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PubMed2004

Epigenetic silencing of the c-fms locus during B-lymphopoiesis occurs in discrete steps and is reversible.

The murine c-fms (Csf1r) gene encodes the macrophage colony-stimulating factor receptor, which is essential for macrophage development. It is expressed at a low level in haematopoietic stem cells and is switched off in all non-macrophage cell types. To examine the role of chromatin structure in this process we studied epigenetic silencing of c-fms during B-lymphopoiesis. c-fms chromatin in stem cells and multipotent progenitors is in the active conformation and bound by transcription factors. A similar result was obtained with specified common myeloid and lymphoid progenitor cells. In developing B cells, c-fms chromatin is silenced in distinct steps, whereby first the binding of transcription factors and RNA expression is lost, followed by a loss of nuclease accessibility. Interestingly, regions of de novo DNA methylation in B cells overlap with an intronic antisense transcription unit that is differently regulated during lymphopoiesis. However, even at mature B cell stages, c-fms chromatin is still in a poised conformation and c-fms expression can be re-activated by conditional deletion of the transcription factor Pax5.

Animals↗
PubMed2005

Generation and analysis of genetically defined liver carcinomas derived from bipotential liver progenitors.

Hepatocellular carcinoma is a chemoresistant cancer and a leading cause of cancer mortality; however, the molecular mechanisms responsible for the aggressive nature of this disease are poorly understood. In this study, we developed a new liver cancer mouse model that is based on the ex vivo genetic manipulation of embryonic liver progenitor cells (hepatoblasts). After retroviral gene transfer of oncogenes or short hairpin RNAs targeting tumor suppressor genes, genetically altered liver progenitor cells are seeded into the liver of otherwise normal recipient mice. We show that histopathology of the engineered liver carcinomas reveals features of the human disease. Furthermore, representational oligonucleotide microarray analysis (ROMA) of murine liver tumors initiated by two defined genetic hits revealed spontaneously acquired genetic alterations that are characteristic for human hepatocellular carcinoma. This model provides a powerful platform for applications like cancer gene discovery or high-throughput preclinical drug testing.

Animals↗
PubMed2005

[Changes of neural stem cells in neonatal rat model of hypoxic-ischemic encephalopathy].

OBJECTIVE: To establish a neonatal rat model of hypoxic-ischemic encephalopathy and clarify the changing features of neural stem cells (NSCs) in episodes of hypoxic-ischemic encephalopathy (HIE) so as to provide experimental and theoretical evidences for treating HIE by applying NSCs at the appropraite time. METHODS: Totally 210 neonatal rats aged 7 d were divided randomly into three groups, normal control group, hypoxic group and hypoxic-ischemic group with 70 rats in each. According to the time of sacrefice, 70 rats of every group were further divided randomly into seven groups including third hour (3 h), the sixth hour (6 h), first day (1 d), third day (3 d), the seventh day (7 d), the fourteenth day (14 d) and the twenty-first day (21 d), with 10 rats in each subgroup. The left common carotid artery of the neonatal rats in hypoxic-ischemic group was ligated and those in the hypoxic group were subjected to inhalation of 8% oxygen for 2.5 h. NSCs from brain tissues of the rats of the three groups were determined with HE staining and immunohistochemical method under light microscope. RESULTS: Most of neonatal rats in hypoxic-ischemic group behaved turning to the left stably 1 h after normal concentration of oxygen was given. In hypoxic-ischemic group, slight brain injury occurred at 3 h, severe brain injury appeared at 1 d, glial cells proliferated at 3 d and 7 d, brain atrophy was found at 14 d and 21 d. NSCs existed in brain tissues of rats in all the three groups. NSCs in normal control and the hypoxic group mainly distributed in hippocampus, subventricular tissues, striatum and cortex. But NSCs in hippocampus located in layers of molecule, cone cell and inner granular cell. NSCs in hypoxic-ischemic group showed obvious regional distribution, less in the regions with pathological changes. At 3 h, 6 h and 14 d, there was no difference in the number of NSCs between hypoxi and hypoxic-ischemic group. At 1 d, 3 d and 7 d, there was a highly significant difference in the number of NSCs between hypoxic and hypoxic-ischemic group. At 21 d, there was a significant difference in the number of NSCs between hypoxic and hypoxic-ischemic group, meanwhile, there was a significant difference in the number of NSCs between control and hypoxic group. At 3 d, there was a very significant difference in the number of NSCs between control and hypoxic-ischemic group. At 7 d and 21 d points, there was a highly significant difference in the number of NSCs between control and hypoxic group. CONCLUSION: The neonatal rat model of HIE was successfully established. NSCs increased in earlier period and decreased in later period of HIE, ultimately, NSCs located in the injured regions died one after anotner. Hypoxia induces NSCs' proliferation.

