Database : MEDLINE
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[PMID]: 25434823
[Au] Autor:Zhang QS; Benedetti E; Deater M; Schubert K; Major A; Pelz C; Impey S; Marquez-Loza L; Rathbun RK; Kato S; Bagby GC; Grompe M
[Ad] Address:Oregon Stem Cell Center, Department of Pediatrics, Oregon Health & Science University, Portland, OR 97239, USA. Electronic address: zhangqi@ohsu.edu....
[Ti] Title:Oxymetholone therapy of fanconi anemia suppresses osteopontin transcription and induces hematopoietic stem cell cycling.
[So] Source:Stem Cell Reports;4(1):90-102, 2015 Jan 13.
[Is] ISSN:2213-6711
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Androgens are widely used for treating Fanconi anemia (FA) and other human bone marrow failure syndromes, but their mode of action remains incompletely understood. Aged Fancd2(-/-) mice were used to assess the therapeutic efficacy of oxymetholone (OXM) and its mechanism of action. Eighteen-month-old Fancd2(-/-) mice recapitulated key human FA phenotypes, including reduced bone marrow cellularity, red cell macrocytosis, and peripheral pancytopenia. As in humans, chronic OXM treatment significantly improved these hematological parameters and stimulated the proliferation of hematopoietic stem and progenitor cells. RNA-Seq analysis implicated downregulation of osteopontin as an important potential mechanism for the drug's action. Consistent with the increased stem cell proliferation, competitive repopulation assays demonstrated that chronic OXM therapy eventually resulted in stem cell exhaustion. These results expand our knowledge of the regulation of hematopoietic stem cell proliferation and have direct clinical implications for the treatment of bone marrow failure.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1501
[Cu] Class update date: 150117
[Lr] Last revision date:150117
[Js] Journal subset:IM
[St] Status:In-Data-Review

  2 / 315805 MEDLINE  
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[PMID]: 25412163
[Au] Autor:Blue EK; Ballman K; Boyle F; Oh E; Kono T; Quinney SK; Thurmond DC; Evans-Molina C; Haneline LS
[Ad] Address:1] Department of Pediatrics, Indiana University School of Medicine, Indianapolis, Indiana [2] Herman B Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, Indiana....
[Ti] Title:Fetal hyperglycemia and a high-fat diet contribute to aberrant glucose tolerance and hematopoiesis in adult rats.
[So] Source:Pediatr Res;77(2):316-25, 2015 Feb.
[Is] ISSN:1530-0447
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: Children exposed to gestational diabetes mellitus (GDM) during pregnancy are at increased risk of obesity, diabetes, and hypertension. Our goal was to identify metabolic and hematopoietic alterations after intrauterine exposure to maternal hyperglycemia that may contribute to the pathogenesis of chronic morbidities. METHODS: Streptozotocin treatment induced maternal hyperglycemia during the last third of gestation in rat dams. Offspring of control mothers (OCM) and diabetic mothers (ODM) were evaluated for weight, glucose tolerance, insulin tolerance, and hematopoiesis defects. The effects of aging were examined in normal and high-fat diet (HFD)-fed young (8-wk-old) and aged (11-mo-old) OCM and ODM rats. RESULTS: Young adult ODM males on a normal diet, but not females, displayed improved glucose tolerance due to increased insulin levels. Aged ODM males and females gained more weight than OCM on a HFD and had worse glucose tolerance. Aged ODM males fed a HFD were also neutrophilic. Increases in bone marrow cellularity and myeloid progenitors preceded neutrophilia in ODM males fed a HFD. CONCLUSION: When combined with other risk factors like HFD and aging, changes in glucose metabolism and hematopoiesis may contribute to the increased risk of obesity, type 2 diabetes, and hypertension observed in children of GDM mothers.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1501
[Cu] Class update date: 150117
[Lr] Last revision date:150117
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1038/pr.2014.185

