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[PMID]: 27270177
[Au] Autor:Ramos CA; Savoldo B; Torrano V; Ballard B; Zhang H; Dakhova O; Liu E; Carrum G; Kamble RT; Gee AP; Mei Z; Wu MF; Liu H; Grilley B; Rooney CM; Brenner MK; Heslop HE; Dotti G
[Ti] Title:Clinical responses with T lymphocytes targeting malignancy-associated κ light chains.
[So] Source:J Clin Invest;126(7):2588-96, 2016 Jul 1.
[Is] ISSN:1558-8238
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: Treatment of B cell malignancies with adoptive transfer of T cells with a CD19-specific chimeric antigen receptor (CAR) shows remarkable clinical efficacy. However, long-term persistence of T cells targeting CD19, a pan-B cell marker, also depletes normal B cells and causes severe hypogammaglobulinemia. Here, we developed a strategy to target B cell malignancies more selectively by taking advantage of B cell light Ig chain restriction. We generated a CAR that is specific for the κ light chain (κ.CAR) and therefore recognizes κ-restricted cells and spares the normal B cells expressing the nontargeted λ light chain, thus potentially minimizing humoral immunity impairment. METHODS: We conducted a phase 1 clinical trial and treated 16 patients with relapsed or refractory κ+ non-Hodgkin lymphoma/chronic lymphocytic leukemia (NHL/CLL) or multiple myeloma (MM) with autologous T cells genetically modified to express κ.CAR (κ.CARTs). Other treatments were discontinued in 11 of the 16 patients at least 4 weeks prior to T cell infusion. Six patients without lymphopenia received 12.5 mg/kg cyclophosphamide 4 days before κ.CART infusion (0.2 × 108 to 2 × 108 κ.CARTs/m2). No other lymphodepletion was used. RESULTS: κ.CART expansion peaked 1-2 weeks after infusion, and cells remained detectable for more than 6 weeks. Of 9 patients with relapsed NHL or CLL, 2 entered complete remission after 2 and 3 infusions of κ.CARTs, and 1 had a partial response. Of 7 patients with MM, 4 had stable disease lasting 2-17 months. No toxicities attributable to κ.CARTs were observed. CONCLUSION: κ.CART infusion is feasible and safe and can lead to complete clinical responses. TRIAL REGISTRATION: ClinicalTrials.gov NCT00881920. FUNDING: National Cancer Institute (NCI) grants 3P50CA126752 and 5P30CA125123 and Leukemia and Lymphoma Society (LLS) Specialized Centers of Research (SCOR) grant 7018.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1607
[Cu] Class update date: 160702
[Lr] Last revision date:160702
[Js] Journal subset:AIM; IM
[St] Status:In-Data-Review

  2 / 469130 MEDLINE  
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[PMID]: 27197066
[Au] Autor:Miller LD; Chou JA; Black MA; Print C; Chifman J; Alistar A; Putti T; Zhou X; Bedognetti D; Hendrickx W; Pullikuth A; Rennhack J; Andrechek ER; Demaria S; Wang E; Marincola FM
[Ad] Address:Department of Cancer Biology, Wake Forest School of Medicine, Winston-Salem, North Carolina. The Comprehensive Cancer Center of Wake Forest University, Winston Salem, North Carolina. ldmiller@wfubmc.edu....
[Ti] Title:Immunogenic Subtypes of Breast Cancer Delineated by Gene Classifiers of Immune Responsiveness.
[So] Source:Cancer Immunol Res;4(7):600-10, 2016 Jul.