Animals↗
PubMed2006

Mesenchymal stromal cells.

PURPOSE OF REVIEW: Our understanding of the biology and properties of mesenchymal stem cells or multipotent mesenchymal stromal cells has expanded dramatically over the last 3 years and is likely to have an impact on clinical practice in the near future, making a review of this topic both timely and relevant RECENT FINDINGS: Recommendations regarding nomenclature and the definition of mesenchymal stromal cells have been proposed, a rapidly dividing population within the mesenchymal stromal cell compartment has been better defined and the ability of these cells to exhibit characteristics of cells from a variety of lineages has been extended. The notion that tissue repair with mesenchymal stromal cells is related to transdifferentiation has been re-evaluated and, for the myocardium at least, may be due rather to a paracrine mechanism. The most dramatic developments have been in identifying some of the complex mechanisms underlying the immunosuppressive and nonimmunogenic properties of mesenchymal stromal cells which have important implications for the management of conditions like acute graft-versus-host disease. SUMMARY: Mesenchymal stromal cells are a biologically important cell population that are able to support hematopoiesis, can differentiate along mesenchymal and nonmesenchymal lineages in vitro, are capable of suppressing alloresponses and appear to be nonimmunogenic. These properties suggest emerging roles for mesenchymal stromal cells in cell therapy.

Animals↗
PubMed1999

The monoclonal antibody SH-2, raised against human mesenchymal stem cells, recognizes an epitope on endoglin (CD105).

Mesenchymal stem cells are multipotent cells resident in the bone marrow throughout adulthood which have the capacity to differentiate into cartilage, bone, fat, muscle, and tendon. A number of monoclonal antibodies raised against human MSCs have been shown to react with surface antigens on these cells in vitro. A protein of molecular mass 92 kDa was immunoprecipitated using the SH-2 monoclonal antibody. This was purified and identified by peptide sequencing analysis and mass spectrometry as endoglin (CD105), the TGF-beta receptor III present on endothelial cells, syncytiotrophoblasts, macrophages, and connective tissue stromal cells. Endoglin on MSCs potentially plays a role in TGF-beta signalling in the control of chondrogenic differentiation of MSCs and also in mediating interactions between MSCs and haematopoietic cells in the bone marrow microenvironment.

Adult↗
PubMed2006

Imaging of cortical astrocytes using 2-photon laser scanning microscopy in the intact mouse brain.

A number of studies over the past decade have shown that astrocytes, the supportive cells of the brain, play important roles in synaptic transmission including regulating the strength of both excitatory and inhibitory synapses. A major challenge for the future is to define the role of astrocytes in complex tasks, such as functional hyperemia and sensory processing, as well as their contribution to acute and degenerative diseases of the nervous system. Multiphoton imaging approaches are ideally suited to study electrically non-excitable astrocytes. We here discuss novel in vivo studies aimed at defining the role of astrocytes in normal and pathological brain function. With a better understanding of the role astrocytes play in information processing and regulation of the brain microenvironment in vivo, and the understanding that astrocytes are heavily implicated in the pathology of many diseases such as epilepsy, Alzheimer's and Parkinson's diseases, astrocytes provide a promising target for future drug therapy approaches.

Animals↗
PubMed2003

[Effect of human cytomegalovirus on hematopoietic system].

