Cell Transplantation (CELL TRANSPLANT)

Publisher: Cell Transplant Society, Cognizant Communication Corporation

Journal description

Cell Transplantation publishes original, peer-reviewed research and review articles on the subject of cell transplantation and its application to human diseases. To ensure high-quality contributions from all areas of transplantation, separate section editors and editorial boards have been established. Articles deal with a wide range of topics including physiological, medical, preclinical, tissue engineering, and device-oriented aspects of transplantation of nervous system, endocrine, growth factor-secreting, bone marrow, epithelial, endothelial, and genetically engineered cells, among others. Basic clinical studies and immunological research papers are also featured. To provide complete coverage of this revolutionary field, Cell Transplantation will report on relevant technological advances, and ethical and regulatory considerations of cell transplants.

Current impact factor: 3.57

Impact Factor Rankings

2015 Impact Factor Available summer 2015
2013 / 2014 Impact Factor 3.57
2012 Impact Factor 4.422
2011 Impact Factor 5.126
2010 Impact Factor 6.204
2009 Impact Factor 5.126
2008 Impact Factor 5.251
2007 Impact Factor 3.871
2006 Impact Factor 3.482
2005 Impact Factor 3.481
2004 Impact Factor 2.497
2003 Impact Factor 2.327
2002 Impact Factor 2.42
2001 Impact Factor 2.19
2000 Impact Factor 2.959
1999 Impact Factor 2.493
1998 Impact Factor 1.818
1997 Impact Factor 1.744

Impact factor over time

Impact factor
Year

Additional details

5-year impact 3.98
Cited half-life 4.20
Immediacy index 0.43
Eigenfactor 0.01
Article influence 0.80
Website Cell Transplantation website
Other titles Cell transplantation
ISSN 0963-6897
OCLC 25644585
Material type Periodical, Internet resource
Document type Journal / Magazine / Newspaper, Internet Resource

Publisher details

Cognizant Communication Corporation

  • Pre-print
    • Author cannot archive a pre-print version
  • Post-print
    • Author cannot archive a post-print version
  • Conditions
    • Creative Commons Attribution Non-Commercial License
    • Publisher's version/PDF must be used
    • On a non-profit server
    • Publisher copyright and source must be acknowledged
    • Applies to Cell Medicine and Cell Transplantation
    • All titles are open access journals
    • This policy is an exception to the default policies of 'Cognizant Communication Corporation'
  • Classification
    ​ blue

