supernatants of macrophage-derived foam cells cultures from 18 hemodialysis patients and 18 apparently healthy individuals controls. Malondialdehyde levels in the supernatant of cell cultures (macrophages stimulated or not with native and oxidized lipoprotein) were significantly increased in uremic patients; no statistically significant difference was found between the supernatant concentrations of nitric oxide by-products, inducible nitric oxide synthase activity, and tumor necrosis factor-α between patients and controls. Our results, obtained with human macrophages and macrophage-derived foam cells, are compatible with the theory that increased cellular oxidative stress and inflammatory activity in ESRD patients could accelerate the atherosclerotic process. The present culture protocol showed it is possible to use human mononuclear cells to evaluate the oxidative metabolism of foam cells, which are considered to be the initial step of atherosclerotic lesions. [Pt] Publication type: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T [Em] Entry month: 1304 [Js] Journal subset: IM [St] Status: In-Process [do] DOI: 10.1111/j.1542-4758.2012.00736.x

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[PMID]: 23185273 [Au] Autor: Rébé C; Filomenko R; Raveneau M; Chevriaux A; Ishibashi M; Lagrost L; Junien JL; Gambert P; Masson D [Ad] Address: Centre de Recherche Institut National de la Santé et de la Recherche Médicale Unité Mixte de Recherche 866, Université de Bourgogne, Dijon, France. [Ti] Title: Identification of biological markers of liver X receptor (LXR) activation at the cell surface of human monocytes. [So] Source: PLoS One;7(11):e48738, 2012. [Is] ISSN: 1932-6203 [Cp] Country of publication: United States [La] Language: eng [Ab] Abstract: BACKGROUND: Liver X receptor (LXR) α and LXR ß (NR1H3 and NR1H2) are oxysterol-activated nuclear receptors involved in the control of major metabolic pathways such as cholesterol homeostasis, lipogenesis, inflammation and innate immunity. Synthetic LXR agonists are currently under development and could find applications in various fields such as cardiovascular diseases, cancer, diabetes and neurodegenerative diseases. The clinical development of LXR agonists requires the identification of biological markers for pharmacodynamic studies. In this context, monocytes represent an attractive target to monitor LXR activation. They are easily accessible cells present in peripheral blood; they express LXR α and ß and respond to LXR agonist stimulation in vitro. The aim of our study was to identify cell surface markers of LXR agonists on monocytes. For this, we focused on clusters of differentiation (CD) markers because they are well characterized and accessible cell surface molecules allowing easy immuno-phenotyping. METHODOLOGY/PRINCIPAL FINDINGS: By using microarray analysis of monocytes treated or not with an LXR agonist in vitro, we selected three CD, i.e. CD82, CD226, CD244 for further analysis by real time PCR and flow cytometry. The three CD were up-regulated by LXR agonist treatment in vitro in a time- and dose- dependent manner and this induction was LXR specific as assessed by a SiRNA or LXR antagonist strategy. By using flow cytometry, we could demonstrate that the expression of these molecules at the cell surface of monocytes was significantly increased after LXR agonist treatment. CONCLUSIONS/SIGNIFICANCE: We have identified three new cell surface markers that could be useful to monitor LXR activation. Future studies will be required to confirm the biological and diagnostic significance of the markers. [Mh] MeSH terms primary: Cell Membrane/metabolism Monocytes/cytology Monocytes/metabolism Orphan Nuclear Receptors/metabolism [Mh] MeSH terms secundary: Antigens, CD/genetics Antigens, CD/metabolism Biological Markers/metabolism Cell Membrane/drug effects Cholesterol/pharmacology Foam Cells/drug effects Foam Cells/metabolism Gene Expression Regulation/drug effects Gene Knockdown Techniques Humans Hydrocarbons, Fluorinated/pharmacology Macrophages/drug effects Macrophages/metabolism Monocytes/drug effects Orphan Nuclear Receptors/agonists RNA, Messenger/genetics RNA, Messenger/metabolism Sulfonamides/pharmacology [Pt] Publication type: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T [Nm] Name of substance: 0 (Antigens, CD); 0 (Biological Markers); 0 (Hydrocarbons, Fluorinated); 0 (Orphan Nuclear Receptors); 0 (RNA, Messenger); 0 (Sulfonamides); 0 (TO-901317); 0 (liver X receptor); 57-88-5 (Cholesterol) [Em] Entry month: 1305 [Js] Journal subset: IM [Da] Date of entry for processing: 121127 [St] Status: MEDLINE [do] DOI: 10.1371/journal.pone.0048738

