Database : MEDLINE
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[PMID]: 25537019
[Au] Autor:Chae M; Peterson TE; Balgeman A; Chen S; Zhang L; Renner DN; Johnson AJ; Parney IF
[Ad] Address:Department of Neurological Surgery (M.C., T.E.P., A.B., S.C., L.Z., I.F.P.) and Department of Immunology, Mayo Clinic, Rochester, Minnesota (D.N.R., A.J.J.)....
[Ti] Title:Increasing glioma-associated monocytes leads to increased intratumoral and systemic myeloid-derived suppressor cells in a murine model.
[So] Source:Neuro Oncol;17(7):978-91, 2015 Jul.
[Is] ISSN:1523-5866
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Patients with glioblastoma multiforme (GBM) exhibit marked intratumoral and systemic immunosuppression. GBM is heavily infiltrated with monocytic cells. Monocytes contacting GBM cells develop features of immunosuppressive myeloid-derived suppressor cells (MDSCs), which are elevated in GBM patients. Therefore, we hypothesized that circulating MDSC levels could be raised in vivo by increasing glioma-associated macrophages. METHODS: GL261-luciferase glioma was implanted intracranially in C57BL/6 mice with or without additional normal syngeneic CD11b+ monocytes. Tumor growth and intratumoral and systemic MDSC (CD11b+/Gr-1+) levels were determined. Green fluorescent protein (GFP)-transgenic monocytes were coinjected intracranially with GL261-luciferase cells. GFP+ cell frequency among splenic and bone marrow MDSCs was determined. Impact of increased MDSC's on spontaneous immune responses to tumor cells expressing a model antigen (ovalbumin [OVA]) was determined. RESULTS: Tumors grew faster and MDSC's were increased in tumor, spleen, and bone marrow in mice receiving GL261-Luc plus monocytes. Many (30%-50%) systemic MDSC's were GFP+ in mice receiving intracranial tumor plus GFP-transgenic monocytes, suggesting that they originated from glioma-associated monocytes. Tumor-infiltrating OVA-specific CD8+ T cells were markedly reduced in mice receiving GL261-OVA and monocytes compared with mice receiving GL261-OVA alone. CONCLUSIONS: Increasing glioma-associated macrophages in intracranial GL261 glioma decreases survival and markedly increases intratumoral and systemic MDSC's, many of which originate directly from glioma-associated macrophages. This is associated with decreased spontaneous immune responses to a model antigen. To our knowledge, this is the first evidence in cancer that systemic MDSC's can arise directly from normal monocytes that have undergone intratumoral immunosuppressive education.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1506
[Cu] Class update date: 150620
[Lr] Last revision date:150620
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1093/neuonc/nou343

  2 / 322246 MEDLINE  
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[PMID]: 26026062
[Au] Autor:Tampella G; Kerns HM; Niu D; Singh S; Khim S; Bosch KA; Garrett ME; Moguche A; Evans E; Browning B; Jahan TA; Nacht M; Wolf-Yadlin A; Plebani A; Hamerman JA; Rawlings DJ; James RG
[Ad] Address:Seattle Children's Research Institute, Seattle WA 98101;...
[Ti] Title:The Tec Kinase-Regulated Phosphoproteome Reveals a Mechanism for the Regulation of Inhibitory Signals in Murine Macrophages.
[So] Source:J Immunol;195(1):246-56, 2015 Jul 1.
