February 6th, 2010 / No Comments » / by pubmed
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Posted in: Report
February 6th, 2010 / No Comments » / by Pottgiesser T, Ahlgrim C, Ruthardt S, Dickhuth HH, Schumacher YO
Hemoglobin mass after 21 days of conventional altitude training at 1816 m.
J Sci Med Sport. 2009 Nov;12(6):673-5
Authors: Pottgiesser T, Ahlgrim C, Ruthardt S, Dickhuth HH, Schumacher YO
The underlying mechanisms of altitude training are still a matter of controversial discussion but erythropoietic adaptations with an increase of total haemoglobin mass (tHb) have been shown in several studies, partly depending on an adequate hypoxic dose. The aim of this retrospective study was to investigate if a 3 weeks sojourn at moderate altitude (1816 m) with conventional training sessions (live and train at moderate altitude), especially under real and uncontrolled conditions, results in an increased tHb. tHb was measured in seven male cyclists competing at elite level (German national cycling team, U23 category) prior to the ascent to altitude and immediately after descent to sea-level. The athletes completed a 21 days altitude training camp living at 1816 m and training at 1800-2400 m during the competitive season. No significant difference was found in tHb after the altitude sojourn (prior 927+/-109g vs. 951+/-113g post, 95% CI -13-61g). Additionally, the analysis of red cell volume, plasma volume and blood volume or haemoglobin concentration [Hb] as well as haematocrit (Hct) did not reveal any significant changes. The data supports the theory that an adequate hypoxic dose is required for adaptations of the erythropoietic system with an increase of tHb and a threshold of approximately 2100-2500 m has to be exceeded.
PMID: 18768367 [PubMed - indexed for MEDLINE]
Posted in: J Sci Med Sport
February 6th, 2010 / No Comments » / by Miccio A, Wang Y, Hong W, Gregory GD, Wang H, Yu X, Choi JK, Shelat S, Tong W, Poncz M, Blobel GA
NuRD mediates activating and repressive functions of GATA-1 and FOG-1 during blood development.
EMBO J. 2010 Jan 20;29(2):442-56
Authors: Miccio A, Wang Y, Hong W, Gregory GD, Wang H, Yu X, Choi JK, Shelat S, Tong W, Poncz M, Blobel GA
GATA transcription factors interact with FOG proteins to regulate tissue development by activating and repressing transcription. FOG-1 (ZFPM1), a co-factor for the haematopoietic factor GATA-1, binds to the NuRD co-repressor complex through a conserved N-terminal motif. Surprisingly, we detected NuRD components at both repressed and active GATA-1/FOG-1 target genes in vivo. In addition, while NuRD is required for transcriptional repression in certain contexts, we show a direct requirement of NuRD also for FOG-1-dependent transcriptional activation. Mice in which the FOG-1/NuRD interaction is disrupted display defects similar to germline mutations in the Gata1 and Fog1 genes, including anaemia and macrothrombocytopaenia. Gene expression analysis in primary mutant erythroid cells and megakaryocytes (MKs) revealed an essential function for NuRD during both the repression and activation of select GATA-1/FOG-1 target genes. These results show that NuRD is a critical co-factor for FOG-1 and underscore the versatile use of NuRD by lineage-specific transcription factors to activate and repress gene transcription in the appropriate cellular and genetic context.
PMID: 19927129 [PubMed - indexed for MEDLINE]
Posted in: EMBO J
February 6th, 2010 / No Comments » / by Banerjee P, Crawford L, Samuelson E, Feuer G
Hematopoietic stem cells and retroviral infection.
Retrovirology. 2010 Feb 4;7(1):8
Authors: Banerjee P, Crawford L, Samuelson E, Feuer G
ABSTRACT: Retroviral induced malignancies serve as ideal models to help us better understand the molecular mechanisms associated with the initiation and progression of leukemogenesis. Numerous retroviruses including AEV, FLV, M-MuLV and HTLV-1 have the ability to infect hematopoietic stem and progenitor cells, resulting in the deregulation of normal hematopoiesis and the development of leukemia/lymphoma. Research over the last few decades has elucidated similarities between retroviral-induced leukemogenesis, initiated by deregulation of innate hematopoietic stem cell traits, and the cancer stem cell hypothesis. Ongoing research in some of these models may provide a better understanding of the processes of normal hematopoiesis and cancer stem cells. Research on retroviral induced leukemias and lymphomas may identify the molecular events which trigger the initial cellular transformation and subsequent maintenance of hematologic malignancies, including the generation of cancer stem cells. This review focuses on the role of retroviral infection in hematopoietic stem cells and the initiation, maintenance and progression of hematological malignancies.