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: The epidermis is a stratified epithelium with a stem cell subpopulation in the basal layer that constantly replicates and periodically detaches from the basis, undergoing to a differentiation process that involves various developmental signals and regulatory pathways. During the last ten years, a number of studies tried to elucidate the intricate scenario that maintains the epithelial shield during the entire life span. In our study we investigated the role of Numb in the skin compartment and, in particular, its involvement in stem cell maintenance. Numb expression in the skin compartment was assessed by immunofluorescence and immunohistochemistry analysis. We evaluated Numb expression in primary epithelial cells at various differentiative stages. Moreover, we overexpressed Numb in the isolated population enriched for undifferentiated progenitors to establish its involvment in in vitro differentiation. We demonstrated that Numb in high proliferating epithelial undifferentiated progenitors contributes to the maintenance of an undifferentiated state. This regulation involves the E3 ligases Itch binding. Moreover, the analysis of a cohort of cutaneous carcinomas showed that Numb is highly expressed in squamous cell carcinoma (SCC). where we observed a direct correlation between the expression of Numb and Ki67. Our data indicate for the first time that Numb is involved in the maintenance of the undifferentiated proliferating stem cell pool in the epithelial basal layer and its expression could become a new marker in skin cancer.
    Cell Transplantation 05/2015;
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    ABSTRACT: Establishing an efficient differentiation procedure is prerequisite for the cell transplantation of pluripotent stem cells. Activating fibroblast growth factor (FGF) signals and inhibiting the activin/nodal pathway are both conserved principles to direct the neural induction (NI) of developing embryos and human embryonic stem cells (hESCs). Wnt signal and OCT4 expression are critical for the hESC pluripotency; however, their roles in cell differentiation are largely unclear. We demonstrate that in the presence of FGF2 and activin inhibitor SB431542, applying a small-molecule Wnt agonist, BIO, efficiently and rapidly steers the NI of all our tested hESCs. A human induced pluripotent stem cell (iPSC), which is refractory for efficient neural conversion by FGF2, effectively differentiated to SOX1+ cells after the BIO/SB431542/FGF2 treatment. In addition, BIO promoted cell survival and transiently sustained OCT4 expression at the early NI stage with FGF2 and SB431542. Interestingly, at the late NI stage, the OCT4 level rapidly declined in the treated hESCs and consequently initiated the formation of neural rosettes with forebrain neuron characteristics. This study illustrates the distinct effects of Wnt activation on maintaining pluripotency and committing neural lineages at the early and late NI stages of hESCs and iPSCs, respectively.
    Cell Transplantation 05/2015; 24(5). DOI:10.3727/096368913X675179
  • Cell Transplantation 04/2015; 24(4). DOI:10.3727/096368915X687813
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    ABSTRACT: Rapid loss of stemness capacity in purified prototype neural stem cells (NSCs) remains a serious challenge to basic and clinical studies aiming to repair the central nervous system. Based on the essential role of mesodermal guidance in the process of neurulation, we hypothesized that coculture of human NSCs (hNSCs) with human bone marrow-derived mesenchymal stromal stem cells (hMSCs) could enhance the stemness of hNSCs through Notch-1 signaling. We have now tested the hypothesis by assessing behaviors of hNSCs and hMSCs under systematically designed coculture conditions relative to monocultures, with or without Notch-1 manipulation in vitro. Our data demonstrate that expression levels of Notch-1 and Hes-1 as determined by immunocytochemistry are significantly higher in hNSCs cocultured with hMSCs than those of controls. Furthermore, coculturing significantly increases immunoreactivity of CD15, a neural stemness marker, but decreases CD24, a marker of neural/neuronal commitment in hNSCs. The effect is independent from the physical status of cell growth since coculture and notch signaling actually promotes hNSC adhesion. Importantly, coculture with hMSCs markedly augments hNSC proliferation rate (e.g., higher yield in G2/M phase subpopulation in a notch-dependent manner detected by flow cytometry) without diminishing their lineage differentiation capabilities. The results suggest that coculture of hNSCs with hMSCs enhances stemness biology of hNSCs partially via activation of Notch-1 signal transduction. Our finding sheds new light on mesoderm‐ectoderm cell fate determination via contact-based hMSC‐hNSC interactions and provides mechanistic leads for devising effective regimens to sustain and augment stemness of in vitro established hNSC and hMSC lines for basic science, translational and clinical applications.
    Cell Transplantation 02/2015; 24(4). DOI:10.3727/096368915X687561