OBJECTIVE: To investigate the mechanism and the suppression effect of human cytomegalovirus (HCMV) on hematopoietic system. METHODS: Semi-solid culture system was used to observe the effect of HCMV AD169 strain on colony forming unit granulocyte/macrophage (CFU-GM), CFU-erythroid (CFU-E), CFU-multipotent (CFU-Mix) and CFU-megakaryocyte (CFU-MK) growth. The techniques of in situ polymerase chain reaction (IS-PCR) and polymerase chain reaction (PCR) were used to demonstrate the existence of HCMV DNA in the colony cells of cultured CFU-GM, CFU-Mix, CFU-MK and CFU-E, respectively. The immediate early antigen (IEA) mRNA in CFU-MK and late antigen (LA) mRNA in CFU-E were detected by reverse transcriptase-polymerase chain reaction (RT-PCR). HCMV early protein P52 was detected with immunohistochemical technique. RESULTS: HCMV AD169 suppressed the differentiation and proliferation of CFU-GM, CFU-E, CFU-Mix and CFU-MK in vitro significantly (P < 0.05). The suppression was dose-dependent. HCMV DNA was successfully detected in CFU-GM, CFU-Mix, CFU-MK colony cells from viral infection groups by IS-PCR, and was detected in CFU-E by PCR, while it was negative in blank control or mock control groups. CFU-MK colony cells expressed HCMV IEA mRNA with the size of 340 bp in virus infection groups of 10(3) plague forming unit (PFU), 10(4) PFU and 10(5) PFU, respectively. The HCMV LA mRNA was detected by RT-PCR and was 263 bp long in positive control group of HCMV-infected human embryonic fibroblasts. The expression of HCMV LA mRNA in CFU-E was negative. The early protein P52 of HCMV in 10(4) PFU group was also identified by immunohistochemical staining. CONCLUSION: HCMV AD169 strains inhibited the differentiation and proliferation of CFU-GM, CFU-E, CFU-Mix and CFU-MK by the infection of the hematopoietic progenitors. HCMV might cause the suppression of hematopoiesis by direct infection, which is thought to be one of the reasons of HCMV infection associated with thrombocytopenia, neutropenia and anemia.

Colony-Forming Units Assay↗
PubMed1999

Flt3 ligand induces the outgrowth of Mac-1+B220+ mouse bone marrow progenitor cells restricted to macrophage differentiation that coexpress early B cell-associated genes.

Flt3 ligand (FL) is an important cytokine that affects the proliferation of hematopoietic stem cells and multipotent progenitors. In addition, FL seems to be strongly involved in the differentiation of B cells and macrophages. These two cell types are derived from separate hematopoietic lineages and display distinct surface markers, for instance, the pan-B cell marker B220 (CD45R) and the myelo/monocytic marker Mac-1 (CD11b), respectively. However, reports during several years have shown that some lineage markers can be coexpressed on factor-dependent progenitor cells as well as on some malignant leukemic clones. In the present study, we describe the ability of FL to induce the development and growth of Mac-1+ progenitor cells coexpressing B220 from c-kit+Lin- mouse bone marrow cells. FL was shown to be necessary but not sufficient for the development of Mac-1(-)B220+ cells, because certain other cytokines, in particular IL-6, had to be added to the cultures. An extended characterization of the cells revealed coexpression of other early B-cell markers, i.e., CD24, CD43, and c-kit. They expressed transcripts for c-fms, the receptor for macrophage-colony stimulating factor (M-CSF), and were able to develop into macrophages at high numbers, but not to other myeloid cells. By RT-PCR analysis we could also demonstrate expression of the B-cell associated genes Pax-5, Rag-2, and TdT. In contrast, Mac-1(+)B220- cells from the same cultures did not express any of the B-cell genes, and retained a broader myeloid differentiation capacity. Despite these B-cell associated features, Mac-1(+)B220- cells could not be induced towards B-cell progenitors. Our data suggest that FL triggers the activation of some B-cell associated genes in progenitor cells predestined to macrophage differentiation.

Animals↗
PubMed2006

Multipotent adult progenitor cell lines originating from the peripheral blood of green fluorescent protein transgenic swine.

