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  • Oxford University Press (OUP)  (8)
  • 1
    Online Resource
    Online Resource
    Hypoxia and serum deprivation-induced apoptosis in mesenchymal stem cells
    Oxford University Press (OUP) ; 2006
    In:  Stem Cells Vol. 24, No. 4 ( 2006-04-01), p. 1141-1141
    Details
    In: Stem Cells, Oxford University Press (OUP), Vol. 24, No. 4 ( 2006-04-01), p. 1141-1141
    Type of Medium: Online Resource
    ISSN: 1066-5099 , 1549-4918
    URL: Article
    DOI: 10.1634/stemcells.2006-erratum3
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2006
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    detail.hit.zdb_id: 1143556-2
    detail.hit.zdb_id: 605570-9
    SSG: 12
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  • 2
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    Hypoxia and Serum Deprivation-Induced Apoptosis in Mesenchymal Stem Cells
    Oxford University Press (OUP) ; 2006
    In:  Stem Cells Vol. 24, No. 2 ( 2006-02-01), p. 416-425
    Details
    In: Stem Cells, Oxford University Press (OUP), Vol. 24, No. 2 ( 2006-02-01), p. 416-425
    Abstract: In recent years, the understanding that regeneration progresses at the level of the myocardium has placed stem cell research at the center stage in cardiology. Despite an increasing interest in cell transplant research, relatively little is known about the biochemical regulation of the stem cell itself after transplantation into an ischemic heart. We demonstrated here, using rat mesenchymal stem cells (MSCs), that cells undergo caspase-dependent apoptosis in response to hypoxia and serum deprivation (SD), which are both components of ischemia in vivo. In particular, the treated cells exhibited mitochondrial dysfunction, including cytochrome C release, loss in ΔΨm, and Bax accumulation, but in a p53-independent manner. Although the cells treated by hypoxia/SD possess the activity of caspase-8, zIEDT-fmk, a specific caspase-8 inhibitor, failed to inhibit cell apoptosis induced in our system. Taken together, our findings indicate that MSCs are sensitive to hypoxia/SD stimuli that involve changes in mitochondrial integrity and function but are potentially independent of caspase-8.
    Type of Medium: Online Resource
    ISSN: 1066-5099 , 1549-4918
    URL: Article
    DOI: 10.1634/stemcells.2005-0121
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2006
    detail.hit.zdb_id: 2030643-X
    detail.hit.zdb_id: 1143556-2
    detail.hit.zdb_id: 605570-9
    SSG: 12
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  • 3
    Online Resource
    Online Resource
    Lysophosphatidic Acid Protects Mesenchymal Stem Cells Against Hypoxia and Serum Deprivation-Induced Apoptosis
    Oxford University Press (OUP) ; 2008
    In:  Stem Cells Vol. 26, No. 1 ( 2008-01-01), p. 135-145
    Details
    In: Stem Cells, Oxford University Press (OUP), Vol. 26, No. 1 ( 2008-01-01), p. 135-145
    Abstract: Bone marrow-derived mesenchymal stem cells (MSCs) have shown great promise for cardiac repair. However, poor viability of transplanted MSCs within the ischemic heart has limited their therapeutic potential. Our previous studies have documented that hypoxia and serum deprivation (hypoxia/SD), induced MSCs apoptosis through the mitochondrial apoptotic pathway. Since serum lysophosphatidic acid (LPA) levels are known to be significantly elevated after acute myocardial infarction and that LPA enhanced survival of other cell systems, we embarked on determining whether LPA protects MSCs against hypoxia/SD-induced apoptosis. We have also investigated the potential mechanism(s) that may mediate such actions of LPA. All experiments were carried out on rat bone marrow MSCs. Apoptosis was induced by exposure of cells to hypoxia/SD in a sealed GENbox hypoxic chamber. Effects of LPA were investigated in the absence and presence of inhibitors that target either Giproteins, the mitogen activated protein kinases ERK1/2, or phosphoinositide 3-kinase (PI3K). The data obtained showed that hypoxia/SD-induced apoptosis was significantly attenuated by LPA through Gi-coupled LPA1 receptors linked to the downstream ERK1/2 and PI3K/Akt signaling pathways that function in parallel. Additional studies have demonstrated that hypoxia/SD-induced activation of mitochondrial dysfunction was virtually abolished by LPA treatment and that inhibition of the LPA1 receptor, Gi proteins, the PI3K/Akt pathway, or ERKs effectively reversed this protective action of LPA. Taken together, our findings indicate that LPA is a novel, potent survival factor for MSCs and this may prove to be of considerable therapeutic significance in terms of exploiting MSC-based therapy in the infracted myocardium. Disclosure of potential conflicts of interest is found at the end of this article.