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[PMID]: 23181442 [Au] Autor: Kim GH; Stevens R; Rodriguez P [Ad] Address: Department of Pathology, Keck School of Medicine of the University of Southern California, USA. genekim@usc.edu [Ti] Title: Anti-human milk fat globulin staining of perifollicular xanthomatosis in Fox-Fordyce disease. [So] Source: J Cutan Pathol;39(12):1057-9, 2012 Dec. [Is] ISSN: 1600-0560 [Cp] Country of publication: United States [La] Language: eng [Mh] MeSH terms primary: Fox-Fordyce Disease/diagnosis Immunoglobulin G/metabolism Lactoglobulins/immunology Xanthomatosis/diagnosis [Mh] MeSH terms secundary: Adult Axilla Carmine/chemistry Coloring Agents/chemistry Female Foam Cells/metabolism Foam Cells/pathology Fox-Fordyce Disease/complications Fox-Fordyce Disease/metabolism Humans Mucins/analysis Mucins/metabolism Staining and Labeling Xanthomatosis/etiology Xanthomatosis/metabolism [Pt] Publication type: CASE REPORTS; JOURNAL ARTICLE [Nm] Name of substance: 0 (Coloring Agents); 0 (Immunoglobulin G); 0 (Lactoglobulins); 0 (Mucins); 1260-17-9 (Carmine); 51395-97-2 (mucicarmine) [Em] Entry month: 1305 [Js] Journal subset: IM [Da] Date of entry for processing: 121127 [St] Status: MEDLINE [do] DOI: 10.1111/cup.12057

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[PMID]: 23498167 [Au] Autor: Yin Y; Liu W; Ji G; Dai Y [Ad] Address: Department of Immunology, Tongji University School of Medicine, 1239 Siping Road, Shanghai 200092, China. [Ti] Title: The essential role of p38 MAPK in mediating the interplay of oxLDL and IL-10 in regulating endothelial cell apoptosis. [So] Source: Eur J Cell Biol;92(4-5):150-9, 2013 Apr-May. [Is] ISSN: 1618-1298 [Cp] Country of publication: Germany [La] Language: eng [Ab] Abstract: Interleukin-10 (IL-10) may have therapeutic potential in various inflammatory diseases, including atherosclerosis, as it can inhibit oxLDL-induced foam cell formation and apoptosis in macrophages. This study investigated the effect of IL-10 on mitogen-activated protein kinase (MAPK) activation, and apoptosis induced by oxidized low-density lipoprotein (oxLDL) in cultured human umbilical vein endothelial cells (HUVEC). The results demonstrated that IL-10 significantly blocked the phosphorylation of p38 MAPK and c-Jun N-terminal kinase (JNK) and apoptosis induced by oxLDL. The inhibitory effect of IL-10 on oxLDL-induced apoptosis was partially dependent on reduced p38, but not JNK, phosphorylation. This study also discovered a linkage between IL-10 and p38 MAPK signaling in oxLDL-induced endothelial cell apoptosis. Interestingly, this study found that lectin-like oxidized LDL receptor-1 (LOX-1) was the only scavenger receptor, on the surface of HUVEC, that was upregulated by oxLDL and the increase in LOX-1 was not suppressed by IL-10. This study confirmed that IL-10 significantly upregulated the expression of suppressor of cytokine signaling-3 (SOCS3), whereas SOCS3 knockdown by siRNA effectively blocked the inhibitory effect of IL-10 on p38 MAPK-dependent apoptosis induced by oxLDL. These results showed for the first time, that IL-10 modulated oxLDL-induced apoptosis by upregulating SOCS3, which then interrupted p38 MAPK activation in endothelial cells. These findings support the essential role of p38 MAPK in the interplay of oxLDL and IL-10 in endothelial apoptosis. [Pt] Publication type: JOURNAL ARTICLE [Em] Entry month: 1305 [Js] Journal subset: IM [St] Status: In-Data-Review

