Duanqing Pei

Chinese Academy of Sciences, Peping, Beijing, China

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Publications (135)917.39 Total impact

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    ABSTRACT: Sox2 is a key factor in maintaining self-renewal of embryonic stem cells (ESCs) and adult stem cells as well as in reprogramming differentiated cells back into pluripotent or multipotent stem cells. Although previous studies have shown that Sox2 is phosphorylated in human ESCs, the biological significance of Sox2 phosphorylation in ESC maintenance and reprogramming has not been well understood. In this study, we have identified new phosphorylation sites on Sox2, and have further demonstrated that Cdk-mediated Sox2 phosphorylation at S39 and S253 is required for establishing the pluripotent state during reprogramming but is dispensable for ESC maintenance. Mass-spectrometry analysis of purified Sox2 protein has identified new phosphorylation sites on two Tyrosine and six Serine/Threonine residues. Cdk2 physically interacts with Sox2 and phosphorylates Sox2 at S39 and S253 in vitro. Surprisingly, Sox2 phosphorylation at S39 and S253 is dispensable for ESC self-renewal and cell cycle progression. In addition, Sox2 phosphorylation enhances its ability to establish the pluripotent state during reprogramming by working with Oct4 and Klf4. Finally, Cdk2 can also modulate the ability of Oct4, Sox2 and Klf4 in reprogramming fibroblasts back into pluripotent stem cells. Therefore, this study has, for the first time, demonstrated that Sox2 phosphorylation by Cdk proteins promotes the establishment, but not the maintenance, of the pluripotent state. It might also help explain why the inactivation of CDK inhibitors, such as p53, p21 and Arf/Ink4, promotes the induction of pluripotent stem cells. Copyright © 2015, The American Society for Biochemistry and Molecular Biology.
    Journal of Biological Chemistry 07/2015; DOI:10.1074/jbc.M115.658195 · 4.57 Impact Factor
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    ABSTRACT: Oncogenic transcription factors are known to mediate the conversion of somatic cells to tumour or induced pluripotent stem cells (iPSCs). Here we report c-Jun as a barrier for iPSC formation. c-Jun is expressed by and required for the proliferation of mouse embryonic fibroblasts (MEFs), but not mouse embryonic stem cells (mESCs). Consistently, c-Jun is induced during mESC differentiation, drives mESCs towards the endoderm lineage and completely blocks the generation of iPSCs from MEFs. Mechanistically, c-Jun activates mesenchymal-related genes, broadly suppresses the pluripotent ones, and derails the obligatory mesenchymal to epithelial transition during reprogramming. Furthermore, inhibition of c-Jun by shRNA, dominant-negative c-Jun or Jdp2 enhances reprogramming and replaces Oct4 among the Yamanaka factors. Finally, Jdp2 anchors 5 non-Yamanaka factors (Id1, Jhdm1b, Lrh1, Sall4 and Glis1) to reprogram MEFs into iPSCs. Our studies reveal c-Jun as a guardian of somatic cell fate and its suppression opens the gate to pluripotency.
    Nature Cell Biology 06/2015; 17(7):856-867. DOI:10.1038/ncb3193 · 20.06 Impact Factor
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    ABSTRACT: Levels of atonal homolog 8 (ATOH8) are reduced in 48% of hepatitis B virus-associated hepatocellular carcinomas (HCCs). ATOH8 downregulation is associated with loss of tumor differentiation, indicating an effect mediated by cancer stem cells. We investigated the effects of loss of ATOH8 in human hepatocellular carcinoma (HCC) cells and cell lines. HCC and adjacent non-tumor tissues were collected, from 2001 through 2012, from 242 patients undergoing hepatectomy at Sun Yat-Sen University Cancer Center in China; 83% of HCCs were associated with HBV infection. CD133+ cells were isolated from tumor tissues by flow cytometry. Experiments were performed in HBV-positive and HBV-negative HCC cell lines, the immortalized liver cell line LO2, and 8 other HCC cell lines. ATOH8 was expressed from lentiviral vectors in PLC8024 and Huh7 cells; levels were knocked down with small interfering RNAs in QSG7701 cells. Cells carrying empty vectors were used as controls. Gene regulation by ATOH8 was assessed in mobility shift and luciferase reporter assays. Cells were analyzed in proliferation, foci formation, and colony formation assays. The tumorigenic and chemo-resistant potential of cells were investigated by assessing growth of xenograft tumors in immunocompromised mice. Metastatic features of cells were