Database : MEDLINE
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[PMID]: 25044556
[Au] Autor:Wen Y; Elliott MJ; Huang Y; Miller TO; Corbin DR; Hussain LR; Ratajczak MZ; Fukui Y; Ildstad ST
[Ad] Address:Institute for Cellular Therapeutics.
[Ti] Title:DOCK2 Is Critical for CD8(+) TCR(-) Graft Facilitating Cells to Enhance Engraftment of Hematopoietic Stem and Progenitor Cells.
[So] Source:Stem Cells;32(10):2732-43, 2014 Oct.
[Is] ISSN:1549-4918
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:CD8(+) TCR(-) graft facilitating cells (FCs) enhance engraftment of hematopoietic stem cells (HSCs) in allogeneic and syngeneic recipients. The mechanisms by which FCs promote HSC engraftment and tolerance induction have not been fully elucidated. Here, we provide data to support a critical role for dedicator of cytokinesis 2 (DOCK2) in multiple aspects of FCs function. DOCK2(-/-) FCs exhibit compromised facilitative function in vivo as evidenced by the loss of engraftment-enhancing capability for c-Kit(+) Sca-1(+) lineage(-) (KSL) cells, and compromised ability to promote KSL cell homing and lodgment in hematopoietic niche. Deletion of DOCK2 abrogates the ability of FCs to induce differentiation of naïve CD4(+) CD25(-) T cells into FoxP3(+) regulatory T cells and interleukin-10-producing type 1 regulatory T cells in vitro. Moreover, DOCK2(-/-) FCs are unable to promote survival of KSL cells when cocultured with KSL cells. DOCK2(-/-) FCs also exhibit compromised migration to stroma-derived factor-1 in vitro and impaired homing to the bone marrow in vivo. In conclusion, our results demonstrate that DOCK2 is critical for FCs to maintain its immunomodulatory function and exert its trophic effects on KSL cells. These findings may have direct clinical relevance to promote HSC engraftment for treatment of autoimmunity, hemoglobinopathies, and to induce transplantation tolerance. Stem Cells 2014;32:2732-2743.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1409
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1002/stem.1780

  2 / 311111 MEDLINE  
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[PMID]: 24989835
[Au] Autor:Hu X; Wu R; Jiang Z; Wang L; Chen P; Zhang L; Yang L; Wu Y; Chen H; Chen H; Xu Y; Zhou Y; Huang X; Webster KA; Yu H; Wang J
[Ad] Address:Department of Cardiology, Second Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, China; Cardiovascular Key Laboratory of Zhejiang Province, Hangzhou, China.
[Ti] Title:Leptin signaling is required for augmented therapeutic properties of mesenchymal stem cells conferred by hypoxia preconditioning.
[So] Source:Stem Cells;32(10):2702-13, 2014 Oct.
[Is] ISSN:1549-4918
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Hypoxia preconditioning enhances the therapeutic effect of mesenchymal stem cells (MSCs). However, the mechanism underlying hypoxia-induced augmentation of the protective effect of MSCs on myocardial infarction (MI) is poorly understood. We show that hypoxia-enhanced survival, mobility, and protection of cocultured cardiomyocytes were paralleled by increased expression of leptin and cell surface receptor CXCR4. The enhanced activities were abolished by either knockdown of leptin with a selective shRNA or by genetic deficiency of leptin or its receptor in MSCs derived, respectively, from ob/ob or db/db mice. To characterize the role of leptin in the regulation of MSC functions by hypoxia and its possible contribution to enhanced therapeutic efficacy, cell therapy using MSCs derived from wild-type, ob/ob, or db/db mice was implemented in mouse models of acute MI. Augmented protection by hypoxia pretreatment was only seen with MSCs from wild-type mice. Parameters that were differentially affected by hypoxia pretreatment included MSC engraftment, c-Kit(+) cell recruitment to the infarct, vascular density, infarct size, and long-term contractile function. These data show that leptin signaling is an early and essential step for the enhanced survival, chemotaxis, and therapeutic properties of MSCs conferred by preculture under hypoxia. Leptin may play a physiological role in priming MSCs resident in the bone marrow endosteum for optimal response to systemic signaling molecules and subsequent tissue repair. Stem Cells 2014;32:2702-2713.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1409
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1002/stem.1784