PMID: 20132553 [PubMed - as supplied by publisher]
Posted in: Retrovirology
February 6th, 2010 / No Comments » / by Mi S, Li Z, Chen P, He C, Cao D, Elkahloun A, Lu J, Pelloso LA, Wunderlich M, Huang H, Luo RT, Sun M, He M, Neilly MB, Zeleznik-Le NJ, Thirman MJ, Mulloy JC, Liu PP, Rowley JD, Chen J
Aberrant overexpression and function of the miR-17-92 cluster in MLL-rearranged acute leukemia.
Proc Natl Acad Sci U S A. 2010 Feb 2;
Authors: Mi S, Li Z, Chen P, He C, Cao D, Elkahloun A, Lu J, Pelloso LA, Wunderlich M, Huang H, Luo RT, Sun M, He M, Neilly MB, Zeleznik-Le NJ, Thirman MJ, Mulloy JC, Liu PP, Rowley JD, Chen J
MicroRNA (miRNA)-17-92 cluster (miR-17-92), containing seven individual miRNAs, is frequently amplified and overexpressed in lymphomas and various solid tumors. We have found that it is also frequently amplified and the miRNAs are aberrantly overexpressed in mixed lineage leukemia (MLL)-rearranged acute leukemias. Furthermore, we show that MLL fusions exhibit a much stronger direct binding to the locus of this miRNA cluster than does wild-type MLL; these changes are associated with elevated levels of histone H3 acetylation and H3K4 trimethylation and an up-regulation of these miRNAs. We further observe that forced expression of this miRNA cluster increases proliferation and inhibits apoptosis of human cells. More importantly, we show that this miRNA cluster can significantly increase colony-forming capacity of normal mouse bone marrow progenitor cells alone and, particularly, in cooperation with MLL fusions. Finally, through combinatorial analysis of miRNA and mRNA arrays of mouse bone marrow progenitor cells transfected with this miRNA cluster and/or MLL fusion gene, we identified 363 potential miR-17-92 target genes that exhibited a significant inverse correlation of expression with the miRNAs. Remarkably, these potential target genes are significantly enriched (P < 0.01; >2-fold) in cell differentiation, hematopoiesis, cell cycle, and apoptosis. Taken together, our studies suggest that overexpression of miR-17-92 cluster in MLL-rearranged leukemias is likely attributed to both DNA copy number amplification and direct up-regulation by MLL fusions, and that the miRNAs in this cluster may play an essential role in the development of MLL-associated leukemias through inhibiting cell differentiation and apoptosis, while promoting cell proliferation, by regulating relevant target genes.
PMID: 20133587 [PubMed - as supplied by publisher]
Posted in: Proc Natl Acad Sci U S A
February 6th, 2010 / No Comments » / by Harnack U, Eckert K, Fichtner I, Pecher G
Comparison of the Effect of Orally Administered Soluble {beta}-(1-3),(1-6)-D-Glucan and of G-CSF on the Recovery of Murine Hematopoiesis.
In Vivo. 2010 Jan-Feb;24(1):59-63
Authors: Harnack U, Eckert K, Fichtner I, Pecher G
beta-Glucans are branched fungal polysaccharide compounds with pleiotropic activating effects on cells of the immune and the hematopoietic system. In this study, the hematopoiesis-promoting effect of an orally administered soluble beta-(1-3),(1-6)-D-glucan and of intravenously (i.v.) injected recombinant human granulocyte colony-stimulating factor (G-CSF/filgrastim) was tested in cyclophosphamide (CY)-conditioned mice. Both agents were administered for 5 consecutive days following treatment with CY. When G-CSF and the carbohydrate compound were co-administered, a small but non-significant increase of granulopoiesis compared to G-CSF alone was detected. beta-Glucan alone failed to augment granulopoiesis in the peripheral blood of CY-treated mice. However, both G-CSF and beta-glucan significantly enhanced the recovery of monocytes in the peripheral blood of leukopenic mice when orally administered as single agents. In conclusion, the present study provides further evidence of a stimulatory function of orally administered beta-glucans on monocyte production and shows a weak additive effect on granulopoiesis when co-administered with G-CSF into leukopenic mice.