    Type of Medium: Online Resource
    ISSN: 1066-5099 , 1549-4918
    URL: Article
    DOI: 10.1634/stemcells.2007-0098
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2008
    detail.hit.zdb_id: 2030643-X
    detail.hit.zdb_id: 1143556-2
    detail.hit.zdb_id: 605570-9
    SSG: 12
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  • 4
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    Online Resource
    Long non-coding RNAs link extracellular matrix gene expression to ischemic cardiomyopathy
    Oxford University Press (OUP) ; 2016
    In:  Cardiovascular Research Vol. 112, No. 2 ( 2016-11), p. 543-554
    Details
    In: Cardiovascular Research, Oxford University Press (OUP), Vol. 112, No. 2 ( 2016-11), p. 543-554
    Type of Medium: Online Resource
    ISSN: 0008-6363 , 1755-3245
    URL: Article
    DOI: 10.1093/cvr/cvw201
    RVK:
    WA 15000
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2016
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  • 5
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    GDF11 enhances therapeutic efficacy of mesenchymal stem cells for myocardial infarction via YME1L-mediated OPA1 processing
    Oxford University Press (OUP) ; 2020
    In:  Stem Cells Translational Medicine Vol. 9, No. 10 ( 2020-10-01), p. 1257-1271
    Details
    In: Stem Cells Translational Medicine, Oxford University Press (OUP), Vol. 9, No. 10 ( 2020-10-01), p. 1257-1271
    Abstract: Growth differentiation factor 11 (GDF11) has been shown to promote stem cell activity, but little is known about the effect of GDF11 on viability and therapeutic efficacy of cardiac mesenchymal stem cells (MSCs) for cardiac injury. To understand the roles of GDF11 in MSCs, mouse heart-derived MSCs were transduced with lentiviral vector carrying genes for both GDF11 and green fluorescent protein (GFP) (MSCsLV-GDF11) or cultured with recombinant GDF11 (MSCsrGDF11). Either MSCsrGDF11 or MSCs LV-GDF11 displayed less cell apoptosis and better paracrine function, as well as preserved mitochondrial morphology and function under hypoxic condition as compared with control MSCs. GDF11 enhanced phosphorylation of Smad2/3, which upregulated expression of YME1L, a mitochondria protease that balances OPA1 processing. Inhibitors of TGF-β receptor (SB431542) or Smad2/3 (SIS3) attenuated the effects of GDF11 on cell viability, mitochondrial function, and expression of YME1L. Transplantation of MSCsGDF11 into infarct heart resulted in improved cell survival and retention, leading to more angiogenesis, smaller scar size, and better cardiac function in comparison with control MSCs. GDF11 enhanced viability and therapeutic efficiency of MSCs by promoting mitochondrial fusion through TGF-β receptor/Smad2/3/YME1L-OPA1 signaling pathway. This novel role of GDF11 may be used for a new approach of stem cell therapy for myocardial infarction.
    Type of Medium: Online Resource
    ISSN: 2157-6564 , 2157-6580
    URL: Article
    DOI: 10.1002/sctm.20-0005
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2020
    detail.hit.zdb_id: 2642270-0
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  • 6
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    Synthesis and Characterization of the First Organically Templated Layered Cerium Phosphate Fluoride: [(CH2)2(NH3)2]0.5[CeIVF3(HPO4)]
    Oxford University Press (OUP) ; 2004
    In:  Chemistry Letters Vol. 33, No. 4 ( 2004-04-01), p. 458-459
    Details
    In: Chemistry Letters, Oxford University Press (OUP), Vol. 33, No. 4 ( 2004-04-01), p. 458-459
    Abstract: A novel organically templated layered cerium phosphate fluoride [(CH2)2(NH3)2]0.5[CeIVF3(HPO4)] has been synthesized by hydrothermal synthesis technology, and characterized by means of single-crystal X-ray diffraction. Its unique layered structure is based on a network of novel CeO3F5 polyhedral and PO4 tetrahedral. The [NH3(CH2)2NH3]+ cations contact with the adjacent layers via hydrogen bonds to compensate the negative charge of the inorganic framework.