  3 / 311111 MEDLINE  
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[PMID]: 24966156
[Au] Autor:Kim HY; Kim H; Oh KW; Oh SI; Koh SH; Baik W; Noh MY; Kim KS; Kim SH
[Ad] Address:Department of Neurology, College of Medicine, Hanyang University, Seoul, South Korea.
[Ti] Title:Biological markers of mesenchymal stromal cells as predictors of response to autologous stem cell transplantation in patients with amyotrophic lateral sclerosis: an investigator-initiated trial and in vivo study.
[So] Source:Stem Cells;32(10):2724-31, 2014 Oct.
[Is] ISSN:1549-4918
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Bone marrow mesenchymal stromal cells (MSCs) can modify disease progression in amyotrophic lateral sclerosis (ALS) model. However, there are currently no accurate biological markers for predicting the efficacy of autologous MSC transplants in ALS patients. This open-label, single-arm, investigator-initiated clinical study was designed to identify markers of MSCs that could be used as potential predictors of response to autologous MSC therapy in patients with ALS. We enrolled 37 patients with ALS who received autologous MSCs via intrathecal injection in two monthly doses. After a 6-month follow-up period, the patients were categorized as responders and non-responders based on their scores on the revised ALS Functional Rating Scale (ALSFRS-R). Biological markers including ß-fibroblast growth factor-2, stromal cell-derived factor-1α, vascular endothelial growth factor (VEGF), insulin-like growth factor-1, brain-derived neurotrophic factor, angiogenin (ANG), interleukin (IL)-4, IL-10, and transforming growth factor-ß (TGF-ß) were measured in the MSC cultures and their levels were compared between the responders and nonresponders. To confirm the markers' predictive ability, MSCs isolated from one patient in each group were transplanted into the cisterna magna of mutant SOD1(G93A) transgenic mice to measure their lifespans, locomotor activity, and motor neuron numbers. The levels of VEGF, ANG, and TGF-ß were significantly higher in responders than in nonresponders. In the mouse model, the recipients of responder MSCs had a significantly slower onset of symptoms and a significantly longer lifespan than the recipients of nonresponders or controls. Our data suggest that VEGF, ANG, and TGF-ß levels in MSCs could be used as potential biological markers to predict the effectiveness of autologous MSC therapy and to identify those patients who could optimally benefit from MSC treatment. Stem Cells 2014;32:2724-2731.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1409
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1002/stem.1770

  4 / 311111 MEDLINE  
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[PMID]: 24906078
[Au] Autor:Leon-Rico D; Aldea M; Sanchez R; Segovia JC; Weiss LA; Hidalgo A; Bueren JA; Almarza E
[Ad] Address:Division of Hematopoietic Innovative Therapies, Centro de Investigaciones Energéticas, Medioambientales y Tecnológicas (CIEMAT) and Centro de Investigación Biomédica en Red de Enfermedades Raras (CIBER-ER), Madrid, Sapin; Instituto de Investigación Sanitaria Fundación Jiménez Díaz (IIS-FJD, UAM), Madrid, Spain.
[Ti] Title:Brief Report: Reduced Expression of CD18 Leads to the In Vivo Expansion of Hematopoietic Stem Cells in Mouse Bone Marrow.
[So] Source:Stem Cells;32(10):2794-8, 2014 Oct.
[Is] ISSN:1549-4918
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Leukocyte adhesion deficiency type-I is a primary immunodeficiency caused by mutations in the ITGB2 gene (CD18 leukocyte integrin) which lead to defects in leukocyte extravasation. To investigate the role of CD18 in hematopoietic stem cell (HSC) biology, we have thoroughly characterized the HSCs of CD18 Itgb2(tm1bay) hypomorphic mice (CD18(HYP) ) both by flow cytometry and using in vitro and in vivo transplantation assays. Flow cytometry analyses and cultures in methyl cellulose revealed that bone marrow (BM) from CD18(HYP) mice was enriched in hematopoietic precursors, mainly early quiescent short-term and long-term Hematopoietic progenitors cells. Strikingly, BM competition assays showed a progressive expansion of CD18(HYP) -derived hematopoiesis in recipient mice. Additionally, we provide evidence that this HSC expansion was not caused by an increased homing capacity of CD18(HYP) HSCs or by alterations in the hematopoietic environment of CD18(HYP) mice due to defects in neutrophils clearance. On the contrary, our data demonstrated that the reduced expression of CD18 causes a cell-autonomous expansion in the HSC compartment, thus revealing unexpected regulatory functions for CD18 in mouse HSCs. Stem Cells 2014;32:2794-2798.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1409
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1002/stem.1762