  3 / 315805 MEDLINE  
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[PMID]: 25139998
[Au] Autor:Jung Y; Wang J; Lee E; McGee S; Berry JE; Yumoto K; Dai J; Keller ET; Shiozawa Y; Taichman RS
[Ad] Address:Department of Periodontics and Oral Medicine, University of Michigan School of Dentistry, Ann Arbor, Michigan....
[Ti] Title:Annexin 2-CXCL12 Interactions Regulate Metastatic Cell Targeting and Growth in the Bone Marrow.
[So] Source:Mol Cancer Res;13(1):197-207, 2015 Jan.
[Is] ISSN:1557-3125
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:UNLABELLED: Annexin 2 (ANXA2) plays a critical role in hematopoietic stem cell (HSC) localization to the marrow niche. In part, ANXA2 supports HSCs by serving as an anchor for stromal-derived factor-1 (CXCL12/SDF-1). Recently, it was demonstrated that prostate cancer cells, like HSCs, use ANXA2 to establish metastases in marrow. The present study determined the capacity of ANXA2 expression by bone marrow stromal cells (BMSC) to facilitate tumor recruitment and growth through ANXA2-CXCL12 interactions. Significantly more CXCL12 was expressed by BMSC(Anxa2) (+/+) than by BMSC(Anxa2) (-/-) resulting in more prostate cancer cells migrating and binding to BMSC(Anxa2) (+/+) than BMSC(Anxa2) (-/-), and these activities were reduced when CXCL12 interactions were blocked. To further confirm that BMSC signaling through ANXA2-CXCL12 plays a critical role in tumor growth, immunocompromised SCID mice were subcutaneously implanted with human prostate cancer cells mixed with BMSC(Anxa2) (+/+) or BMSC(Anxa2) (-/-). Significantly larger tumors grew in the mice when the tumors were established with BMSC(Anxa2) (+/+) compared with the tumors established with BMSC(Anxa2) (-/-). In addition, fewer prostate cancer cells underwent apoptosis when cocultured with BMSC(Anxa2) (+/+) compared with BMSC(Anxa2) (-/-), and similar results were obtained in tumors grown in vivo. Finally, significantly more vascular structures were observed in the tumors established with the BMSC(Anxa2) (+/+) compared with the tumors established with BMSC(Anxa2) (-/-). Thus, ANXA2-CXCL12 interactions play a crucial role in the recruitment, growth, and survival of prostate cancer cells in the marrow. IMPLICATIONS: The tumor microenvironment interaction between ANXA2-CXCL12 is critical for metastatic phenotypes and may impact chemotherapeutic potential. Mol Cancer Res; 13(1); 197-207. ©2014 AACR.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1501
[Cu] Class update date: 150117
[Lr] Last revision date:150117
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1158/1541-7786.MCR-14-0118

  4 / 315805 MEDLINE  
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[PMID]: 25548223
[Au] Autor:Nakagawa Y; Gallo RL
[Ad] Address:Division of Dermatology, University of California, San Diego, San Diego, CA 92161.
[Ti] Title:Endogenous Intracellular Cathelicidin Enhances TLR9 Activation in Dendritic Cells and Macrophages.
[So] Source:J Immunol;194(3):1274-84, 2015 Feb 1.
[Is] ISSN:1550-6606
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Cathelicidins are a gene family best known for their antimicrobial action, but the diverse mature peptides they encode also have other host defense functions. The human cathelicidin peptide LL-37 enhances recognition of nucleic acids, an action whose significance is seen in human diseases such as psoriasis where it is associated with increased type 1 IFN production. This function has been attributed to the extracellular action of the peptide to facilitate uptake of nucleic acids. In this study, we demonstrate that the murine mature cathelicidin peptide (CRAMP), encoded by the mouse gene (Camp), is functionally distinct from the human mature peptide (LL-37), as it does not facilitate CpG entry. However, mouse cathelicidin does influence recognition of CpG as bone marrow-derived dendritic cells from Camp(-/-) mice have impaired CpG responses and Camp(-/-) mice had impaired response to CpG given i.v. or s.c. We show that cathelicidin concentrates in Lamp1 positive compartments, is colocalized with CpG in the endolysosome, can be immunoprecipitated with TLR9, and binds to CpG intracellulary. Collectively, these results indicate that the functions of cathelicidin in control of TLR9 activation may include both intracellular and extracellular effects.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1501
[Cu] Class update date: 150117
[Lr] Last revision date:150117
[Js] Journal subset:AIM; IM
[St] Status:In-Data-Review
[do] DOI:10.4049/jimmunol.1402388