[Is] ISSN:1550-6606
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Previous work has shown conflicting roles for Tec family kinases in regulation of TLR-dependent signaling in myeloid cells. In the present study, we performed a detailed investigation of the role of the Tec kinases Btk and Tec kinases in regulating TLR signaling in several types of primary murine macrophages. We demonstrate that primary resident peritoneal macrophages deficient for Btk and Tec secrete less proinflammatory cytokines in response to TLR stimulation than do wild-type cells. In contrast, we found that bone marrow-derived and thioglycollate-elicited peritoneal macrophages deficient for Btk and Tec secrete more proinflammatory cytokines than do wild-type cells. We then compared the phosphoproteome regulated by Tec kinases and LPS in primary peritoneal and bone marrow-derived macrophages. From this analysis we determined that Tec kinases regulate different signaling programs in these cell types. In additional studies using bone marrow-derived macrophages, we found that Tec and Btk promote phosphorylation events necessary for immunoreceptor-mediated inhibition of TLR signaling. Taken together, our results are consistent with a model where Tec kinases (Btk, Tec, Bmx) are required for TLR-dependent signaling in many types of myeloid cells. However, our data also support a cell type-specific TLR inhibitory role for Btk and Tec that is mediated by immunoreceptor activation and signaling via PI3K.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1506
[Cu] Class update date: 150620
[Lr] Last revision date:150620
[Js] Journal subset:AIM; IM
[St] Status:In-Data-Review
[do] DOI:10.4049/jimmunol.1403238

  3 / 322246 MEDLINE  
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[PMID]: 26002975
[Au] Autor:Wang Y; Park NY; Jang Y; Ma A; Jiang Q
[Ad] Address:Department of Nutrition Science, Purdue University, West Lafayette, IN 47907; and....
[Ti] Title:Vitamin E γ-Tocotrienol Inhibits Cytokine-Stimulated NF-κB Activation by Induction of Anti-Inflammatory A20 via Stress Adaptive Response Due to Modulation of Sphingolipids.
[So] Source:J Immunol;195(1):126-33, 2015 Jul 1.
[Is] ISSN:1550-6606
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:NF-κB plays a central role in pathogenesis of inflammation and cancer. Many phytochemicals, including γ-tocotrienol (γTE), a natural form of vitamin E, have been shown to inhibit NF-κB activation, but the underlying mechanism has not been identified. In this study, we show that γTE inhibited cytokine-triggered activation of NF-κB and its upstream regulator TGF--activated kinase-1 in murine RAW 264.7 macrophages and primary bone marrow-derived macrophages. In these cells, γTE induced upregulation of A20, an inhibitor of NF-κB. Knockout of A20 partially diminished γTE's anti-NF-κB effect, but γTE increased another NF-κB inhibitor, Cezanne, in A20(-/-) cells. In search of the reason for A20 upregulation, we found that γTE treatment increased phosphorylation of translation initiation factor 2, IκBα, and JNK, indicating induction of endoplasmic reticulum stress. Liquid chromatography-tandem mass spectrometry analyses revealed that γTE modulated sphingolipids, including enhancement of intracellular dihydroceramides, sphingoid bases in de novo synthesis of the sphingolipid pathway. Chemical inhibition of de novo sphingolipid synthesis partially reversed γTE's induction of A20 and the anti-NF-κB effect. The importance of dihydroceramide increase is further supported by the observation that C8-dihydroceramide mimicked γTE in upregulating A20, enhancing endoplasmic reticulum stress, and attenuating TNF-triggered NF-κB activation. Our study identifies a novel anti-NF-κB mechanism where A20 is induced by stress-induced adaptive response as a result of modulation of sphingolipids, and it demonstrates an immunomodulatory role of dihydrocermides.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1506
[Cu] Class update date: 150620
[Lr] Last revision date:150620
[Js] Journal subset:AIM; IM
[St] Status:In-Data-Review
[do] DOI:10.4049/jimmunol.1403149

  4 / 322246 MEDLINE  
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[PMID]: 25994969
[Au] Autor:Eddens T; Elsegeiny W; Nelson MP; Horne W; Campfield BT; Steele C; Kolls JK
[Ad] Address:Department of Immunology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15224; Richard King Mellon Foundation Institute for Pediatric Research, Children's Hospital of Pittsburgh of University of Pittsburgh Medical Center, Pittsburgh, PA 15224;...
[Ti] Title:Eosinophils Contribute to Early Clearance of Pneumocystis murina Infection.
[So] Source:J Immunol;195(1):185-93, 2015 Jul 1.