[Is] ISSN:2326-6074
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The abundance and functional orientation of tumor-infiltrating lymphocytes in breast cancer is associated with distant metastasis-free survival, yet how this association is influenced by tumor phenotypic heterogeneity is poorly understood. Here, a bioinformatics approach defined tumor biologic attributes that influence this association and delineated tumor subtypes that may differ in their ability to sustain durable antitumor immune responses. A large database of breast tumor expression profiles and associated clinical data was compiled, from which the ability of phenotypic markers to significantly influence the prognostic performance of a classification model that incorporates immune cell-specific gene signatures was ascertained. Markers of cell proliferation and intrinsic molecular subtype reproducibly distinguished two breast cancer subtypes that we refer to as immune benefit-enabled (IBE) and immune benefit-disabled (IBD). The IBE tumors, comprised mostly of highly proliferative tumors of the basal-like, HER2-enriched, and luminal B subtypes, could be stratified by the immune classifier into significantly different prognostic groups, while IBD tumors could not, indicating the potential for productive engagement of metastasis-protective immunity in IBE tumors, but not in IBD tumors. The prognostic stratification in IBE was independent of conventional variables. Gene network analysis predicted the activation of TNFα/IFNγ signaling pathways in IBE tumors and the activation of the transforming growth factor-ß pathway in IBD tumors. This prediction supports a model in which breast tumors can be distinguished on the basis of their potential for metastasis-protective immune responsiveness. Whether IBE and IBD represent clinically relevant contexts for evaluating sensitivity to immunotherapeutic agents warrants further investigation. Cancer Immunol Res; 4(7); 600-10. ©2016 AACR.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1607
[Cu] Class update date: 160702
[Lr] Last revision date:160702
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1158/2326-6066.CIR-15-0149

  3 / 469130 MEDLINE  
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[PMID]: 27197294
[Au] Autor:Sigel C; Cavalcanti MS; Daniel T; Vakiani E; Shia J; Sigel K
[Ad] Address:Department of Pathology, Memorial Sloan Kettering Cancer Center, New York, New York....
[Ti] Title:Clinicopathologic Features of Colorectal Carcinoma in HIV-Positive Patients.
[So] Source:Cancer Epidemiol Biomarkers Prev;25(7):1098-104, 2016 Jul.
[Is] ISSN:1538-7755
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: Emerging evidence suggests differences in colorectal cancer in HIV-infected patients (HIV(+)) compared with HIV(-) patients. Microsatellite instability (MSI), occurring in a subset of colorectal cancer, is present at a higher rate in certain cancers in HIV(+) patients. Colorectal cancer with MSI share some characteristics with those reported for HIV(+) colorectal cancer. On this premise, we studied clinical and pathologic features of HIV(+) colorectal cancer and evaluated for MSI using matched HIV(-) colorectal cancer controls. METHODS: Two nested, matched cohorts were identified from a hospital-based cohort of colorectal cancer patients. HIV(+) colorectal cancers were identified and random control patients were matched for selected characteristics. Mismatch repair protein (MMR) IHC was performed as the detection method for MSI. Variables were compared between cases and controls using fixed-effects logit modeling to account for matching. RESULTS: We included 184 colorectal cancer samples (38 HIV(+), 146 HIV(-) control). Median patient age at colorectal cancer onset was 55. When compared with HIV(-) colorectal cancer, HIV(+) patients were more likely to have smoked (P = 0.001), have right-sided colorectal cancer (37% vs. 14%; P = 0.003), and tumor-infiltrating lymphocytes (TIL) above 50/10 high-power fields (21% vs. 7%). There was no difference in MMR protein expression (P = 0.6). HIV(+) colorectal cancer patients had reduced overall survival (P = 0.02) but no difference in progression-free survival. CONCLUSIONS: HIV(+) patients developed colorectal cancer at a lower median age than population estimates, had a higher frequency of right-sided disease, and increased TILs, suggesting potential biologic differences compared with uninfected patients. IMPACT: Clinicopathologic differences in colorectal cancer of HIV(+) persons may have implications for tumor pathogenesis. Cancer Epidemiol Biomarkers Prev; 25(7); 1098-104. ©2016 AACR.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1607
[Cu] Class update date: 160702
[Lr] Last revision date:160702
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1158/1055-9965.EPI-15-1179

  4 / 469130 MEDLINE  
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[PMID]: 26680540
[Au] Autor:Liu Q; Zhang B
[Ad] Address:Department of Biomedical Informatics, Vanderbilt University School of Medicine , Nashville, Tennessee 37232, United States....