assessed in Matrigel invasion assays and wound healing analyses. Levels of ATOH8 mRNA were reduced by more than 4-fold, compared to non-tumor tissues, in 118/242 HCC samples (48.8%). Patients with tumor reductions in ATOH8 had significantly shorter times of disease-free survival (mean, 41.4 months) than patients with normal tissue levels (mean, 52.6 months). ATOH8 expression was reduced in HepG2, Huh7, PLC8024 and CRL8064 HCC cells, as well as CD133+ cells isolated from human HCC samples. Transgenic expression of ATOH8 in HCC cell lines significantly reduced proliferation and foci colony formation, as well as their invasive and migratory abilities. Transgenic expression of ATOH8 reduced the ability of HBV-positive PLC8024 cells to form tumors in mice, compared to control cells. Cells with ATOH8 knockdown formed xenograft tumors more rapidly, in more mice, than control cells. ATOH8 repressed transcription of stem-cell associated genes including OCT4, NANOG, and CD133. Knockdown of ATOH8 in CD133-negative QSG7701 cells caused them to express CD133; acquire self-renewal, differentiation, chemo-resistance properties; form more xenograft tumors in mice; and generate induced pluripotent stem cells (based on staining for alkaline phosphatase and their ability to form embryoid bodies and teratomas). Alternatively, expression of ATOH8 in PLC8024 and Huh7 cells significantly reduced the numbers of cells expressing CD133, and increased the chemo-sensitivity of Huh7 cells to 5-fluorouracil (5-FU) and cisplatin, in vitro and in mice. ATOH8 appears to be a tumor suppressor that induces stem-cell features and chemoresistance in HCC cells. Strategies to restore its levels and activities might be developed to treat patients with liver cancer. Copyright © 2015 AGA Institute. Published by Elsevier Inc. All rights reserved.
    Gastroenterology 06/2015; DOI:10.1053/j.gastro.2015.06.010 · 13.93 Impact Factor
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    ABSTRACT: The mouse is an organism that is widely used as a mammalian model for studying human physiology or disease, and the development of immunodeficient mice has provided a valuable tool for basic and applied human disease research. Following the development of large-scale mouse knockout programs and genome-editing tools, it has become increasingly efficient to generate genetically modified mouse strains with immunodeficiency. However, due to the lack of a standardized system for evaluating the immuno-capacity that prevents tumor progression in mice, an objective choice of the appropriate immunodeficient mouse strains to be used for tumor engrafting experiments is difficult. In this study, we developed a tumor engraftment index (TEI) to quantify the immunodeficiency response to hematologic malignant cells and solid tumor cells of six immunodeficient mouse strains and C57BL/6 wild-type mouse (WT). Mice with a more severely impaired immune system attained a higher TEI score. We then validated that the NOD-scid-IL2Rg-/- (NSI) mice, which had the highest TEI score, were more suitable for xenograft and allograft experiments using multiple functional assays. The TEI score was effectively able to reflect the immunodeficiency of a mouse strain.
    Journal of Hematology & Oncology 05/2015; 8(1):59. DOI:10.1186/s13045-015-0156-y · 4.93 Impact Factor
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    ABSTRACT: We describe robust induction of autophagy during the reprogramming of mouse fibroblasts to induced pluripotent stem cells by four reprogramming factors (Sox2, Oct4, Klf4 and c-Myc), henceforth 4F. This process occurs independently of p53 activation, and is mediated by the synergistic downregulation of mechanistic target of rapamycin complex 1 (mTORC1) and the induction of autophagy-related genes. The 4F coordinately repress mTORC1, but bifurcate in their regulation of autophagy-related genes, with Klf4 and c-Myc inducing them but Sox2 and Oct4 inhibiting them. On one hand, inhibition of mTORC1 facilitates reprogramming by promoting cell reshaping (mitochondrial remodelling and cell size reduction). On the other hand, mTORC1 paradoxically impairs reprogramming by triggering autophagy. Autophagy does not participate in cell reshaping in reprogramming but instead degrades p62, whose accumulation in autophagy-deficient cells facilitates reprogramming. Our results thus reveal a complex signalling network involving mTORC1 inhibition and autophagy induction in the early phase of reprogramming, whose delicate balance ultimately determines reprogramming efficiency.