[Is] ISSN:1550-6606
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Pneumocystis pneumonia remains a common opportunistic infection in the diverse immunosuppressed population. One clear risk factor for susceptibility to Pneumocystis is a declining CD4(+) T cell count in the setting of HIV/AIDS or primary immunodeficiency. Non-HIV-infected individuals taking immunosuppressive drug regimens targeting T cell activation are also susceptible. Given the crucial role of CD4(+) T cells in host defense against Pneumocystis, we used RNA sequencing of whole lung early in infection in wild-type and CD4-depleted animals as an unbiased approach to examine mechanisms of fungal clearance. In wild-type mice, a strong eosinophil signature was observed at day 14 post Pneumocystis challenge, and eosinophils were increased in the bronchoalveolar lavage fluid of wild-type mice. Furthermore, eosinophilopoiesis-deficient Gata1(tm6Sho)/J mice were more susceptible to Pneumocystis infection when compared with BALB/c controls, and bone marrow-derived eosinophils had in vitro Pneumocystis killing activity. To drive eosinophilia in vivo, Rag1(-/-) mice were treated with a plasmid expressing IL-5 (pIL5) or an empty plasmid control via hydrodynamic injection. The pIL5-treated mice had increased serum IL-5 and eosinophilia in the lung, as well as reduced Pneumocystis burden, compared with mice treated with control plasmid. In addition, pIL5 treatment could induce eosinophilia and reduce Pneumocystis burden in CD4-depleted C57BL/6 and BALB/c mice, but not eosinophilopoiesis-deficient Gata1(tm6Sho)/J mice. Taken together, these results demonstrate that an early role of CD4(+) T cells is to recruit eosinophils to the lung and that eosinophils are a novel candidate for future therapeutic development in the treatment of Pneumocystis pneumonia in the immunosuppressed population.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1506
[Cu] Class update date: 150620
[Lr] Last revision date:150620
[Js] Journal subset:AIM; IM
[St] Status:In-Data-Review
[do] DOI:10.4049/jimmunol.1403162

  5 / 322246 MEDLINE  
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[PMID]: 26041023
[Au] Autor:Suhett GD; de Souza SA; Carvalho AB; de Pinho Rachid R; da Cunha-E-Silva NL; de Carvalho AC; da Fonseca LM; Dos Santos Goldenberg RC; Gutfilen B
[Ad] Address:Laboratrio de Cardiologia Celular e Molecular, Instituto de Biofsica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro (UFRJ), Av. Carlos Chagas Filho, 373, Bloco G. Ilha do Fundo, Cidade Universitria, Rio de Janeiro, 21941-902, Brasil. grazisuhett@gmail.com....
[Ti] Title:99m-Technetium binding site in bone marrow mononuclear cells.
[So] Source:Stem Cell Res Ther;6:115, 2015.