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[PMID]: 23549373 [Au] Autor: Li N; Zhang Q; Gao S; Song Q; Huang R; Wang L; Liu L; Dai J; Tang M; Cheng G [Ad] Address: Suzhou Key Laboratory of Nanobiomedicine & Division of Nanobiomedicine, Suzhou Institute of Nano-Tech and Nano-Bionics, Chinese Academy of Sciences, Suzhou, P. R. China. [Ti] Title: Three-dimensional graphene foam as a biocompatible and conductive scaffold for neural stem cells. [So] Source: Sci Rep;3:1604, 2013 Apr 3. [Is] ISSN: 2045-2322 [Cp] Country of publication: England [La] Language: eng [Ab] Abstract: Neural stem cell (NSC) based therapy provides a promising approach for neural regeneration. For the success of NSC clinical application, a scaffold is required to provide three-dimensional (3D) cell growth microenvironments and appropriate synergistic cell guidance cues. Here, we report the first utilization of graphene foam, a 3D porous structure, as a novel scaffold for NSCs in vitro. It was found that three-dimensional graphene foams (3D-GFs) can not only support NSC growth, but also keep cell at an active proliferation state with upregulation of Ki67 expression than that of two-dimensional graphene films. Meanwhile, phenotypic analysis indicated that 3D-GFs can enhance the NSC differentiation towards astrocytes and especially neurons. Furthermore, a good electrical coupling of 3D-GFs with differentiated NSCs for efficient electrical stimulation was observed. Our findings implicate 3D-GFs could offer a powerful platform for NSC research, neural tissue engineering and neural prostheses. [Pt] Publication type: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S. [Em] Entry month: 1304 [Js] Journal subset: IM [St] Status: In-Process [do] DOI: 10.1038/srep01604

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[PMID]: 23306836 [Au] Autor: McConnell R; Wu W; Berhane K; Liu F; Verma G; Peden D; Diaz-Sanchez D; Fruin S [Ad] Address: Department of Preventive Medicine, Keck School of Medicine, University of Southern California, Los Angeles, CA 90089, USA. rmcconne@usc.edu [Ti] Title: Inflammatory cytokine response to ambient particles varies due to field collection procedures. [So] Source: Am J Respir Cell Mol Biol;48(4):497-502, 2013 Apr. [Is] ISSN: 1535-4989 [Cp] Country of publication: United States [La] Language: eng [Ab] Abstract: In vitro assays of biological activity induced by particulate matter (PM) are a tool for investigating mechanisms of PM health effects. They have potential application to exposure assessment in chronic disease epidemiology. However, there has been little reporting of the impact of real-world PM collection techniques on assay results. Therefore, we examined the effect of sampling duration and postsampling delays in freezing on PM-induced biological activity. Duplicate samples of respirable ambient Los Angeles PM were collected on polyurethane foam filters during 17 days and during three contemporaneous consecutive shorter periods. After collection, one duplicate was stored at ambient temperature for 24 hours before freezing; the other was frozen immediately. Cytokine response (IL-1ß, IL-6, IL-8, and TNF-α) to PM aqueous extract was assessed in THP-1 cells, a model for evaluating monocyte/macrophage lineage cell responses. There was consistent 3- to 4-fold variation in PM-induced cytokine levels across the three collection intervals. Compared with levels induced by PM pooled across the three periods, continuously collected PM-induced levels were reduced by 25% (IL-6) to 39% (IL-8). The pattern of cytokine gene expression response was similar. Cytokine level variation by time to freezing was not statistically significant. PM-induced inflammatory response varied substantially over a weekly time scale. We conclude that long PM sampling interval induced less activity than the average of equivalent shorter consecutive sampling intervals. Time to freezing was less important. Implications for development of metrics of long-term spatial variation in biological exposure metrics for study of chronic disease merit further investigation. [Pt] Publication type: JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S. [Em] Entry month: 1304 [Js] Journal subset: IM [St] Status: In-Process [do] DOI: 10.1165/rcmb.2012-0320OC