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    ABSTRACT: The 7th Pan Pacific Symposium on Stem Cells and Cancer Research (PPSSC) was held in Taichung, Taiwan on April 12-14, 2014. The main themes for this symposium were advancing translational and regenerative medicine in stem cells therapy, current clinical applications of induced pluripotent stem (iPS) cells, nanotechnology and medical devices, new drug discovery and development, and patent validation and patent appraisals. Among them, 19 topics were selected for this special issue.
    Cell Transplantation 02/2015; 24(3). DOI:10.3727/096368915X686814
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    ABSTRACT: Neurovascular niches serve as the hosts for adult neural stem cells in both the hippocampus and subventricular zone (SVZ). The rostral migratory stream (RMS) vasculature has been found to be important for neuroblast migration, while its roles in hosting putative neural stem cells have not been investigated. Here we investigated the organization of RMS vasculature and its contribution to the production of new neurons. A single pulse of Bromodeoxyuridine (BrdU) administration revealed locally formed new neurons within RMS were located adjacent to blood vessels. In addition, BrdU Label-Retaining Cells (LRCs) that are putative neural stem cells were also found close to the vasculature. Sodium fluorescein perfusion assay demonstrated that the blood-brain barrier (BBB) organization was especially 'leaky' in the neurogenic niches. Immunohistochemical visualization of some BBB component molecules indicated a thinner BBB in the RMS region, compared to that in the frontal cortex of adult rats. Finally, the expression of Vascular endothelial growth factor (VEGF) was strong and specialized in the RMS region, implying that the region was active in cell proliferation and migration. Here we show that the RMS vasculature associated with surrounding astrocytes provides a highly organized neurovascular niche for adult neural stem cell proliferation, in addition to the function of neuroblast migration support. This result points to a new vasculature supporting neurogenic region in the brain.
    Cell Transplantation 02/2015; 24(3). DOI:10.3727/096368915X686878
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    ABSTRACT: Effects of leukemia inhibitory factor (LIF) and fibroblast growth factor 2 (FGF2) on establishment and maintenance of rabbit embryonic stem cell (rESC) lines were assessed. When grown on MEF feeders, rESC lines derived from fertilized embryos were established and maintained in medium containing paracrine factors LIF (via STAT3) and/or FGF2 (via MEK-ERK1/2 and PI3K-AKT). However, high levels of ERK1/2 and AKT activities in rESCs were crucial for maintaining their undifferentiated proliferation. Although rESCs under the influence of either LIF (500, 1,000 and 2,000 U/mL) or FGF2 (5, 10 and 20 ng/mL) alone had enhanced expression of pluripotency markers, peak expression occurred when both LIF (1,000 U/mL) and FGF2 (10 ng/mL) were applied. Induced dephosphorylation of STAT3, ERK1/2 and AKT by specific inhibitors limited growth of rESCs and caused remarkable losses of self-renewal capacity; therefore, we inferred that STAT3, ERK and AKT had essential roles in maintaining rESC proliferation and self-renewal. We concluded that LIF and FGF2 jointly maintained the undifferentiated state and self-renewal of rabbit ESCs through an integrative signaling module.
    Cell Transplantation 02/2015; 24(3). DOI:10.3727/096368915X686832
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    ABSTRACT: Acute hepatic failure (AHF) is a severe liver injury leading to sustained damage and complications. Induced pluripotent stem cells (iPSCs) may be an alternative option for the treatment of AHF. In this study, we reprogrammed human dental pulp-derived fibroblasts into iPSCs (DP-iPSCs), which exhibited pluripotency and the capacity to differentiate into tridermal lineages, including hepatocyte-like cells (iPSC-Heps). These iPSC-Heps resembled human ESC-derived hepatocyte-like cells in gene signature and hepatic markers/functions. To improve iPSC-Heps engraftment, we next developed an injectable carboxymethyl-hexanoyl chitosan hydrogel (CHC) with sustained hepatocyte growth factor (HGF) release (HGF-CHC) and investigated the hepatoprotective activity of HGF-CHC-delivered iPSC-Heps in vitro and in an immunocompromised AHF mouse model induced by thioacetamide (TAA). Intrahepatic delivery of HGF-CHC-iPSC-Heps reduced the TAA-induced hepatic necrotic area and rescued liver function and recipient viability. Compared with PBS-delivered iPSC-Heps, the HGF-CHC-delivered iPSC-Heps exhibited higher antioxidant and anti-apoptotic activities that reduced hepatic necrotic area. Importantly, these HGF-CHC-mediated responses could be abolished by administering anti-HGF neutralizing antibodies. In conclusion, our findings demonstrated that HGF mediated the enhancement of iPSC-Hep antioxidant/antiapoptotic capacities and hepatoprotection and that HGF-CHC is as an excellent vehicle for iPSC-Hep engraftment in iPSC-based therapy against AHF.
    Cell Transplantation 02/2015; 24(3). DOI:10.3727/096368915X686986