  5 / 315805 MEDLINE  
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[PMID]: 25535285
[Au] Autor:Kant CD; Akiyama Y; Tanaka K; Shea S; Yamada Y; Connolly SE; Marino J; Tocco G; Benichou G
[Ad] Address:Transplantation Research Center, Department of Surgery, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114....
[Ti] Title:Both rejection and tolerance of allografts can occur in the absence of secondary lymphoid tissues.
[So] Source:J Immunol;194(3):1364-71, 2015 Feb 1.
[Is] ISSN:1550-6606
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:In this study, we showed that aly/aly mice, which are devoid of lymph nodes and Peyer's patches, acutely rejected fully allogeneic skin and heart grafts. They mounted potent inflammatory direct alloresponses but failed to develop indirect alloreactivity after transplantation. Remarkably, skin allografts also were rejected acutely by splenectomized aly/aly (aly/aly-spl(-)) mice devoid of all secondary lymphoid organs. In these recipients, the rejection was mediated by alloreactive CD8(+) T cells presumably primed in the bone marrow. In contrast, cardiac transplants were not rejected by aly/aly-spl(-) mice. Actually, aly/aly-spl(-) mice that spontaneously accepted a heart allotransplant and displayed donor-specific tolerance also accepted skin grafts from the same, but not a third-party, donor via a mechanism involving CD4(+) regulatory T cells producing IL-10 cytokine. Therefore, direct priming of alloreactive T cells, as well as rejection and regulatory tolerance of allogeneic transplants, can occur in recipient mice lacking secondary lymphoid organs.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1501
[Cu] Class update date: 150117
[Lr] Last revision date:150117
[Js] Journal subset:AIM; IM
[St] Status:In-Data-Review
[do] DOI:10.4049/jimmunol.1401157

  6 / 315805 MEDLINE  
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[PMID]: 25527787
[Au] Autor:Yao Y; Matsushima H; Ohtola JA; Geng S; Lu R; Takashima A
[Ad] Address:Department of Medical Microbiology and Immunology, University of Toledo College of Medicine, Toledo, OH 43614....
[Ti] Title:Neutrophil Priming Occurs in a Sequential Manner and Can Be Visualized in Living Animals by Monitoring IL-1ß Promoter Activation.
[So] Source:J Immunol;194(3):1211-24, 2015 Feb 1.
[Is] ISSN:1550-6606
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Rapid enhancement of phagocyte functionality is a hallmark of neutrophil priming. GeneChip analyses unveiled elevated CD54, dectin-2, and IL-1ß mRNA expression by neutrophils isolated from inflammatory sites. In fact, CD54 and dectin-2 protein expression was detected on neutrophils recovered from skin, peritoneal, and lung inflammation lesions but not on those in bone marrow or peripheral blood. Neutrophils increased CD54 and dectin-2 mRNA during migration in Boyden chambers and acquired CD54 and dectin-2 surface expression after subsequent exposure to GM-CSF. Neutrophils purified from IL-1ß promoter-driven DsRed-transgenic mice acquired DsRed signals during cell migration or exposure to GM-CSF. CD54 and dectin-2 were expressed by DsRed(+) (but not DsRed(-)) neutrophils in GM-CSF-supplemented cultures, and neutrophils recovered from inflammatory sites exhibited strong DsRed signals. The dynamic process of neutrophil priming was studied in chemically induced inflammatory skin lesions by monitoring DsRed expression using confocal microscopy. A majority (>80%) of Ly6G(+) neutrophils expressed DsRed, and those DsRed(+)/Ly6G(+) cells exhibited crawling motion with a higher velocity compared with their DsRed(-)/Ly6G(+) counterparts. This report unveils motile behaviors of primed neutrophils in living animals. We propose that neutrophil priming occurs in a sequential manner with rapid enhancement of phagocyte functionality, followed by CD54 and dectin-2 mRNA and protein expression, IL-1ß promoter activation, and accelerated motility. Not only do these findings provide a new conceptual framework for our understanding of the process of neutrophil priming, they also unveil new insights into the pathophysiology of many inflammatory disorders that are characterized by neutrophil infiltration.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1501
[Cu] Class update date: 150117
[Lr] Last revision date:150117
[Js] Journal subset:AIM; IM
[St] Status:In-Data-Review
[do] DOI:10.4049/jimmunol.1402018