    Type of Medium: Online Resource
    ISSN: 0366-7022 , 1348-0715
    URL: Article
    DOI: 10.1246/cl.2004.458
    RVK:
    VA 3560
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2004
    detail.hit.zdb_id: 2063626-X
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  • 7
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    Enhanced Cardioprotection by Human Endometrium Mesenchymal Stem Cells Driven by Exosomal MicroRNA-21
    Oxford University Press (OUP) ; 2017
    In:  Stem Cells Translational Medicine Vol. 6, No. 1 ( 2017-01-01), p. 209-222
    Details
    In: Stem Cells Translational Medicine, Oxford University Press (OUP), Vol. 6, No. 1 ( 2017-01-01), p. 209-222
    Abstract: Our group recently reported positive therapeutic benefit of human endometrium-derived mesenchymal stem cells (EnMSCs) delivered to infarcted rat myocardium, an effect that correlated with enhanced secretion of protective cytokines and growth factors compared with parallel cultures of human bone marrow MSCs (BMMSCs). To define more precisely the molecular mechanisms of EnMSC therapy, in the present study, we assessed in parallel the paracrine and therapeutic properties of MSCs derived from endometrium, bone marrow, and adipose tissues in a rat model of myocardial infarction (MI). EnMSCs, BMMSCs, and adipose-derived MSCs (AdMSCs) were characterized by fluorescence-activated cell sorting (FACS). Paracrine and cytoprotective actions were assessed in vitro by coculture with neonatal cardiomyocytes and human umbilical vein endothelial cells. A rat MI model was used to compare cell therapy by intramyocardial injection of BMMSCs, AdMSCs, and EnMSCs. We found that EnMSCs conferred superior cardioprotection relative to BMMSCs or AdMSCs and supported enhanced microvessel density. Inhibitor studies indicated that the enhanced paracrine actions of EnMSCs were mediated by secreted exosomes. Analyses of exosomal microRNAs (miRs) by miR array and quantitative polymerase chain reaction revealed that miR-21 expression was selectively enhanced in exosomes derived from EnMSCs. Selective antagonism of miR-21 by anti-miR treatment abolished the antiapoptotic and angiogenic effects of EnMSCs with parallel effects on phosphatase and tensin homolog (PTEN), a miR-21 target and downstream Akt. The results of the present study confirm the superior cardioprotection by EnMSCs relative to BMMSCs or AdMSCs and implicates miR-21 as a potential mediator of EnMSC therapy by enhancing cell survival through the PTEN/Akt pathway. The endometrium might be a preferential source of MSCs for cardiovascular cell therapy.
    Type of Medium: Online Resource
    ISSN: 2157-6564 , 2157-6580
    URL: Article
    DOI: 10.5966/sctm.2015-0386
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2017
    detail.hit.zdb_id: 2642270-0
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  • 8
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    Online Resource
    Loss of ten-eleven translocation 2 induces cardiac hypertrophy and fibrosis through modulating ERK signaling pathway
    Oxford University Press (OUP) ; 2021
    In:  Human Molecular Genetics Vol. 30, No. 10 ( 2021-05-29), p. 865-879
    Details
    In: Human Molecular Genetics, Oxford University Press (OUP), Vol. 30, No. 10 ( 2021-05-29), p. 865-879
    Abstract: The ten-eleven translocation (Tet) family of dioxygenases convert 5-methylcytosine to 5-hydroxymethylcytosine (5hmC). Previous studies have shown that 5hmC-mediated epigenetic modifications play essential roles in diverse biological processes and diseases. Here, we show that Tet proteins and 5hmC display dynamic features during postnatal cardiac development and that Tet2 is the predominant dioxygenase present in heart. Tet2 knockout results in abnormal cardiac function, progressive cardiac hypertrophy and fibrosis. Mechanistically, Tet2 deficiency leads to reduced hydroxymethylation in the cardiac genome and alters the cardiac transcriptome. Mechanistically, Tet2 loss leads to a decrease of Hspa1b expression, a regulator of the extracellular signal-regulated protein kinase (Erk) signaling pathway, which leads to over-activation of Erk signaling. Acute Hspa1b knock down (KD) increased the phosphorylation of Erk and induced hypertrophy of cardiomyocytes, which could be blocked by Erk signaling inhibitor. Consistently, ectopic expression of Hspa1b was able to rescue the deficits of cardiomyocytes induced by Tet2 depletion. Taken together, our study’s results reveal the important roles of Tet2-mediated DNA hydroxymethylation in cardiac development and function.
    Type of Medium: Online Resource
    ISSN: 0964-6906 , 1460-2083
    URL: Article
    DOI: 10.1093/hmg/ddab046
    RVK:
    XA 10000
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2021
    detail.hit.zdb_id: 1474816-2
    SSG: 12
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