PMID: 20133977 [PubMed - in process]
Posted in: In Vivo
February 5th, 2010 / No Comments » / by Bernard JJ, Seweryniak KE, Koniski AD, Spinelli SL, Blumberg N, Francis CW, Taubman MB, Palis J, Phipps RP
Foxp3 regulates megakaryopoiesis and platelet function.
Arterioscler Thromb Vasc Biol. 2009 Nov;29(11):1874-82
Authors: Bernard JJ, Seweryniak KE, Koniski AD, Spinelli SL, Blumberg N, Francis CW, Taubman MB, Palis J, Phipps RP
OBJECTIVE: Platelets are crucial for hemostasis and are vital regulators of inflammation. Foxp3 is a key transcription factor for T regulatory cell development. Humans with IPEX (immune dysregulation, polyendocrinopathy, enteropathy, x-linked) and the scurfy (Foxp3(sf)) mouse have mutations in the Foxp3 gene that lead to a host of pathologies including autoimmunity and skin diseases. Scurfy mice and some humans with IPEX are also thrombocytopenic. The purpose of this study was to determine whether the absence of functional Foxp3 leads to defects in megakaryocytes and platelets. METHODS AND RESULTS: We discovered that human and mouse megakaryocytes express Foxp3 mRNA and protein. Using shRNA and Foxp3(sf) mice, we demonstrated that Foxp3-deficient mouse and human megakaryocyte progenitors exhibited proliferation defects. Striking platelet abnormalities were observed in both an IPEX patient and Foxp3(sf) mice. Impaired platelet spreading and release of TGF-beta and CD40 ligand (CD40L), and abnormal levels of plasma CD40L were observed in a case of IPEX syndrome. Foxp3(sf) mice were thrombocytopenic and had increased platelet volume and altered serum levels of CD40L, TXB(2), and TGF-beta. CONCLUSIONS: These findings provide compelling new evidence that Foxp3 is needed for proper megakaryopoiesis and plays a role in regulating platelet function including spreading and release.
PMID: 19661482 [PubMed - indexed for MEDLINE]
Posted in: Arterioscler Thromb Vasc Biol
February 5th, 2010 / No Comments » / by Bernard JJ, Seweryniak KE, Koniski AD, Spinelli SL, Blumberg N, Francis CW, Taubman MB, Palis J, Phipps RP
Foxp3 regulates megakaryopoiesis and platelet function.
Arterioscler Thromb Vasc Biol. 2009 Nov;29(11):1874-82
Authors: Bernard JJ, Seweryniak KE, Koniski AD, Spinelli SL, Blumberg N, Francis CW, Taubman MB, Palis J, Phipps RP
OBJECTIVE: Platelets are crucial for hemostasis and are vital regulators of inflammation. Foxp3 is a key transcription factor for T regulatory cell development. Humans with IPEX (immune dysregulation, polyendocrinopathy, enteropathy, x-linked) and the scurfy (Foxp3(sf)) mouse have mutations in the Foxp3 gene that lead to a host of pathologies including autoimmunity and skin diseases. Scurfy mice and some humans with IPEX are also thrombocytopenic. The purpose of this study was to determine whether the absence of functional Foxp3 leads to defects in megakaryocytes and platelets. METHODS AND RESULTS: We discovered that human and mouse megakaryocytes express Foxp3 mRNA and protein. Using shRNA and Foxp3(sf) mice, we demonstrated that Foxp3-deficient mouse and human megakaryocyte progenitors exhibited proliferation defects. Striking platelet abnormalities were observed in both an IPEX patient and Foxp3(sf) mice. Impaired platelet spreading and release of TGF-beta and CD40 ligand (CD40L), and abnormal levels of plasma CD40L were observed in a case of IPEX syndrome. Foxp3(sf) mice were thrombocytopenic and had increased platelet volume and altered serum levels of CD40L, TXB(2), and TGF-beta. CONCLUSIONS: These findings provide compelling new evidence that Foxp3 is needed for proper megakaryopoiesis and plays a role in regulating platelet function including spreading and release.
PMID: 19661482 [PubMed - indexed for MEDLINE]
Posted in: Arterioscler Thromb Vasc Biol
February 5th, 2010 / No Comments » / by Swijnenburg RJ, Govaert JA, van der Bogt KE, Pearl JI, Huang M, Stein W, Hoyt G, Vogel H, Contag CH, Robbins RC, Wu JC
Timing of bone marrow cell delivery has minimal effects on cell viability and cardiac recovery after myocardial infarction.