[Is] ISSN:1757-6512
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:INTRODUCTION: The increasing interest in 99m-technetium ((99m)Tc)-labeled stem cells encouraged us to study the (99m)Tc binding sites in stem cell compartments. METHODS: Bone marrow mononuclear cells were collected from femurs and tibia of rats. Cells were labeled with (99m)Tc by a direct method, in which reduced molecules react with (99m)Tc with the use of chelating agents, and lysed carefully in an ultrasonic apparatus. The organelles were separated by means of differential centrifugation. At the end of this procedure, supernatants and pellets were counted, and the percentages of radioactivity (in megabecquerels) bound to the different cellular fractions were determined. Percentages were calculated by dividing the radioactivity in each fraction by total radioactivity in the sample. The pellets were separated and characterized by their morphology on electron microscopy. RESULTS: The labeling procedure did not affect viability of bone marrow mononuclear cells. Radioactivity distributions in bone marrow mononuclear cell organelles, obtained in five independent experiments, were approximately 38.5 % in the nuclei-rich fraction, 5.3 % in the mitochondria-rich fraction, 2.2 % in microsomes, and 54 % in the cytosol. Our results showed that most of the radioactivity remained in the cytosol; therefore, this is an intracellular labeling procedure that has ribosomes unbound to membrane and soluble molecules as targets. However, approximately 39 % of the radioactivity remained bound to the nuclei-rich fraction. To confirm that cell disruption and organelle separation were efficient, transmission electron microscopy assays of all pellets were performed. CONCLUSIONS: Our results showed that most of the radioactivity was present in the cytosol fraction. More studies to elucidate the mechanisms involved in the cellular uptake of (99m)Tc in bone marrow cells are ongoing.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1506
[Cu] Class update date: 150620
[Lr] Last revision date:150620
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1186/s13287-015-0107-0

  6 / 322246 MEDLINE  
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[PMID]: 26012584
[Au] Autor:Ma L; Aijima R; Hoshino Y; Yamaza H; Tomoda E; Tanaka Y; Sonoda S; Song G; Zhao W; Nonaka K; Shi S; Yamaza T
[Ad] Address:Department of Molecular Cell Biology and Oral Anatomy, Kyushu University Graduate School of Dental Science, 3-1-1 Maidashi, Higashi-ku, Fukuoka, 812-8582, Japan. malan2010@dent.kyushu-u.ac.jp....
[Ti] Title:Transplantation of mesenchymal stem cells ameliorates secondary osteoporosis through interleukin-17-impaired functions of recipient bone marrow mesenchymal stem cells in MRL/lpr mice.
[So] Source:Stem Cell Res Ther;6:104, 2015.
[Is] ISSN:1757-6512
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:INTRODUCTION: Secondary osteoporosis is common in systemic lupus erythematosus and leads to a reduction in quality of life due to fragility fractures, even in patients with improvement of the primary disorder. Systemic transplantation of mesenchymal stem cells could ameliorate bone loss and autoimmune disorders in a MRL/lpr mouse systemic lupus erythematosus model, but the detailed therapeutic mechanism of bone regeneration is not fully understood. In this study, we transplanted human bone marrow mesenchymal stem cells (BMMSCs) and stem cells from exfoliated deciduous teeth (SHED) into MRL/lpr mice and explored their therapeutic mechanisms in secondary osteoporotic disorders of the systemic lupus erythematosus model mice. METHODS: The effects of systemic human mesenchymal stem cell transplantation on bone loss of MRL/lpr mice were analyzed in vivo and ex vivo. After systemic human mesenchymal stem cell transplantation, recipient BMMSC functions of MRL/lpr mice were assessed for aspects of stemness, osteogenesis and osteoclastogenesis, and a series of co-culture experiments under osteogenic or osteoclastogenic inductions were performed to examine the efficacy of interleukin (IL)-17-impaired recipient BMMSCs in the bone marrow of MRL/lpr mice. RESULTS: Systemic transplantation of human BMMSCs and SHED recovered the reduction in bone density and structure in MRL/lpr mice. To explore the mechanism, we found that impaired recipient BMMSCs mediated the negative bone metabolic turnover by enhanced osteoclastogenesis and suppressed osteoblastogenesis in secondary osteoporosis of MRL/lpr mice. Moreover, IL-17-dependent hyperimmune conditions in the recipient bone marrow of MRL/lpr mice damaged recipient BMMSCs to suppress osteoblast capacity and accelerate osteoclast induction. To overcome the abnormal bone metabolism, systemic transplantation of human BMMSCs and SHED into MRL/lpr mice improved the functionally impaired recipient BMMSCs through IL-17 suppression in the recipient bone marrow and then maintained a regular positive bone metabolism via the balance of osteoblasts and osteoclasts. CONCLUSIONS: These findings indicate that IL-17 and recipient BMMSCs might be a therapeutic target for secondary osteoporosis in systemic lupus erythematosus.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1506
[Cu] Class update date: 150620
[Lr] Last revision date:150620
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1186/s13287-015-0091-4

  7 / 322246 MEDLINE  
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[PMID]: 26070484
[Au] Autor:Askenase MH; Han SJ; Byrd AL; Morais da Fonseca D; Bouladoux N; Wilhelm C; Konkel JE; Hand TW; Lacerda-Queiroz N; Su XZ; Trinchieri G; Grainger JR; Belkaid Y
[Ad] Address:Program in Barrier Immunity and Repair, Mucosal Immunology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, MD 20892, USA; Immunology Graduate Group, University of Pennsylvania, Philadelphia, PA 19104, USA....