    Nature Cell Biology 05/2015; 17(6). DOI:10.1038/ncb3172 · 20.06 Impact Factor
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    ABSTRACT: Heteroplasmic cells, harboring both mutant and normal mitochondrial DNAs (mtDNAs), must accumulate mutations to a threshold level before respiratory activity is affected. This phenomenon has led to the hypothesis of mtDNA complementation by inter-mitochondrial content mixing. The precise mechanisms of heteroplasmic complementation are unknown, but it depends both on the mtDNA nucleoid dynamics among mitochondria as well as the mitochondrial dynamics as influenced by mtDNA. We tracked nucleoids among the mitochondria in real time to show that they are shared after complete fusion but not 'kiss-and-run'. Employing a cell hybrid model, we further show that mtDNA-less mitochondria, which have little ATP production and extensive Opa1 proteolytic cleavage, exhibit weak fusion activity among themselves, yet remain competent in fusing with healthy mitochondria in a mitofusin- and OPA1-dependent manner, resulting in restoration of metabolic function. Depletion of mtDNA by overexpression of the matrix-targeted nuclease UL12.5 resulted in heterogeneous mitochondrial membrane potential (ΔΨm) at the organelle level in mitofusin-null cells but not in wild type. In this system, overexpression of mitofusins or application of the fusion-promoting drug M1 could partially rescue the metabolic damage caused by UL12.5. Interestingly, mtDNA transcription/translation is not required for normal mitochondria to restore metabolic function to mtDNA-less mitochondria by fusion. Thus, interplay between mtDNA and fusion capacity governs a novel 'initial metabolic complementation'.
    Cellular and Molecular Life Sciences CMLS 02/2015; 72(13). DOI:10.1007/s00018-015-1863-9 · 5.86 Impact Factor
  • Duanqing Pei · Yasong Wu · Yuan Li · Baoming Qin
    02/2015; DOI:10.1038/protex.2015.001
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    ABSTRACT: Human pluripotent stem cells (hPSCs) are a promising cell source with pluripotency and capacity to differentiate into all human somatic cell types. Designing simple and safe biomaterials with an innate ability to induce osteoblastic lineage from hPSCs is desirable to realize their clinical adoption in bone regenerative medicine. To address the issue, here we developed a fully defined synthetic peptides-decorated two dimensional (2D) microenvironment assisted via polydopamine (pDA) chemistry and subsequent carboxymethyl chitosan (CMC) grafting to enhance the culture and osteogenic potential of hPSCs in vitro. The hPSCs including human embryonic stem cells (hESCs) and human induced pluripotent stem cells (hiPSCs) were successfully cultured on the peptides-decorated surface without Matrigel- and ECM protein-coating and underwent promoted osteogenic differentiation in vitro, determined from the alkaline phosphate (ALP) activity, gene expression, and protein production as well as calcium deposit amount. It was found that directed osteogenic differentiation of hPSCs could be achieved through a peptides-decorated niche. This chemical-defined and safe 2D microenvironment which facilitates proliferation and osteo-differentiation of hPSCs, not only helps to accelerate the translational perspectives of hPSCs, but also provides tissue-specific functions such as directing stem cell differentiation commitment, having great potential in bone tissue engineering and presenting new avenues for bone regenerative medicine.
    ACS Applied Materials & Interfaces 02/2015; 7(8). DOI:10.1021/acsami.5b00188 · 6.72 Impact Factor
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    ABSTRACT: Successful expansion of hematopoietic stem cells (HSCs) would benefit the use of HSC transplants in the clinic. Angiopoietin-like 7 promotes the expansion of hematopoietic stem and progenitor cells (HSPC) in vitro and ex vivo. However, the impact of loss of Angptl7 on HSPCs in vivo has not been characterized. Here, we generated Angptl7-deficient mice by TALEN-mediated gene targeting and found that HSC compartments in Angptl7-null mice were compromised. In addition, wild type (WT) HSPCs failed to repopulate in the BM of Angptl7-null mice after serial transplantations while the engraftment of Angptl7-deficient HSPCs in WT mice was not impaired. These results suggest that Angptl7 is required for HSPCs repopulation in a non-cell autonomous manner. Electronic supplementary material The online version of this article (doi:10.1186/s13045-014-0102-4) contains supplementary material, which is available to authorized users.