[Ti] Title:Integrative Omics Analysis Reveals Post-Transcriptionally Enhanced Protective Host Response in Colorectal Cancers with Microsatellite Instability.
[So] Source:J Proteome Res;15(3):766-76, 2016 Mar 4.
[Is] ISSN:1535-3907
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Microsatellite instability (MSI) is a frequent and clinically relevant molecular phenotype in colorectal cancer. MSI cancers have favorable survival compared with microsatellite stable cancers (MSS), possibly due to the pronounced tumor-infiltrating lymphocytes observed in MSI cancers. Consistent with the strong immune response that MSI cancers trigger in the host, previous transcriptome expression studies have identified mRNA signatures characteristic of immune response in MSI cancers. However, proteomics features of MSI cancers and the extent to which the mRNA signatures are reflected at the protein level remain largely unknown. Here, we performed a comprehensive comparison of global proteomics profiles between MSI and MSS colorectal cancers in The Cancer Genome Atlas (TCGA) cohort. We found that protein signatures of MSI are also associated with increased immunogenicity. To reliably quantify post-transcription regulation in MSI cancers, we developed a resampling-based regression method by integrative modeling of transcriptomics and proteomics data sets. Compared with the popular simple method, which detects post-transcriptional regulation by either identifying genes differentially expressed at the mRNA level but not at the protein level or vice versa, our method provided a quantitative, more sensitive, and accurate way to identify genes subject to differential post-transcriptional regulation. With this method, we demonstrated that post-transcriptional regulation, coordinating protein expression with key players, initiates de novo and enhances protective host response in MSI cancers.
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Entry month:1603
[Cu] Class update date: 160310
[Lr] Last revision date:160310
[Js] Journal subset:IM
[St] Status:In-Process
[do] DOI:10.1021/acs.jproteome.5b00847

  5 / 469130 MEDLINE  
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[PMID]: 26745254
[Au] Autor:Schreiner F; Plamper M; Dueker G; Schoenberger S; Gámez-Díaz L; Grimbacher B; Hilger AC; Gohlke B; Reutter H; Woelfle J
[Ad] Address:Pediatric Endocrinology (F.S., M.P., B.Go., J.W.), Pediatric Gastroenterology and Hepatology (G.D.), and Pediatric Hematology and Oncology (S.S.), Children's Hospital, University of Bonn, 53113 Bonn, Germany; Center for Chronic Immunodeficiency (L.G.-D., B.Gr.), University Medical Center and Univers...
[Ti] Title:Infancy-Onset T1DM, Short Stature, and Severe Immunodysregulation in Two Siblings With a Homozygous LRBA Mutation.
[So] Source:J Clin Endocrinol Metab;101(3):898-904, 2016 Mar.
[Is] ISSN:1945-7197
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:CONTEXT: Type 1 diabetes mellitus (T1DM) is caused by autoimmunity against pancreatic ß-cells. Although a significant number of T1DM patients have or will develop further autoimmune disorders during their lifetime, coexisting severe immunodysregulation is rare. OBJECTIVE: Presuming autosomal-recessive inheritance in a complex immunodysregulation disorder including T1DM and short stature in two siblings, we performed whole-exome sequencing. CASE PRESENTATION: Two Libyan siblings born to consanguineous parents were presented to our diabetology department at ages 12 and 5 years, respectively. Apart from T1DM diagnosed at age 2 years, patient 1 suffered from chronic restrictive lung disease, mild enteropathy, hypogammaglobulinemia, and GH deficiency. Fluorescence-activated cell sorting analysis revealed B-cell deficiency. In addition, CD4(+)/CD25(+) and CD25(high)/FoxP3(+) cells were diminished, whereas an unusual CD25(-)/FoxP3(+) population was detectable. The younger brother, patient 2, also developed T1DM during infancy. Although his enteropathy was more severe and electrolyte derangements repeatedly led to hospitalization, he did not have significant pulmonary problems. IgG levels and B-lymphocytes were within normal ranges. RESULTS: By whole-exome sequencing we identified a homozygous truncating mutation (c.2445_2447del(C)3ins(C)2, p.P816Lfs*4) in the lipopolysaccharide-responsive beige-like anchor (LRBA) gene in both siblings. The diagnosis of LRBA deficiency was confirmed by a fluorescence-activated cell sorting-based immunoassay showing the absence of LRBA protein in phytohemagglutinin-stimulated peripheral blood mononuclear cells. CONCLUSION: We identified a novel truncating LRBA mutation in two siblings with T1DM, short stature, and severe immunodysregulation. LRBA mutations have previously been reported to cause multiorgan autoimmunity and immunodysfunction. In light of the variable phenotypes reported so far in LRBA-mutant individuals, LRBA deficiency should be considered in all patients presenting with T1DM and signs of severe immunodysregulation.