[Ti] Title:Bone-Marrow-Resident NK Cells Prime Monocytes for Regulatory Function during Infection.
[So] Source:Immunity;42(6):1130-42, 2015 Jun 16.
[Is] ISSN:1097-4180
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Tissue-infiltrating Ly6C(hi) monocytes play diverse roles in immunity, ranging from pathogen killing to immune regulation. How and where this diversity of function is imposed remains poorly understood. Here we show that during acute gastrointestinal infection, priming of monocytes for regulatory function preceded systemic inflammation and was initiated prior to bone marrow egress. Notably, natural killer (NK) cell-derived IFN-γ promoted a regulatory program in monocyte progenitors during development. Early bone marrow NK cell activation was controlled by systemic interleukin-12 (IL-12) produced by Batf3-dependent dendritic cells (DCs) in the mucosal-associated lymphoid tissue (MALT). This work challenges the paradigm that monocyte function is dominantly imposed by local signals after tissue recruitment, and instead proposes a sequential model of differentiation in which monocytes arepre-emptively educated during development in the bone marrow to promote their tissue-specific function.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1506
[Cu] Class update date: 150620
[Lr] Last revision date:150620
[Js] Journal subset:IM
[St] Status:In-Data-Review

  8 / 322246 MEDLINE  
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[PMID]: 26085896
[Au] Autor:Lue K; Emtage JB; Parias MA; Dhillon J; Pow-Sang J
[Ad] Address:University of South Florida, College of Medicine, Tampa, FL;...
[Ti] Title:An extramedullary plasmacytoma in the testicle: A case report and review of the literature.
[So] Source:Can Urol Assoc J;9(3-4):E240-2, 2015 Mar-Apr.
[Is] ISSN:1911-6470
[Cp] Country of publication:Canada
[La] Language:eng
[Ab] Abstract:We present a rare case of testicular extramedullary plasmacytoma (EMP) in a 43-year-old man with multiple myeloma and diffuse systemic involvement refractory to chemotherapy. Multiple myeloma is typically found within the bone marrow and rarely involves other organs and sites. EMPs are most frequently associated with the head and neck region, but in rare cases testicular involvement have been seen. These mimic other causes of testicular swelling and therefore require a full diagnostic workup and management similar to that of any scrotal pathology. Radical inguinal orchiectomy is the treatment of choice with the addition of adjunct or salvage radiation therapy if necessary. The prognosis with these lesions is poor and in cases of primary testicular plasmacytoma, progression to multiple myeloma is likely.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1506
[Cu] Class update date: 150620
[Lr] Last revision date:150620
[Da] Date of entry for processing:150618
[St] Status:PubMed-not-MEDLINE
[do] DOI:10.5489/cuaj.2531

  9 / 322246 MEDLINE  
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[PMID]: 25964477
[Au] Autor:Kim PD; Xia-Juan X; Crump KE; Abe T; Hajishengallis G; Sahingur SE
[Ad] Address:Department of Periodontics, School of Dentistry, Virginia Commonwealth University, Richmond, Virginia, USA Department of Microbiology and Immunology, School of Medicine, Virginia Commonwealth University, Richmond, Virginia, USA....
[Ti] Title:Toll-Like Receptor 9-Mediated Inflammation Triggers Alveolar Bone Loss in Experimental Murine Periodontitis.
[So] Source:Infect Immun;83(7):2992-3002, 2015 Jul.