    Journal of Hematology & Oncology 02/2015; 8(1):7. DOI:10.1186/s13045-014-0102-4 · 4.93 Impact Factor
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    ABSTRACT: Successful expansion of hematopoietic stem cells would benefit the use of hematopoietic stem cell transplants in the clinic. Several angiopoietin-like proteins, including angiopoietin-like 7, can support the activity of hematopoietic stem cells. However, effects of ANGPTL7 on human hematopoietic stem cells and the downstream signaling cascade activated by ANGPTL7 are poorly understood. Here, we established a human hematopoietic stem and progenitor cell-supportive mouse fetal liver cell line that specifically expressed the Angptl7 protein. Furthermore, we found ANGPTL7 is capable of stimulating human hematopoietic stem and progenitor cell expansion and increasing the repopulation activities of human hematopoietic progenitors in xenografts. RNA-sequencing analysis showed that ANGPTL7 activated the expression of CXCR4, HOXB4 and Wnt downstream targets in human hematopoietic progenitors. In addition, chemical manipulation of Wnt signaling diminished the effects of ANGPTL7 on human hematopoietic stem and progenitor cells in culture. In summary, we identify the secreted growth factor ANGPTL7 as a regulator of both human hematopoietic stem and progenitor cells expansion and regeneration. Copyright © 2015, Ferrata Storti Foundation.
    Haematologica 01/2015; 100(5). DOI:10.3324/haematol.2014.118612 · 5.87 Impact Factor
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    ABSTRACT: Valproic acid (VPA) is widely used to treat epilepsy, migraine, chronic headache, bipolar disorder, and as adjuvant chemotherapy, but potentially causes idiosyncratic liver injury. Alpers syndrome (AHS), a neurometabolic disorder caused by mutations in the mitochondrial DNA polymerase gamma (POLG), is associated with an increased risk of developing fatal VPA hepatotoxicity. However, the mechanistic link of this clinical mystery remains unknown. Here, fibroblasts from two AHS patients were reprogrammed to induced pluripotent stem cells, and then differentiated to hepatocyte-like cells (AHS iPSCs-Hep). Both AHS iPSCs-Hep are more sensitive to VPA-induced mitochondrial dependent apoptosis than controls, showing more activated caspase-9 and cytochrome c release. Strikingly, levels of both soluble and oligomeric OPA1, which together keep cristae junctions tight, are reduced in AHS iPSCs-Hep. Furthermore, POLG mutation cells show reduced POLG expression, mitochondrial DNA (mtDNA) amount, mitochondrial ATP production as well as abnormal mitochondrial ultrastructure following differentiation to hepatocyte-like cells. Superoxide flashes, spontaneous bursts of superoxide generation, caused by opening of the mitochondrial permeability transition pore (mPTP), occur more frequently in AHS iPSCs-Hep. Moreover, the mPTP inhibitor, cyclosporine A (CsA), rescues VPA-induced apoptotic sensitivity in AHS iPSCs-Hep. This result suggests that targeting mPTP opening could be an effective method to prevent hepatotoxicity by VPA in AHS patients. In addition, carnitine or N-acetylcysteine (NAC), which has been used in the treatment of VPA-induced hepatotoxicity, is able to rescue VPA-induced apoptotic sensitivity in AHS iPSCs-Hep. Conclusion: AHS iPSCs-Hep are more sensitive to the VPA-induced mitochondrial dependent apoptotic pathway, and this effect is mediated by mPTP opening. This is the first toxicity model in genetic diseases using iPSCs, which also will enable the evaluation of drugs for the therapeutic target. This article is protected by copyright. All rights reserved.
    Hepatology 01/2015; 61(5). DOI:10.1002/hep.27712 · 11.19 Impact Factor
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    ABSTRACT: Hematopoiesis is a progressive process collectively controlled by an elaborate network of transcription factors (TFs). Among these TFs, GATA2 has been implicated to be critical for regulating multiple steps of hematopoiesis in mouse models. However, whether similar function of GATA2 is conserved in human hematopoiesis, especially during early embryonic development stage, is largely unknown. To examine the role of GATA2 in human background, we generated homozygous GATA2 knockout human embryonic stem cells (GATA2 (-/-) hESCs) and analyzed their blood differentiation potential. Our results demonstrated that GATA2 (-/-) hESCs displayed attenuated generation of CD34(+)CD43(+) hematopoietic progenitor cells (HPCs), due to the impairment of endothelial to hematopoietic transition (EHT). Interestingly, GATA2 (-/-) hESCs retained the potential to generate erythroblasts and macrophages, but never granulocytes. We further identified that SPI1 downregulation was partially responsible for the defects of GATA2 (-/-) hESCs in generation of CD34(+)CD43(+) HPCs and granulocytes. Furthermore, we found that GATA2 (-/-) hESCs restored the granulocyte potential in the presence of Notch signaling. Our findings revealed the essential roles of GATA2 in EHT and granulocyte development through regulating SPI1, and uncovered a role of Notch signaling in granulocyte generation during hematopoiesis modeled by human ESCs.