  5 / 311111 MEDLINE  
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[PMID]: 25221594
[Au] Autor:Huang L; Li R; Liu W; Dai J; Du Z; Wang X; Ma J; Zhao J
[Ad] Address:Department of Joint Surgery, Orthopedics Hospital of the Second Hospital of Jilin University, Changchun, Jilin Province, China....
[Ti] Title:Dynamic culture of a thermosensitive collagen hydrogel as an extracellular matrix improves the construction of tissue-engineered peripheral nerve.
[So] Source:Neural Regen Res;9(14):1371-8, 2014 Jul 15.
[Is] ISSN:1673-5374
[Cp] Country of publication:India
[La] Language:eng
[Ab] Abstract:Tissue engineering technologies offer new treatment strategies for the repair of peripheral nerve injury, but cell loss between seeding and adhesion to the scaffold remains inevitable. A thermosensitive collagen hydrogel was used as an extracellular matrix in this study and combined with bone marrow mesenchymal stem cells to construct tissue-engineered peripheral nerve composites in vitro. Dynamic culture was performed at an oscillating frequency of 0.5 Hz and 35° swing angle above and below the horizontal plane. The results demonstrated that bone marrow mesenchymal stem cells formed membrane-like structures around the poly-L-lactic acid scaffolds and exhibited regular alignment on the composite surface. Collagen was used to fill in the pores, and seeded cells adhered onto the poly-L-lactic acid fibers. The DNA content of the bone marrow mesenchymal stem cells was higher in the composites constructed with a thermosensitive collagen hydrogel compared with that in collagen I scaffold controls. The cellular DNA content was also higher in the thermosensitive collagen hydrogel composites constructed with the thermosensitive collagen hydrogel in dynamic culture than that in static culture. These results indicate that tissue-engineered composites formed with thermosensitive collagen hydrogel in dynamic culture can maintain larger numbers of seeded cells by avoiding cell loss during the initial adhesion stage. Moreover, seeded cells were distributed throughout the material.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1409
[Da] Date of entry for processing:140915
[St] Status:PubMed-not-MEDLINE
[do] DOI:10.4103/1673-5374.137590

  6 / 311111 MEDLINE  
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[PMID]: 25220590
[Au] Autor:Byrne M; Bennett RL; Cheng X; Stratford May W
[Ad] Address:Department of Medicine, Division of Hematology and Oncology and the University of Florida Health Cancer Center, Gainesville, FL 32610....
[Ti] Title:Progressive Genomic Instability in the Nup98-HoxD13 Model of MDS Correlates with Loss of the PIG-A Gene Product.
[So] Source:Neoplasia;16(8):627-33, 2014 Aug.
[Is] ISSN:1476-5586
[Cp] Country of publication:Canada
[La] Language:eng
[Ab] Abstract:The Nup98-HoxD13 (NHD13) fusion gene was identified in a patient with therapy-related myelodysplastic syndrome (MDS). When transgenically expressed in hematopoietic cells, mice faithfully recapitulate human disease with serial progression from peripheral blood (PB) cytopenias and increased bone marrow (BM) blasts to acute leukemia. It is well accepted that genomic instability in dysplastic hematopoietic stem/progenitor cells (HSPC) drives the evolution of MDS to acute leukemia. Findings here demonstrate that reticulocytes, myeloid and lymphoid PB cells of NHD13 mice, display an increase in the age-associated loss of glycosylphosphatidylinositol-linked surface proteins versus wild type controls. These data correlate with a progressive increase in the DNA damage response as measured by γ-H2AX activity, accumulating BM blasts as the disease progresses and finally development of acute leukemia. These findings clearly demonstrate a state of progressive genomic instability that increases the likelihood of a "second hit" or complimentary mutation later in the disease to trigger development of acute leukemia and underscores the mechanistic nature of how the NUP98-HoxD13 transgene induces progression of MDS to acute leukemia. Additionally, these data support the use of the PIG-A assay as an efficient, real-time surrogate marker of the genomic instability that occurs in the MDS HSPCs. Key Point The PIG-A assay is a sensitive, nonlethal method for the serial assessment of genomic instability in mouse models of MDS.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1409
[Js] Journal subset:IM
[St] Status:In-Data-Review