  7 / 315805 MEDLINE  
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[PMID]: 25527786
[Au] Autor:Li Y; Chen HL; Bannick N; Henry M; Holm AN; Metwali A; Urban JF; Rothman PB; Weiner GJ; Blazar BR; Elliott DE; Ince MN
[Ad] Address:Department of Internal Medicine, Carver College of Medicine, University of Iowa, Iowa City, IA 52242;...
[Ti] Title:Intestinal Helminths Regulate Lethal Acute Graft-versus-Host Disease and Preserve the Graft-versus-Tumor Effect in Mice.
[So] Source:J Immunol;194(3):1011-20, 2015 Feb 1.
[Is] ISSN:1550-6606
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Donor T lymphocyte transfer with hematopoietic stem cells suppresses residual tumor growth (graft-versus-tumor [GVT]) in cancer patients undergoing bone marrow transplantation (BMT). However, donor T cell reactivity to host organs causes severe and potentially lethal inflammation called graft-versus-host disease (GVHD). High-dose steroids or other immunosuppressive drugs are used to treat GVHD that have limited ability to control the inflammation while incurring long-term toxicity. Novel strategies are needed to modulate GVHD, preserve GVT, and improve the outcome of BMT. Regulatory T cells (Tregs) control alloantigen-sensitized inflammation of GVHD, sustain GVT, and prevent mortality in BMT. Helminths colonizing the alimentary tract dramatically increase the Treg activity, thereby modulating intestinal or systemic inflammatory responses. These observations led us to hypothesize that helminths can regulate GVHD and maintain GVT in mice. Acute GVHD was induced in helminth (Heligmosomoides polygyrus)-infected or uninfected BALB/c recipients of C57BL/6 donor grafts. Helminth infection suppressed donor T cell inflammatory cytokine generation and reduced GVHD-related mortality, but maintained GVT. H. polygyrus colonization promoted the survival of TGF-ß-generating recipient Tregs after a conditioning regimen with total body irradiation and led to a TGF-ß-dependent in vivo expansion/maturation of donor Tregs after BMT. Helminths did not control GVHD when T cells unresponsive to TGF-ß-mediated immune regulation were used as donor T lymphocytes. These results suggest that helminths suppress acute GVHD using Tregs and TGF-ß-dependent pathways in mice. Helminthic regulation of GVHD and GVT through intestinal immune conditioning may improve the outcome of BMT.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1501
[Cu] Class update date: 150117
[Lr] Last revision date:150117
[Js] Journal subset:AIM; IM
[St] Status:In-Data-Review
[do] DOI:10.4049/jimmunol.1303099

  8 / 315805 MEDLINE  
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[PMID]: 24469043
[Au] Autor:Sales KU; Friis S; Konkel JE; Godiksen S; Hatakeyama M; Hansen KK; Rogatto SR; Szabo R; Vogel LK; Chen W; Gutkind JS; Bugge TH
[Ad] Address:1] Oral and Pharyngeal Cancer Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD, USA [2] Clinical Research Core, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD, USA....
[Ti] Title:Non-hematopoietic PAR-2 is essential for matriptase-driven pre-malignant progression and potentiation of ras-mediated squamous cell carcinogenesis.
[So] Source:Oncogene;34(3):346-56, 2015 Jan 15.
[Is] ISSN:1476-5594
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:The membrane-anchored serine protease, matriptase, is consistently dysregulated in a range of human carcinomas, and high matriptase activity correlates with poor prognosis. Furthermore, matriptase is unique among tumor-associated proteases in that epithelial stem cell expression of the protease suffices to induce malignant transformation. Here, we use genetic epistasis analysis to identify proteinase-activated receptor (PAR)-2-dependent inflammatory signaling as an essential component of matriptase-mediated oncogenesis. In cell-based assays, matriptase was a potent activator of PAR-2, and PAR-2 activation by matriptase caused robust induction of nuclear factor (NF)κB through Gαi. Importantly, genetic elimination of PAR-2 from mice completely prevented matriptase-induced pre-malignant progression, including inflammatory cytokine production, inflammatory cell recruitment, epidermal hyperplasia and dermal fibrosis. Selective ablation of PAR-2 from bone marrow-derived cells did not prevent matriptase-driven pre-malignant progression, indicating that matriptase activates keratinocyte stem cell PAR-2 to elicit its pro-inflammatory and pro-tumorigenic effects. When combined with previous studies, our data suggest that dual induction of PAR-2-NFκB inflammatory signaling and PI3K-Akt-mTor survival/proliferative signaling underlies the transforming potential of matriptase and may contribute to pro-tumorigenic signaling in human epithelial carcinogenesis.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1501
[Cu] Class update date: 150117
[Lr] Last revision date:150117
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1038/onc.2013.563