    01/2015; 4(1):4. DOI:10.1186/s13619-015-0018-7
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    ABSTRACT: Recent studies have boosted our understanding of long noncoding RNAs (lncRNAs) in numerous biological processes, but few have examined their roles in somatic cell reprogramming. Through expression profiling and functional screening, we have identified that the large intergenic noncoding RNA p21 (lincRNA-p21) impairs reprogramming. Notably, lincRNA-p21 is induced by p53 but does not promote apoptosis or cell senescence in reprogramming. Instead, lincRNA-p21 associates with the H3K9 methyltransferase SETDB1 and the maintenance DNA methyltransferase DNMT1, which is facilitated by the RNA-binding protein HNRNPK. Consequently, lincRNA-p21 prevents reprogramming by sustaining H3K9me3 and/or CpG methylation at pluripotency gene promoters. Our results provide insight into the role of lncRNAs in reprogramming and establish a novel link between p53 and heterochromatin regulation.Cell Research advance online publication 16 December 2014; doi:10.1038/cr.2014.165.
    Cell Research 12/2014; 25(1). DOI:10.1038/cr.2014.165 · 11.98 Impact Factor
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    ABSTRACT: Sorting nexin 10 (SNX10), the unique member of the SNX family having vacuolation activity in cells, was shown to be involved in the development of Autosomal Recessive Osteopetrosis (ARO) in recent genetic studies. However, the molecular mechanism of the disease-related mutations affecting the biological function of SNX10 is unclear. Here, we report the crystal structure of human SNX10 to 2.6 Å resolution. The structure reveals that SNX10 contains the extended PX domain we previously proposed. Our study provides the structural details of those disease-related mutations. Combined with the vacuolation study of those mutations, we found that Tyr32 and Arg51 are important for the protein stability and both play a critical role in vacuolation activity, while Arg16Leu may affect the function of SNX10 in osteoclast through protein-protein interactions. © Proteins 2014;. © 2014 Wiley Periodicals, Inc.
    Proteins Structure Function and Bioinformatics 12/2014; 82(12). DOI:10.1002/prot.24689 · 2.92 Impact Factor
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    ABSTRACT: Reactivation of the pluripotency network during somatic cell reprogramming by exogenous transcription factors involves chromatin remodeling and the recruitment of RNA polymerase II (Pol II) to target loci. Here, we report that Pol II is engaged at pluripotency promoters in reprogramming but remains paused and inefficiently released. We also show that bromodomain-containing protein 4 (BRD4) stimulates productive transcriptional elongation of pluripotency genes by dissociating the pause release factor P-TEFb from an inactive complex containing HEXIM1. Consequently, BRD4 overexpression enhances reprogramming efficiency and HEXIM1 suppresses it, whereas Brd4 and Hexim1 knockdown do the opposite. We further demonstrate that the reprogramming factor KLF4 helps recruit P-TEFb to pluripotency promoters. Our work thus provides a mechanism for explaining the reactivation of pluripotency genes in reprogramming and unveils an unanticipated role for KLF4 in transcriptional pause release.
  • Xiaodong Shu · Duanqing Pei
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    ABSTRACT: The process that converts somatic cells to pluripotent ones has enormous potential not only as a tool to generate cells for disease therapy and modeling, but also as an experimental system to investigate fundamental biological questions. The discovery of mesenchymal-to-epithelial transitions at the initial phase of reprogramming provides a conceptual framework to understand reprogramming in a cellular context and it helps to resolve the mechanistic roles of the original Yamanaka factors as well as newly identified modulators of reprogramming. Emerging concept such as sequential EMT-MET in reprogramming further suggests the value of this model to the understanding of cell fate conversions. We highlight recent advances about the function and regulation of MET in reprogramming and discuss their potential implications here.