[Is] ISSN:1098-5522
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Chronic periodontitis is a local inflammatory disease induced by a dysbiotic microbiota and leading to destruction of the tooth-supporting structures. Microbial nucleic acids are abundantly present in the periodontium, derived through release after phagocytic uptake of microbes and/or from biofilm-associated extracellular DNA. Binding of microbial DNA to its cognate receptors, such as Toll-like receptor 9 (TLR9), can trigger inflammation. In this study, we utilized TLR9 knockout (TLR9(-/-)) mice and wild-type (WT) controls in a murine model of Porphyromonas gingivalis-induced periodontitis and report the first in vivo evidence that TLR9 signaling mediates the induction of periodontal bone loss. P. gingivalis-infected WT mice exhibited significantly increased bone loss compared to that in sham-infected WT mice or P. gingivalis-infected TLR9(-/-) mice, which were resistant to bone loss. Consistent with this, the expression levels of interleukin 6 (IL-6), tumor necrosis factor (TNF), and receptor-activator of nuclear factor kappa B ligand (RANKL) were significantly elevated in the gingival tissues of the infected WT mice but not in infected TLR9(-/-) mice compared to their levels in controls. Ex vivo studies using splenocytes and bone marrow-derived macrophages revealed significantly diminished cytokine production in TLR9(-/-) cells relative to the cytokine production in WT cells in response to P. gingivalis, thereby implicating TLR9 in inflammatory responses to this organism. Intriguingly, compared to the cytokine production in WT cells, TLR9(-/-) cells exhibited significantly decreased proinflammatory cytokine production upon challenge with lipopolysaccharide (LPS) (TLR4 agonist) or Pam3Cys (TLR2 agonist), suggesting possible cross talk between TLR9, TLR4, and TLR2. Collectively, our results provide the first proof-of-concept evidence implicating TLR9-triggered inflammation in periodontal disease pathogenesis, thereby identifying a new potential therapeutic target to control periodontal inflammation.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1506
[Cu] Class update date: 150620
[Lr] Last revision date:150620
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1128/IAI.00424-15

  10 / 322246 MEDLINE  
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[PMID]: 25714596
[Au] Autor:Kawashiri MA; Nakanishi C; Tsubokawa T; Shimojima M; Yoshida S; Yoshimuta T; Konno T; Yamagishi M; Hayashi K
[Ad] Address:Division of Cardiovascular Medicine, Kanazawa University Graduate School of Medicine, Kanazawa, Japan.
[Ti] Title:Impact of Enhanced Production of Endogenous Heme Oxygenase-1 by Pitavastatin on Survival and Functional Activities of Bone Marrow-derived Mesenchymal Stem Cells.
[So] Source:J Cardiovasc Pharmacol;65(6):601-6, 2015 Jun.
[Is] ISSN:1533-4023
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Although mesenchymal stem cells (MSCs) have a therapeutic potential for the repair of tissue injuries, their poor viability in damaged tissue limits their effectiveness. Statins can induce an increased production of heme oxygenase-1 (HO-1), which may prevent this detrimental effect in MSCs. We investigated the protective effect of statin-induced overexpression of HO-1 by examining changes in gene expression and function in MSCs after pitavastatin treatment. The relative expression of the HO-1 and endothelial nitric oxide synthase genes in MSCs was significantly increased after treatment with pitavastatin (MSCs). Immunocytological analysis showed that MSCs also stained with phospho-Akt. After exposure to oxidative stress, MSCs showed increased resistance to induced cell death compared with control MSCs. Under serum starvation conditions, MSCs treated with 1 M pitavastatin showed enhanced cell proliferation and a marked increase in vascular endothelial growth factor production compared with control MSCs. Interestingly, MSCs showed enhanced tube formation under both normoxia and hypoxia. These results demonstrate that pitavastatin can enhance endogenous HO-1 expression in MSCs, which may protect the cells into the environment of oxidative stress with partial activation of endothelial nitric oxide synthase and Akt phosphorylation.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1506
[Cu] Class update date: 150620
[Lr] Last revision date:150620
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1097/FJC.0000000000000231


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