  9 / 315805 MEDLINE  
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[PMID]: 25404732
[Au] Autor:Stewart MD; Ramani VC; Sanderson RD
[Ad] Address:From the Department of Pathology.
[Ti] Title:Shed Syndecan-1 Translocates to the Nucleus of Cells Delivering Growth Factors and Inhibiting Histone Acetylation: A NOVEL MECHANISM OF TUMOR-HOST CROSS-TALK.
[So] Source:J Biol Chem;290(2):941-9, 2015 Jan 9.
[Is] ISSN:1083-351X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The heparan sulfate proteoglycan syndecan-1 is proteolytically shed from the surface of multiple myeloma cells and is abundant in the bone marrow microenvironment where it promotes tumor growth, angiogenesis, and metastasis. In this study, we demonstrate for the first time that shed syndecan-1 present in the medium conditioned by tumor cells is taken up by bone marrow-derived stromal cells and transported to the nucleus. Translocation of shed syndecan-1 (sSDC1) to the nucleus was blocked by addition of exogenous heparin or heparan sulfate, pretreatment of conditioned medium with heparinase III, or growth of cells in sodium chlorate, indicating that sulfated heparan sulfate chains are required for nuclear translocation. Interestingly, cargo bound to sSDC1 heparan sulfate chains (i.e. hepatocyte growth factor) was transported to the nucleus along with sSDC1, and removal of heparan sulfate-bound cargo from sSDC1 abolished its translocation to the nucleus. Once in the nucleus, sSDC1 binds to the histone acetyltransferase enzyme p300, and histone acetyltransferase activity and histone acetylation are diminished. These findings reveal a novel function for shed syndecan-1 in mediating tumor-host cross-talk by shuttling growth factors to the nucleus and by altering histone acetylation in host cells. In addition, this work has broad implications beyond myeloma because shed syndecan-1 is present in high levels in many tumor types as well as in other disease states.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1501
[Cu] Class update date: 150117
[Lr] Last revision date:150117
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1074/jbc.M114.608455

  10 / 315805 MEDLINE  
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[PMID]: 25573522
[Au] Autor:Norman G; Fayter D; Lewis-Light K; Chisholm J; McHugh K; Levine D; Jenney M; Mandeville H; Gatz S; Phillips B
[Ad] Address:Centre for Reviews and Dissemination, University of York, York, North Yorkshire, UK....
[Ti] Title:An emerging evidence base for PET-CT in the management of childhood rhabdomyosarcoma: systematic review.
[So] Source:BMJ Open;5(1):e006030, 2015.
[Is] ISSN:2044-6055
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:INTRODUCTION: Rhabdomyosarcoma (RMS) management depends on risk stratification at diagnosis and treatment response. Assessment methods include CT, MRI, bone scintigraphy, histological analysis and bone marrow biopsy. Advanced functional imaging (FI) has potential to improve staging accuracy and management strategies. METHODS AND ANALYSIS: We conducted a systematic review (PROSPERO 2013:CRD42013006128) of diagnostic accuracy and clinical effectiveness of FI in histologically proven paediatric RMS. PRISMA guidance was followed. We searched 10 databases to November 2013. Studies with ≥10 patients with RMS which compared positron emission tomography (PET), PET-CT or diffusion-weighted imaging (DWI) MRI to conventional imaging at any treatment stage were included. Study quality was assessed. Limited, heterogeneous effectiveness data required narrative synthesis, illustrated by plotting sensitivity and specificity in receiver operating curve (ROC) space. RESULTS: Eight studies (six PET-CT, two PET) with 272 RMS patients in total were included. No DWI-MRI studies met inclusion criteria. Pooled estimates were not calculated due to sparseness of data. Limited evidence indicated initial PET-CT results were predictive of survival. PET-CT changed management of 7/40 patients. Nodal involvement PET-CT: sensitivity ranged from 80% to 100%; specificity from 89% to 100%. Distant metastatic involvement: PET-CT sensitivity ranged from 95% to 100%; specificity from 80% to100%. Data on metastases in different sites were sparse. Limited data were found on outcome prediction by PET-CT response. DISSEMINATION AND ETHICS: PET/PET-CT may increase initial staging accuracy in paediatric RMS, specifically in the detection of nodal involvement and distant metastatic spread. There is a need to further assess PET-CT for this population, ideally in a representative, unbiased and transparently selected cohort of patients.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1501
[Cu] Class update date: 150117
[Lr] Last revision date:150117
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1136/bmjopen-2014-006030


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