Circ Cardiovasc Imaging. 2010 Jan;3(1):77-85
Authors: Swijnenburg RJ, Govaert JA, van der Bogt KE, Pearl JI, Huang M, Stein W, Hoyt G, Vogel H, Contag CH, Robbins RC, Wu JC
BACKGROUND: Despite ongoing clinical trials, the optimal time for delivery of bone marrow mononuclear cells (BMCs) after myocardial infarction is unclear. We compared the viability and effects of transplanted BMCs on cardiac function in the acute and subacute inflammatory phases of myocardial infarction. METHODS AND RESULTS: The time course of acute inflammatory cell infiltration was quantified by FACS analysis of enzymatically digested hearts of FVB mice (n=12) after left anterior descending artery ligation. Mac-1(+)Gr-1(high) neutrophil infiltration peaked at day 4. BMCs were harvested from transgenic FVB mice expressing firefly luciferase (Fluc) and green fluorescent protein (GFP). Afterward, 2.5x10(6) BMCs were injected into the left ventricle of wild-type FVB mice either immediately (acute BMC) or 7 days (subacute BMC) after myocardial infarction, or after a sham procedure (n=8 per group). In vivo bioluminescence imaging showed an early signal increase in both BMC groups at day 7, followed by a nonsignificant trend (P=0.203) toward improved BMC survival in the subacute BMC group that persisted until the bioluminescence imaging signal reached BACKGROUND: <0.01) and 6 weeks (both BMC groups versus saline; P<0.05) but no significant differences between the 2 BMC groups. FACS analysis of BMC-injected hearts at day 7 revealed that GFP(+) BMCs expressed hematopoietic (CD45, Mac-1, Gr-1), minimal progenitor (Sca-1, c-kit), and no endothelial (CD133, Flk-1) or cardiac (Trop-T) cell markers. CONCLUSIONS: Timing of BMC delivery has minimal effects on intramyocardial retention and preservation of cardiac function. In general, there is poor long-term engraftment and BMCs tend to adopt inflammatory cell phenotypes.
PMID: 19920031 [PubMed - indexed for MEDLINE]
Posted in: Circ Cardiovasc Imaging
February 5th, 2010 / No Comments » / by Swijnenburg RJ, Govaert JA, van der Bogt KE, Pearl JI, Huang M, Stein W, Hoyt G, Vogel H, Contag CH, Robbins RC, Wu JC
Timing of bone marrow cell delivery has minimal effects on cell viability and cardiac recovery after myocardial infarction.
Circ Cardiovasc Imaging. 2010 Jan;3(1):77-85
Authors: Swijnenburg RJ, Govaert JA, van der Bogt KE, Pearl JI, Huang M, Stein W, Hoyt G, Vogel H, Contag CH, Robbins RC, Wu JC
BACKGROUND: Despite ongoing clinical trials, the optimal time for delivery of bone marrow mononuclear cells (BMCs) after myocardial infarction is unclear. We compared the viability and effects of transplanted BMCs on cardiac function in the acute and subacute inflammatory phases of myocardial infarction. METHODS AND RESULTS: The time course of acute inflammatory cell infiltration was quantified by FACS analysis of enzymatically digested hearts of FVB mice (n=12) after left anterior descending artery ligation. Mac-1(+)Gr-1(high) neutrophil infiltration peaked at day 4. BMCs were harvested from transgenic FVB mice expressing firefly luciferase (Fluc) and green fluorescent protein (GFP). Afterward, 2.5x10(6) BMCs were injected into the left ventricle of wild-type FVB mice either immediately (acute BMC) or 7 days (subacute BMC) after myocardial infarction, or after a sham procedure (n=8 per group). In vivo bioluminescence imaging showed an early signal increase in both BMC groups at day 7, followed by a nonsignificant trend (P=0.203) toward improved BMC survival in the subacute BMC group that persisted until the bioluminescence imaging signal reached BACKGROUND: <0.01) and 6 weeks (both BMC groups versus saline; P<0.05) but no significant differences between the 2 BMC groups. FACS analysis of BMC-injected hearts at day 7 revealed that GFP(+) BMCs expressed hematopoietic (CD45, Mac-1, Gr-1), minimal progenitor (Sca-1, c-kit), and no endothelial (CD133, Flk-1) or cardiac (Trop-T) cell markers. CONCLUSIONS: Timing of BMC delivery has minimal effects on intramyocardial retention and preservation of cardiac function. In general, there is poor long-term engraftment and BMCs tend to adopt inflammatory cell phenotypes.
PMID: 19920031 [PubMed - indexed for MEDLINE]
Posted in: Circ Cardiovasc Imaging