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Entry month:1603
[Js] Journal subset:AIM; IM
[St] Status:In-Process
[do] DOI:10.1210/jc.2015-3382

  6 / 469130 MEDLINE  
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[PMID]: 26906195
[Au] Autor:Dygai AM; Skurikhin EG; Pershina OV; Ermakova NN; Krupin VA; Ermolaeva LA; Stakheeva MN; Choinzonov EL; Goldberg VE; Reikhart DV; Ellinidi VN; Kravtsov VY
[Ad] Address:E. D. Goldberg Research Institute of Pharmacology and Regene rative Medicine, Tomsk, Russia....
[Ti] Title:Role of Hematopoietic Stem Cells in Inflammation of the Pancreas during Diabetes Mellitus.
[So] Source:Bull Exp Biol Med;160(4):474-9, 2016 Feb.
[Is] ISSN:1573-8221
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The model of streptozotocin-induced diabetes mellitus in C57Bl/6 mice was employed to study the role of precursors of insulin-producing ß-cells, hematopoietic stem cells, and progenitor hematopoietic cells in inflammation. In addition to provoking hyperglycemia, streptozotocin elevated serum levels of IL-1ß and hyaluronic acid, induced edema in the pancreatic insular tissue and its infiltration by inflammatory cells (neutrophils, lymphocytes, and macrophages) and fibroblasts. Inflammation in pancreatic islets was accompanied by necrotic processes and decreasing counts of multipotent progenitor ß-cells (CD45(-), TER119(-), c-kit-1(-), and Flk-1(-)), oligopotent progenitor ß-cells (CD45(-), TER119(-), CD133(+), and CD49f(low)), and insulinproducing ß-cells (Pdx1(+)). Pancreatic infl ammation was preceded by elevation of the number of short-term hematopoietic stem cells (Lin-Sca-1(+)c-kit(+)CD34(+)) relative to long-term cells (Lin(-)Sca-1(+)c-kit(+)CD34(-)) in the bone marrow as well as recruitment of hematopoietic stem and progenitor cells into circulation. Transplantation of bone marrow hematopoietic stem and progenitor cells from diabetic C57Bl/6 donor mice to recipient CBA mice with 5-fluorouracilinduced leukopenia accelerated regeneration of granulocytopoiesis in recipient mice.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1603
[Js] Journal subset:IM
[St] Status:In-Process
[do] DOI:10.1007/s10517-016-3200-1

  7 / 469130 MEDLINE  
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[PMID]: 26059005
[Au] Autor:Pham OH; McSorley SJ
[Ad] Address:Department of Anatomy, Physiology, and Cell Biology, Center for Comparative Medicine, UC Davis, Davis, California, USA.
[Ti] Title:Divergent behavior of mucosal memory T cells.
[So] Source:Mucosal Immunol;8(4):731-4, 2015 Jul.
