Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P02794 (ferritin)
 17,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We studied the effect of myelodysplastic syndrome (MDS)-derived adherent cells on colony formation of granulocyte-macrophage progenitors (CFU-GM) in both normal and MDS bone marrow cells. MDS-adherent cells suppressed the growth of normal CFU-GM colony formation. Antibodies against ferritin almost totally neutralized the haematopoietic inhibitory activity. Antibody against gamma-interferon (gamma-IFN) did not have such effect. By cytogenetic analysis using G-staining method, MDS-derived CFU-GM colony showed abnormal clones. MDS have been recognized to be a mosaic of normal and abnormal clones. MDS-macrophages suppressed the growth of progenitor cells derived from normal clones by soluble factors, but did not suppress the growth of those from abnormal clones. It is suggested that progenitor cells derived from abnormal clones are freed from the negative myelopoietic regulator that may be related to the progress of leukaemia.
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PMID:MDS-macrophage derived inhibitory activity on myelopoiesis of MDS abnormal clones. 848 44

A variety of cytokines and chemokines exert potent myelosuppressive effects that play a role in the maintenance of hematopoiesis, which, if unchecked, may result in pathological impairment of blood cell production. Processes that modulate these myelosuppressive effects are not well defined. Here we demonstrate that stromal cell-derived factor-1 (SDF-1/CXCL12), known for its ability to attract and to promote survival of hematopoietic progenitor cells (HPCs) and stem cells, blocks the effects of a broad range of myelosuppressive chemokines on proliferation of HPCs in vitro. The regulatory effects of SDF/CXCL12 on colony formation by mouse bone marrow granulocyte-macrophage (CFUGM), erythroid (BFU-E), and multipotential (CFU-GEMM) progenitor cells were assessed. These cells were stimulated to proliferate by combinations of growth factors, such that responses of immature HPCs could be assessed. SDF-1/CXCL12 potently blocked myelosuppressive responses induced by CCL2/MCP-1, CCL3/MIP-1alpha, CCL19/CKbeta-11, CCL25/TECK, CXCL4/PF4, CXCL8/IL-8, CXCL10/IP-10, and XCL1/Lymphotactin. However, SDF/CDL12 did not influence myelosuppression induced by tumor necrosis factor (TNF)-alpha, interferon (IFN)-gamma, transforming growth factor (TGF)-beta or the iron-binding proteins H-ferritin or lactoferrin (LF). LF, previously shown to suppress release of growth factors, is shown here to also suppress proliferation of immature subsets of HPCs. HPCs from marrows of mice expressing an SDF-1/CXCL12 transgene were insensitive to inhibition by SDF/CXCL12-sensitive myelosuppressive chemokines, but not to SDF/CCL12-insensitive cytokines (TNF-alpha, IFN-gamma, TGF-beta, H-Ferritin, or LF). Thus, SDF-1/CXCL12 differentially and selectively regulates suppression of HPC proliferation by chemokines. These effects may counter myelosuppressive effects of certain chemokines in vivo, where proliferation of HPCs must be sustained.
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PMID:Stromal cell-derived factor-1/CXCL12 selectively counteracts inhibitory effects of myelosuppressive chemokines on hematopoietic progenitor cell proliferation in vitro. 1591 Feb 46

The purpose of this investigation was to determine whether echinacea supplementation results in alterations of erythroid growth factors and erythropoietic status. Twenty-four men age 24.9 +/- 4.2 y, height 1.7 +/- 0.8 m, weight 87.9 +/- 14.6 kg, and 19.3% +/- 6.5% body fat were grouped using a double-blind design and self- administered an 8000-mg/d dose of either echinacea (ECH) or placebo (PLA) in 5 x 400 mg x 4 times/d for 28 d. Blood samples were collected and analyzed for red blood cells (RBCs), hematocrit (Hct), hemoglobin (Hb), mean corpuscular volume, mean corpuscular hemoglobin content, prostaglandin E2, ferritin, erythropoietin (EPO), interleukin 3 (IL-3), and granulocyte-macrophage-colony-stimulating factor using automated flow cytometry and ELISA. ANOVA was used to determine significant differences (P ? 0.05). EPO was greater (P < 0.001) in ECH at Days 7, 14, and 21 and reflected a 44%, 63%, and 36% increase, respectively. IL-3 was greater (P = 0.011) in ECH at Days 14 and 21, which indicated a 65% and 73% increase, respectively. These data indicate that ECH supplementation resulted in an increase in EPO and IL-3 but did not significantly alter RBCs, Hb, or Hct.
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PMID:The effect of 4 wk of oral echinacea supplementation on serum erythropoietin and indices of erythropoietic status. 1796 12


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