Multipotent self-renewing stem cell lines have been established using peripheral blood mononuclear cells from adult green fluorescent protein transgenic swine. These cells proliferate as nonadherent spheroids in primordial-specific culture media and readily differentiate into angiogenic, osteogenic, adipogenic, and neurogenic phenotypes when cultured under the appropriate conditions. These cells are designated peripheral blood-derived multipotent adult progenitor cells (PBD-MAPCs). When differentiated in endothelial-specific media, these cells exhibit a cobblestone morphology and express von Willebrand factor (vWF), take up 1,1'-dioctadecyl-3,3,3',3'-tetramethyl-indocarboxyanine-labeled acetylated low-density lipoprotein DiI-Ac-LDL, and form tubes with lumens when grown on pads of Matrigel. Under different culture conditions, the cells appear whorl-like in appearance and express alpha-actin, indicative of smooth muscle phenotype. In the presence of dexamethasone and ascorbic acid, PBD-MAPCs differentiate into cells that produce Alizarin Red-staining extracellular mineral, consistent with an osteogenic potential. Under different conditions the cells produce Oil Red O-staining lipid vacuoles, suggestive of an adipocyte phenotype. We have also developed conditions that induce PBDMAPCs to differentiate into neural cells, confirmed by the expression of specific neuron- and glial-specific markers. Upon transplantation into rat brain, the neurogenic cells survive and migrate throughout the striatum and corpus callosum. The cells remain brightly fluorescent throughout their time in culture, during in vitro differentiation, and after in vivo transplantation. PBD-MAPCs have been maintained in primordial cell media for more than 100 doublings, yet can be induced to differentiate rapidly and efficiently into distinct cell types. PBD-MAPCs are ideal tools to study the mechanisms of differentiation and may be superior to embryonic stem cells as cellular therapeutics.

Actins↗
PubMed2002

Grafted lineage-restricted precursors differentiate exclusively into neurons in the adult spinal cord.

Multipotent neural stem cells (NSCs) have the potential to differentiate into neuronal and glial cells and are therefore candidates for cell replacement after CNS injury. Their phenotypic fate in vivo is dependent on the engraftment site, suggesting that the environment exerts differential effects on neuronal and glial lineages. In particular, when grafted into the adult spinal cord, NSCs are restricted to the glial lineage, indicating that the host spinal cord environment is not permissive for neuronal differentiation. To identify the stage at which neuronal differentiation is inhibited we examined the survival, differentiation, and integration of neuronal restricted precursor (NRP) cells, derived from the embryonic spinal cord of transgenic alkaline phosphatase rats, after transplantation into the adult spinal cord. We found that grafted NRP cells differentiate into mature neurons, survive for at least 1 month, appear to integrate within the host spinal cord, and extend processes in both the gray and white matter. Conversely, grafted glial restricted precursor cells did not differentiate into neurons. We did not observe glial differentiation from the grafted NRP cells, indicating that they retained their neuronal restricted properties in vivo. We conclude that the adult nonneurogenic CNS environment does not support the transition of multipotential NSCs to the neuronal commitment stage, but does allow the survival, maturation, and integration of NRP cells.

Alkaline Phosphatase↗
PubMed1986

A model of hemopoietic stress in a lactate dehydrogenase mouse mutant with hemolytic anemia.

A codominantly inherited mutation of the lactate dehydrogenase (LDH) in the C3H mouse causes a severe hemolytic anemia in homozygous mutants, whereas viability and fertility are close to normal. Investigation of multipotent hemopoietic stem cells (CFU-S), myeloid (GM-CFC) and erythroid progenitors (BFU-E, CFU-E) in femur and spleen indicates a general shift from bone marrow to splenic hemopoiesis. In terms of total body hemopoiesis, however, the BFU-E pool is 1.4- and the CFU-E pool 19-fold enlarged, whereas CFU-S and GM-CFC show little or no deviation from normal. It is concluded that this mouse mutant is an appropriate model of long-term hemopoietic stress showing that compensation in this severe hemolytic anemia is achieved primarily by an increase of the number of the most mature erythroid progenitors.

Anemia, Hemolytic↗
PubMed1998

Expression and function of a retinoic acid receptor in budding ascidians.

Retinoic acid is thought to induce transdifferentiation of multipotent epithelial stem cells in the developing buds of the ascidian Polyandrocarpa misakiensis. We isolated a cDNA clone from this species, named PmRAR, encoding a retinoic acid receptor (RAR) homologue. PmRAR clusters with other RARs on phylogenetic trees constructed by three different methods. Within the cluster, PmRAR is on a separate branch from all the subtypes of RARs, suggesting that RAR subtypes arose in the ancestral vertebrates after divergence of vertebrates and urochordates. The embryos of another ascidian species Ciona intestinalis were co-electroporated with a mixture of a PmRAR expression vector and a lacZ reporter plasmid containing vertebrate-type retinoic acid response elements. The expression of lacZ depended on the presence of both retinoic acid and PmRAR, suggesting that PmRAR is a functional receptor. PmRAR mRNA is expressed in the epidermis and mesenchyme cells of the Polyandrocarpa developing bud. The mRNA is not detectable in the mesenchyme cells in the adult body wall, but its expression can be induced by retinoic acid in vitro. These results suggest that the PmRAR is a mediator of retinoic acid signalling in transdifferentiation during asexual reproduction of protochordates.