[Is] ISSN:1935-3456
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Memory CD4 T cells are strategically positioned at mucosal surfaces to initiate a robust adaptive immune response. The detection of specific antigen via the T-cell receptor causes these memory T cells to unleash a potent antimicrobial response that includes rousing local innate immune populations for tissue-specific defense. Paradoxically, these same memory T cells can also be stimulated by nonantigen-specific signals that are generated by the activity of local innate immune cells. This versatility of mucosal memory T cells in both the initiation and the sensing of local innate immunity could be a vitally important asset during pathogen defense but alternatively could be responsible for initiating and maintaining chronic inflammation in sensitive mucosal tissues.
[Mh] MeSH terms primary: CD4-Positive T-Lymphocytes/immunology
Crohn Disease/immunology
Immunity, Innate
Nasal Polyps/immunology
Receptors, Interleukin-18/immunology
Receptors, Tumor Necrosis Factor, Member 25/immunology
[Mh] MeSH terms secundary: Humans
[Pt] Publication type:COMMENT; JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Name of substance:0 (Receptors, Interleukin-18); 0 (Receptors, Tumor Necrosis Factor, Member 25)
[Em] Entry month:1603
[Cu] Class update date: 160702
[Lr] Last revision date:160702
[Js] Journal subset:IM
[Da] Date of entry for processing:150624
[St] Status:MEDLINE
[do] DOI:10.1038/mi.2015.52

  8 / 469130 MEDLINE  
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[PMID]: 27369569
[Au] Autor:Yang Y; Xue X; Yang Y; Chen X; Du A
[Ad] Address:Institute of Preventive Veterinary Medicine & Zhejiang Provincial Key Laboratory of Preventive Veterinary Medicine, College of Animal Sciences, Zhejiang University, Hangzhou 310058, China....
[Ti] Title:Efficacy of a potential DNA vaccine encoding Cryptosporidium baileyi rhomboid protein against homologous challenge in chickens.
[So] Source:Vet Parasitol;225:5-11, 2016 Jul 30.
[Is] ISSN:1873-2550
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:The parasite Cryptosporidium baileyi can infect the larynx, trachea, bursa and cloaca of poultry, causing high mortality during severe infection and leading to substantial economic losses of the poultry industry. The rhomboid protein is very important in Cryptosporidium infection. In this study, a nucleic acid based vaccine candidate pEGFP-CbROM was constructed. After orally challenging with C. baileyi oocysts, the corresponding immune responses induced were analyzed and the immunoprotective effect evaluated in chickens. Obtained results revealed that this nucleic acid based vaccine could induce antibody responses and peripheral blood T lymphocytes proliferation significantly (P<0.05), while the peripheral blood B lymphocyte proliferation increased significantly (P<0.05) only at a high dose of 100µg of pEGFP-CbROM, compared with the PBS control group. After C. baileyi infection, the duration of oocysts shedding was shortened by 2days in the 100µg pEGFP-CbROM group, and the rate of reduction could reach to around 71.3%. While no significant difference in body weight gain was observed among the immunized groups (P>0.05), the differences between the immunized and the non-immunized groups were found to be significant (P<0.05). Our data provides a useful basis for further work in cryptosporidiosis prevention and treatment.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1607
[Js] Journal subset:IM
[St] Status:In-Data-Review

  9 / 469130 MEDLINE  
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[PMID]: 27369932
[Au] Autor:de Bragança AC; Volpini RA; Mehrotra P; Andrade L; Basile DP
[Ad] Address:Division of Nephrology, Laboratory of Basic Science LIM-12, University of São Paulo School of Medicine, São Paulo, Brazil ana.braganca@hc.fm.usp.br....
[Ti] Title:Vitamin D deficiency contributes to vascular damage in sustained ischemic acute kidney injury.
[So] Source:Physiol Rep;4(13), 2016 Jul.