    Current Opinion in Genetics & Development 08/2014; 28C:32-37. DOI:10.1016/j.gde.2014.08.005 · 8.57 Impact Factor
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    ABSTRACT: Differentiation of neural lineages from human pluripotent stem cells (hPSCs) raises the hope of generating functional cells for the treatment of neural diseases. However, current protocols for differentiating hPSCs into neural lineages remain inefficient and largely variable between different hPSC lines. We report that microRNA 376c (miR-376c) significantly enhanced neural differentiation of hPSCs in a defined condition by suppressing SMAD4, the co-SMAD for TGF-β signaling. Downstream, SMAD4 directly bound and suppressed PAX6, the critical neural lineage specification factor. Interestingly, we also found that SMAD4 binds and suppresses miR-376c clusters in undifferentiated hESCs. In summary, our findings revealed a reciprocal antagonism between miR-376c and SMAD signaling that regulates cell fate during human neural differentiation.-Liu, J., Wang, L., Su, Z., Wu, W., Cai, X., Li, D., Hou, J., Pei, D., Pan, G. A reciprocal antagonism between miR-376c and TGF-β signaling regulates neural differentiation of hPSCs.
    The FASEB Journal 08/2014; 28(11). DOI:10.1096/fj.13-249342 · 5.48 Impact Factor
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    ABSTRACT: Accumulating evidence indicates that the mesenchymal-epithelial transition (MET) and epithelial-mesenchymal transition (EMT) are basic mechanisms for cell fate conversion and may help us understand both physiologic and pathologic processes such as development and carcinogenesis. Here, we further suggest that mammalian cells fall into two grand divisions, mesenchymal or epithelial; interconversions between these two grand divisions through EMT/MET resonate with some ancient Chinese philosophic ideas.
    Cell Research 07/2014; 24(10). DOI:10.1038/cr.2014.93 · 11.98 Impact Factor
  • Pengfei Liu · Yanmei Zhang · Shubin Chen · Jinglei Cai · Duanqing Pei
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    ABSTRACT: The stem-cell-based tissue-engineering approaches are widely applied in establishing functional organs and tissues for regenerative medicine. Successful generation of induced pluripotent stem cells (iPS cells) and rapid progress of related technical platform provide great promise in the development of regenerative medicine, including organ regeneration. We have previously reported that iPS cells could be an appealing stem cells source contributing to tooth regeneration. In the present paper, we mainly review the application of iPS technology in dental bioengineering and discuss the challenges for iPS cells in the whole tooth regeneration.
    Stem Cell Reviews and Reports 06/2014; 10(5). DOI:10.1007/s12015-014-9531-2 · 3.21 Impact Factor
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    ABSTRACT: Hemophilia A (HA) is a severe, congenital bleeding disorder caused by the deficiency of clotting factor VIII (FVIII). For years, traditional laboratory animals have been used to study HA and its therapies, although animal models may not entirely mirror the human pathophysiology. Human induced pluripotent stem cells (iPSCs) can undergo unlimited self-renewal and differentiate into all cell types. This study aims to generate hemophilia A (HA) patient-specific iPSCs that differentiate into disease-affected hepatocyte cells. These hepatocytes are potentially useful for in vitro disease modeling and provide an applicable cell source for autologous cell therapy after genetic correction.
    Life Sciences 05/2014; 108(1). DOI:10.1016/j.lfs.2014.05.004 · 2.30 Impact Factor

Publication Stats

4k Citations
917.39 Total Impact Points

Institutions

  • 2006–2015
    • Chinese Academy of Sciences
      • • South China Institute for Stem Cell Biology and Regenerative Medicine
      • • Guangzhou Institutes of Biomedicine and Health
      Peping, Beijing, China
  • 2014
    • The University of Hong Kong
      Hong Kong, Hong Kong
  • 2013
    • University of Science and Technology of China
      • School of Life Sciences
      Luchow, Anhui Sheng, China
  • 2011
    • University of Natural Resources and Life Science Vienna
      Wien, Vienna, Austria
  • 2009–2011
    • Institute for Stem Cell Biology and Regenerative Medicine
      Bengalūru, Karnataka, India
  • 2003–2006
    • Tsinghua University
      • School of Medicine
      Peping, Beijing, China