  7 / 311111 MEDLINE  
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[PMID]: 25220589
[Au] Autor:Chen WT; Ha D; Kanel G; Lee AS
[Ad] Address:Department of Biochemistry and Molecular Biology, University of Southern California, Keck School of Medicine, USC Norris Comprehensive Cancer Center, 1441 Eastlake Avenue, NOR 5308, Los Angeles, CA, 90089-9176, USA. Electronic address: chenwant@usc.edu....
[Ti] Title:Targeted Deletion of ER Chaperone GRP94 in the Liver Results in Injury, Repopulation of GRP94-Positive Hepatocytes, and Spontaneous Hepatocellular Carcinoma Development in Aged Mice.
[So] Source:Neoplasia;16(8):617-26, 2014 Aug.
[Is] ISSN:1476-5586
[Cp] Country of publication:Canada
[La] Language:eng
[Ab] Abstract:Hepatocellular carcinoma (HCC) often results from chronic liver injury and severe fibrosis or cirrhosis, but the underlying molecular pathogenesis is unclear. We previously reported that deletion of glucose regulated protein 94 (GRP94), a major endoplasmic reticulum chaperone, in the bone marrow and liver leads to progenitor/stem cell expansion. Since liver progenitor cell (LPC) proliferation can contribute to liver tumor formation, here we examined the effect of GRP94 deficiency on spontaneous liver tumorigenesis. Utilizing liver-specific Grp94 knockout mice driven by Albumin-Cre (cGrp94(f/f)), we discovered that while wild-type livers are tumor free up to 24 months, cGrp94(f/f) livers showed abnormal small nodules at 15 months and developed HCC and ductular reactions (DRs) by 21 months of age, associating with increased liver injury, apoptosis and fibrosis. cGrp94(f/f) livers were progressively repopulated by GRP94-positive hepatocytes. At 15 months, we observed expansion of LPCs and mild DRs, as well as increase in cell proliferation. In examining the underlying mechanisms for HCC development in cGrp94(f/f) livers, we detected increase in TGF-ß1, activation of SMAD2/3, ERK, and JNK, and cyclin D1 upregulation at the premalignant stage. While epithelial-mesenchymal transition (EMT) was not evident, E-cadherin expression was elevated. Correlating with the recurrence of GRP94 positive-hepatocytes, the HCC was found to be GRP94-positive, whereas the expanded LPCs and DRs remained GRP94-negative. Collectively, this study uncovers that GRP94 deficiency in the liver led to injury, LPC expansion, increased proliferation, activation of oncogenic signaling, progressive repopulation of GRP94-positive hepatocytes and HCC development in aged mice.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1409
[Js] Journal subset:IM
[St] Status:In-Data-Review

  8 / 311111 MEDLINE  
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[PMID]: 25146676
[Au] Autor:Arahira T; Todo M
[Ad] Address:Interdisciplinary Graduate School of Engineering Sciences, Kyushu University, Fukuoka, Japan; Currently, Fukuoka Dental College, Fukuoka, Japan.
[Ti] Title:Effects of Proliferation and Differentiation of Mesenchymal Stem Cells on Compressive Mechanical Behavior of Collagen/ß-TCP Composite Scaffold.
[So] Source:J Mech Behav Biomed Mater;39:218-30, 2014 Nov.
[Is] ISSN:1878-0180
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:The primary aim of this study is to characterize the effects of cell culture on the compressive mechanical behavior of the collagen/ß-tricalcium phosphate (TCP) composite scaffold. The composite and pure collagen scaffolds were fabricated by the solid-liquid phase separation technique and the subsequent freeze-drying method. Rat bone marrow mesenchymal stem cells (rMSCs) were then cultured in these scaffolds up to 28 days. Compression test of the scaffolds with rMSCs were conducted periodically. Biological properties such as cell number, alkaline phosphatase (ALP) activity, and gene expressions of osteogenetic bone markers were evaluated during cell culture. The microstructural changes in the scaffolds during cell culture were also examined using a scanning electron microscope. The compressive elastic modulus was then correlated with those of the biological properties and microstructures to understand the mechanism of variational behavior of the macroscopic elastic property. The composite scaffold exhibited higher ALP activity and more active generation of osteoblastic markers than the collagen scaffold, indicating that ß-TCP can activate the differentiation of rMSCs into osteoblasts and extracellular matrix (ECM) formation such as type I collagen and the following mineralization. The variational behavior of the compressive modulus of the composite scaffold was affected by both the material degradation and the proliferation of cells and the ECM formation. In the first stage, the modulus of the composite scaffold tended to increase due to cell proliferation and the following formation of network structure. In the second stage, the modulus tended to decrease because the material degradation such as ductile deformation of collagen and decomposition of ß-TCP were more effective on the property than the ECM formation. In the third stage, active calcification by formation and growth of mineralized nodules resulted in the recovery of modulus. It is concluded that the introduction of ß-TCP powder into the porous collagen matrix is very effective to improve the mechanical and biological properties of collagen scaffold prepared for bone tissue engineering. Furthermore, the compressive modulus of the composite scaffold is strongly affected by the material degradation and the ECM formation by stem cells under in vitro culture condition.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1409
[Js] Journal subset:IM
[St] Status:In-Data-Review