[Is] ISSN:2051-817X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Reductions in renal microvasculature density and increased lymphocyte activity may play critical roles in the progression of chronic kidney disease (CKD) following acute kidney injury (AKI) induced by ischemia/reperfusion injury (IRI). Vitamin D deficiency is associated with tubulointerstitial damage and fibrosis progression following IRI-AKI We evaluated the effect of vitamin D deficiency in sustained IRI-AKI, hypothesizing that such deficiency contributes to the early reduction in renal capillary density or alters the lymphocyte response to IRI Wistar rats were fed vitamin D-free or standard diets for 35 days. On day 28, rats were randomized into four groups: control, vitamin D deficient (VDD), bilateral IRI, and VDD+IRI Indices of renal injury and recovery were evaluated for up to 7 days following the surgical procedures. VDD rats showed reduced capillary density (by cablin staining), even in the absence of renal I/R. In comparison with VDD and IRI rats, VDD+IRI rats manifested a significant exacerbation of capillary rarefaction as well as higher urinary volume, kidney weight/body weight ratio, tissue injury scores, fibroblast-specific protein-1, and alpha-smooth muscle actin. VDD+IRI rats also had higher numbers of infiltrating activated CD4(+) and CD8(+) cells staining for interferon gamma and interleukin-17, with a significant elevation in the Th17/T-regulatory cell ratio. These data suggest that vitamin D deficiency impairs renal repair responses to I/R injury, exacerbates changes in renal capillary density, as well as promoting fibrosis and inflammation, which may contribute to the transition from AKI to CKD.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1607
[Da] Date of entry for processing:160702
[St] Status:PubMed-not-MEDLINE

  10 / 469130 MEDLINE  
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[PMID]: 27367604
[Au] Autor:Chang J; Luo Y; Wang Y; Pathak R; Sridharan V; Jones T; Mao XW; Nelson G; Boerma M; Hauer-Jensen M; Zhou D; Shao L
[Ad] Address:Division of Radiation Health, Department of Pharmaceutical Sciences, University of Arkansas for Medical Sciences, Little Rock, Arkansas, United States of America....
[Ti] Title:Low Doses of Oxygen Ion Irradiation Cause Acute Damage to Hematopoietic Cells in Mice.
[So] Source:PLoS One;11(7):e0158097, 2016.
[Is] ISSN:1932-6203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:One of the major health risks to astronauts is radiation on long-duration space missions. Space radiation from sun and galactic cosmic rays consists primarily of 85% protons, 14% helium nuclei and 1% high-energy high-charge (HZE) particles, such as oxygen (16O), carbon, silicon, and iron ions. HZE particles exhibit dense linear tracks of ionization associated with clustered DNA damage and often high relative biological effectiveness (RBE). Therefore, new knowledge of risks from HZE particle exposures must be obtained. In the present study, we investigated the acute effects of low doses of 16O irradiation on the hematopoietic system. Specifically, we exposed C57BL/6J mice to 0.1, 0.25 and 1.0 Gy whole body 16O (600 MeV/n) irradiation and examined the effects on peripheral blood (PB) cells, and bone marrow (BM) hematopoietic stem cells (HSCs) and hematopoietic progenitor cells (HPCs) at two weeks after the exposure. The results showed that the numbers of white blood cells, lymphocytes, monocytes, neutrophils and platelets were significantly decreased in PB after exposure to 1.0 Gy, but not to 0.1 or 0.25 Gy. However, both the frequency and number of HPCs and HSCs were reduced in a radiation dose-dependent manner in comparison to un-irradiated controls. Furthermore, HPCs and HSCs from irradiated mice exhibited a significant reduction in clonogenic function determined by the colony-forming and cobblestone area-forming cell assays. These acute adverse effects of 16O irradiation on HSCs coincided with an increased production of reactive oxygen species (ROS), enhanced cell cycle entry of quiescent HSCs, and increased DNA damage. However, none of the 16O exposures induced apoptosis in HSCs. These data suggest that exposure to low doses of 16O irradiation induces acute BM injury in a dose-dependent manner primarily via increasing ROS production, cell cycling, and DNA damage in HSCs. This finding may aid in developing novel strategies in the protection of the hematopoietic system from space radiation.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1607
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1371/journal.pone.0158097


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