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[PMID]: 23234806 [Au] Autor: Debata PR; Castellanos MR; Fata JE; Baggett S; Rajupet S; Szerszen A; Begum S; Mata A; Murty VV; Opitz LM; Banerjee P [Ad] Address: Department of Chemistry, The College of Staten Island (CUNY), Staten Island, NY 10314, USA. [Ti] Title: A novel curcumin-based vaginal cream Vacurin selectively eliminates apposed human cervical cancer cells. [So] Source: Gynecol Oncol;129(1):145-53, 2013 Apr. [Is] ISSN: 1095-6859 [Cp] Country of publication: United States [La] Language: eng [Ab] Abstract: OBJECTIVE: Human papillomavirus (HPV) infections remain a leading cause of mortality worldwide. In the U.S. strategies via screening and vaccination prevent HPV-associated cervical neoplasms, but consume immense healthcare costs. The spice component curcumin has potent anticancer and antiviral properties, which have been difficult to harness as a treatment, due to its poor systemic bioavailability. This project tests the possibility of developing a curcumin-based therapy for cervical cancer. METHODS: Using four HPV(+) cervical cancer cell lines and normal fibroblasts we first tested the selectivity and potency of curcumin in eliminating HPV(+) cells. Subsequently, we developed a curcumin-based cervical cream and tested its efficacy in eliminating apposed HPV(+) cells and also its possible side effects on the vaginal epithelium of healthy mice. RESULTS: Curcumin selectively eliminates a variety of HPV(+) cervical cancer cells (HeLa, ME-180, SiHa, and SW756), suppresses the transforming antigen E6, dramatically inhibits the expression of the pro-cancer protein epidermal growth factor receptor (EGFR), and concomitantly induces p53. Additionally, Vacurin, a uniform colloidal solution of curcumin in a clinically used amphipathic vaginal cream, eliminates apposed HeLa cells while suppressing the expression of EGFR. In mice, daily intravaginal application of Vacurin for three weeks produced no change in body weight and when the mice were sacrificed, the vaginal tract epithelium showed no Vacurin-evoked adverse effects. CONCLUSION: We have developed a curcumin-based vaginal cream, which effectively eradicates HPV(+) cancer cells and does not affect non-cancerous tissue. Our preclinical data support a novel approach for the treatment of cervical HPV infection. [Mh] MeSH terms primary: Curcumin/administration & dosage Uterine Cervical Neoplasms/drug therapy Vaginal Creams, Foams, and Jellies [Mh] MeSH terms secundary: Animals Cell Survival/drug effects Female HeLa Cells Humans Mice Oncogene Proteins, Viral/antagonists & inhibitors Papillomaviridae/isolation & purification Receptor, Epidermal Growth Factor/antagonists & inhibitors Repressor Proteins/antagonists & inhibitors Uterine Cervical Neoplasms/pathology Uterine Cervical Neoplasms/virology [Pt] Publication type: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T [Nm] Name of substance: 0 (E6 protein, Human papillomavirus type 16); 0 (Oncogene Proteins, Viral); 0 (Repressor Proteins); 0 (Vaginal Creams, Foams, and Jellies); 458-37-7 (Curcumin); EC 2.7.10.1 (Receptor, Epidermal Growth Factor) [Em] Entry month: 1305 [Js] Journal subset: IM [Da] Date of entry for processing: 130325 [St] Status: MEDLINE

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