Amino Acid Sequence↗
PubMed2004

Multiple signaling pathways are involved in erythropoietin-independent differentiation of erythroid progenitors in polycythemia vera.

Polycythemia vera (PV) is a myeloproliferative disorder arising in a multipotent hematopoietic stem cell. The pathogenesis of PV remains poorly understood; however, the biologic hallmark of this disease is the presence of erythropoietin (Epo)-independent colony formation (endogenous erythroid colony [EEC]) and cytokine hypersensitivity. We have developed a simple liquid culture from CD34+ cells to study PV erythroid differentiation. PV erythroid differentiation was characterized in this culture system by two types of abnormalities: 1) an increased proliferation of progenitors in response to cytokines, associated with strict cytokine dependency for preventing apoptosis; and 2) Epo-independent terminal erythroid differentiation in the presence of stem cell factor and interleukin-3 as evidenced by the acquisition of glycophorin A. The level of Epo-independent terminal differentiation correlates in PV patients with the number of EEC. Epo-independent terminal differentiation as well as normal Epo-induced differentiation were repressed by inhibitors of JAK2 (AG490), PI3K (LY294002), and the Src family kinases (PP2). In contrast, an inhibitor of the ERK/MAP kinase pathway (PD98059) had no effect on Epo-independent terminal differentiation. These signaling abnormalities were not mediated by a decreased expression or activity of the membrane tyrosine phosphatase CD45, which dephosphorylates JAK2 and Src family kinases. This study demonstrates that early steps of PV erythroid differentiation are strictly cytokine dependent. In contrast, late erythroid differentiation is an Epo-independent phenomenon that is mediated by signaling pathways identical to those in Epo-induced differentiation.

Antigens, CD34↗
PubMed2006

A close developmental relationship between the lymphoid and myeloid lineages.

The classic dichotomy model of hematopoiesis postulates that the first step of differentiation beyond the multipotent hematopoietic stem cell generates the common myelo-erythroid progenitors and common lymphoid progenitors (CLPs). Previous studies in fetal mice showed, however, that myeloid potential persists in the T- and B-cell branches even after these lineages have diverged, indicating that the simple dichotomy model is invalid, at least for fetal hematopoiesis. Nevertheless, CLPs have persisted in models of adult hematopoiesis; results from several groups support the presence of CLPs in bone marrow. Recent evidence challenges the dichotomy model in the adult, and it is proposed here that the alternative myeloid-based model is applicable to both fetal and adult hematopoiesis.

Animals↗
PubMed2005

The transcriptional basis of adipocyte development.

Adipogenesis is the developmental process by which a multipotent mesenchymal stem cell differentiates into a mature adipocyte. This process involves a highly regulated and coordinated cascade of transcription factors that together lead to the establishment of the differentiated state. In the presence of the correct hormonal cues, committed pre-adipocytes express the bZIP factors C/EBPb and C/EBPd. These factors in turn induce the expression of C/EBPa and peroxisome proliferator-activated receptor g (PPARg). C/EBPa and PPARg together promote differentiation by activating adipose-specific gene expression and by maintaining each others expression at high levels. We have investigated the relative contributions of PPARg and C/EBPa to adipogenesis by selectively ablating these genes in mouse embryonic fibroblasts (MEFs). MEFs that lack C/EBPa are able to undergo adipogenesis, but only when PPARg is ectopically expressed. Interestingly, these cells are not sensitive to the metabolic actions of insulin. By way of contrast, cells that lack PPARg are utterly incapable of adipogenic conversion, even when supplemented with high levels of C/EBPa. Our current investigations are centered on the identification of novel adipogenic transcription factors, utilizing a variety of techniques, ranging from BAC transgenics to computational approaches. These approaches will be discussed, along with the roles of some new transcriptional players in adipogenesis, including the O/E family of proteins.