  9 / 311111 MEDLINE  
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[PMID]: 24751726
[Au] Autor:Han NR; Oh HA; Nam SY; Moon PD; Kim DW; Kim HM; Jeong HJ
[Ad] Address:Department of Pharmacology, College of Korean Medicine, Kyung Hee University, Dongdaemun-gu, Seoul, Republic of Korea....
[Ti] Title:TSLP Induces Mast Cell Development and Aggravates Allergic Reactions through the Activation of MDM2 and STAT6.
[So] Source:J Invest Dermatol;134(10):2521-30, 2014 Oct.
[Is] ISSN:1523-1747
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Thymic stromal lymphopoietin (TSLP) is known to promote T helper type 2 cell-associated inflammation. Mast cells are major effector cells in allergic inflammatory responses. We noted that the population and maturation of mast cells were reduced in TSLP-deficient mice (TSLP-/-). Thus, we hypothesized that TSLP might affect mast cell development. We found that TSLP induced the proliferation and differentiation of mast cells from bone marrow progenitors. TSLP-induced mast cell proliferation was abolished by depletion of mouse double minute 2 (MDM2) and signal transducers and activators of transcription 6 (STAT6), as an upstream activator of MDM2. TSLP-/-, in particular, had a considerable deficit in the expression of MDM2 and STAT6. Also, the TSLP deficiency attenuated mast cell-mediated allergic reactions through the downregulation of STAT6 and MDM2. In an antibody microarray chip analysis, MDM2 expression was increased in atopic dermatitis patients. These observations indicate that TSLP is a factor for mast cell development, and that it aggravates mast cell-mediated immune responses.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1409
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1038/jid.2014.198

  10 / 311111 MEDLINE  
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[PMID]: 24714203
[Au] Autor:Liu S; Jiang L; Li H; Shi H; Luo H; Zhang Y; Yu C; Jin Y
[Ad] Address:1] Research and Development Center for Tissue Engineering, Fourth Military Medical University, Xi'an, Shaanxi, China [2] Department of Oral Histology and Pathology, School of Stomatology, Fourth Military Medical University, Xi'an, Shaanxi, China....
[Ti] Title:Mesenchymal Stem Cells Prevent Hypertrophic Scar Formation via Inflammatory Regulation when Undergoing Apoptosis.
[So] Source:J Invest Dermatol;134(10):2648-57, 2014 Oct.
[Is] ISSN:1523-1747
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The cutaneous wound-healing process can lead to hypertrophic scar formation, during which exaggerated inflammation has been demonstrated to have an important role. Therefore, an exploration of strategies designed to regulate this inflammatory process is warranted. Mesenchymal stem cells (MSCs) have recently been demonstrated to regulate inflammation in various diseases. In this regard, using a rabbit model, we locally injected human mesenchymal stem cells (hMSCs) derived from bone marrow to treat hypertrophic scar formation, and explored their underlying mechanisms. We found that hMSC therapy efficiently regulated inflammation and prevented scar formation. We attributed the therapeutic effects of hMSCs to their secretion of an anti-inflammatory protein, TNF-alpha-stimulated gene/protein 6 (TSG-6). Unexpectedly, after injection, the number of surviving hMSCs decreased markedly and the hMSCs underwent extensive apoptosis, which was demonstrated to promote their secretion of TSG-6, partially through the activation of caspase-3. Moreover, H2O2-induced apoptotic hMSCs showed higher inflammatory regulatory abilities. The inhibition of caspase-3 decreased the inflammatory regulatory abilities of hMSCs and attenuated their therapeutic effects. Our results demonstrate that hMSCs can efficiently prevent hypertrophic scar formation via inflammatory regulation. In addition, we found that apoptosis has an important role in the activation of the inflammatory regulatory abilities of hMSCs.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1409
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1038/jid.2014.169


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