Adipocytes↗
PubMed2006

Characterization and induction of human pre-adipocytes.

Human processed lipoaspirate is a source of multipotent adult stem cells that are able to differentiate between mesenchymal and neurogenic lineage. We characterized PLA cells by cytometry and then they were cultured to induce differentiation into myogenic and neurogenic lineage. Lipoaspirates were digested with collagenase to obtain the pellet, which was labelled with anti-CD44, anti-CD45, and anti-CD90. We used BD FACS Calibur flow cytometer to acquire cellular events. Some cells were cultured at 37 degrees C and 5% CO(2) in neurogenic or myogenic medium and analysed by immunocytochemistry, using Neuron specific enolase, Vimentin, Glial fibrillary acidic protein, Tau, MAP2 to confirm neurogenic differentiation, MyoD1, Myosin heavy chain, Actin smooth muscle, vimentin to confirm myogenic differentiation. The cytometry results suggest that a part of the cells are of a mesenchymal origin, among which there are progenitor endothelial cells and leucocytes. Microscopy observation already reveals neuronal morphology and longitudinal multinucleated cells compared to control cells. Neurogenic cells only express NSE (early neuronal progenitor marker), but not GFAP, Tau, MAP2 (mature neuron and glial markers); myogenic cells are positive for MyoD1 and Myosin heavy chain. This demonstrates that lipoaspirate cells are capable of differentiating in vitro over a short period of time, and could be employed in biological and clinical research, like mesenchymal adult stem cells.

Adipocytes↗
PubMed1988

Decreased interleukin-1 production in aplastic anemia.

PURPOSE: Interleukin-1 (IL-1), a monocyte factor, plays a central role in the regulation of the immune response; recent data have suggested that IL-1 is the same molecule as hemopoietin-1, a growth factor acting on the multipotent hematopoietic stem cell. IL-1 affects hematopoiesis (1) in vitro, by inducing the release of colony-stimulating factors and regulating early hematopoietic progenitor cells, and (2) in vivo, by stimulating stem cell recovery in irradiated or chemotherapy-treated mice. Several lines of evidence suggest that aplastic anemia may be mediated by cells of the immune system. We address the issue of abnormal IL-1 production in severe aplastic anemia and attempt to correlate normalization of the levels with response to anti-thymocyte globulin (ATG) therapy. PATIENTS AND METHODS: We studied IL-1 production by monocytes from 21 patients with aplastic anemia using a bioassay for IL-1 activity. Fifteen patients were evaluated before ATG therapy. Eight patients were studied before and three months after ATG. In addition, five patients were evaluated only after ATG treatment. One patient did not respond to ATG but did respond to intravenous acyclovir, and was studied before and after acyclovir therapy. Twenty patients with other hematologic disorders requiring transfusions and 30 normal healthy volunteers were also assessed. RESULTS: IL-1 production was markedly decreased in 75 percent of patients with aplastic anemia when compared with that in normal control subjects (p less than 0.005). Hematologic recovery correlated with normalization of IL-1 production in all but two cases (p less than 0.04). CONCLUSION: These observations represent the first evidence of monocyte dysfunction and deficient hematopoietic growth factor production in aplastic anemia. Decreased IL-1 production may have a pathologic role in some cases of aplastic anemia.

Adult↗
PubMed1988

Monoclonal anti-Thy-1.2 antibody induced hematopoiesis in vivo.

The intravenous injection of a monoclonal anti-Thy-1.2 alloantibody (IgM class) induced a rapid increase in the number, and the ratio, of multipotent hematopoietic stem cells (CFU-S) in S-phase. The onset of hematopoiesis was thymus-independent. Reconstitution of lethally-irradiated mice with bone marrow cells from mice injected with antibody augmented the T-cell responsiveness to mitogens. No activation was observed in granulocyte/macrophage progenitors. The monoclonal antibody did not directly stimulate CFU-S in vitro, although hematopoietic activity could be found in the sera of antibody-injected mice. Immediately after injection, the antibody was found bound on Thy-1+ cells in spleen. No decrease in the number of peripheral T cells was seen. These results seem to indicate that Thy-1.2-positive cells bound with anti-Thy-1.2 alloantibody may secrete a factor which induces the proliferation of hematopoietic stem cells.

Animals↗