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    ABSTRACT: Currently, there is not an effective therapy for cirrhosis of the liver except for liver transplant. However, finding a compatible liver is difficult due to the low supply and increased demand for healthy livers. Stem cell therapy may be a solution for liver cirrhosis. In our previous report, stem cells from Wharton's jelly and bone marrow were shown to improve liver function in a chemically-induced liver fibrosis animal model. However the immunological rejection of an allograft is always a risk for clinical application. In this study proposal, we suggest using human adipose-derived stem cells (ADSCs) because they are an immune-privileged cell type; they lack human leukocyte antigen-DR expression, and they also suppress the proliferation of activated allogenic lymphocytes and inhibit the production of inflammatory cytokines. In addition, ADSCs contain a sufficient amount of adult stem cells for autologous transplantation. Based on these benefits, ADSCs are promising candidates for clinical application when compared to other stem cell types. The aim of our study will be to investigate the safety and efficacy of autologous ADSCs for the clinical treatment of liver cirrhosis.
    Cell Transplantation 02/2015; 24(3). DOI:10.3727/096368915X687228
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    ABSTRACT: Adult stem cell therapy for the treatment of tendon injuries is a growing area of research. This study is aimed to investigate the efficacy of human adipose-derived stem cell (hADSC) injection on the tendon during its healing process in a rat model of rotator cuff injury. Human ADSCs were injected 3 days after collagenase induced rotator cuff injuries in experimental groups while the control group received saline as a placebo. Histological and biomechanical analyses were performed on 7, 14, 21 and 28 days after collagenase injection. Compared to the control group, it was found that inflammatory cells were significantly decreased in the hADSC-treated group after collagenase injection for 7 days and 14 days. In the hADSC-injected group, the fiber arrangement and tendon organization had also been improved. On the 7th day after collagenase injection, the load-to-failure of the hADSC-injected group (15.87±2.20N) was notably higher than that of the saline-injected group (11.20±1.35N). It is suggested that the tensile strength of the supraspinatus tendon was significantly enhanced. Local administration of hADSCs might have the possibility to restore the tensile strength and attenuate the progression of tendinitis. Taken together, these findings demonstrate that the recovery processes in damaged tendons can be facilitated architecturally and functionally after hADSC injection.
    Cell Transplantation 02/2015; 24(3). DOI:10.3727/096368915X686968
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    ABSTRACT: As assuring cell quality is an essential parameter for the success of stem cell therapy, the impact of various senescence-inducing stress signals, and strategies to circumvent them, has been an important area of focus in stem cell research. The aim of this study was to demonstrate the capacity of trans-cinnamaldehyde (TC) in reversing stress-induced senescence and maintaining the quality of stem cells in a chemically (H2O2)-induced cell senescence model. Because of the availability and the promising application potential in regenerative medicine, adipose-derived stem cells (ADSCs) were chosen for the study. We found that H2O2 treatment resulted in the expression of senescence characteristics in the ADSCs, including decreased proliferation rate, increased senescence associated-β-galactosidase (SA-β-gal) activity, decreased SIRT1 (silent mating type information regulation 2 homolog) expression and decreased telomerase activity. However, TC treatment was sufficient to rescue or reduce the effects of H2O2 induction, ultimately leading to an increased proliferation rate, a decrease in the percentage of SA-β-gal positive cells, upregulation of SIRT1 expression, and increased telomerase activity of the senescent ADSCs at the cellular level. Moreover, a chemically induced liver fibrosis animal model was used to evaluate the functionality of these rescued cells in vivo. Liver dysfunction was established by injecting 200 mg/kg thioacetamide (TAA) intraperitoneally into Wistar rats every third day for 60 days. The experimental rats were separated into groups; normal group (rats without TAA induction), sham group (without ADSC transplantation), positive control group (transplanted with normal ADSCs); H2O2 group (transplanted with H2O2 -induced senescent ADSCs), and H2O2+TC group (transplanted with ADSCs pretreated with H2O2 and then further treated with TC). In the transplantation group, 1 × 10(6) human ADSCs were introduced into each rat via direct liver injection. Based on the biochemical analysis and immunohistochemical staining results, it was determined that the therapeutic effects on liver fibrosis by the induced senescent ADSCs (H2O2 group) were not as significant as those exerted by the normal ADSCs (the positive control group). However, the H2O2+TC group showed significant reversal of liver damage when compared to the H2O2 group 1 week post transplantation. These data confirmed that the TC treatment had the potential to reduce the effects of H2O2-induced senescence and to restore in vivo functionality of the induced-senescent ADSCs. It is therefore suggested that TC has potential applications in maintaining the quality of stem cells and could aid in treating senescence-related disorders.
    Cell Transplantation 02/2015; 24(3). DOI:10.3727/096368915X686959
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    ABSTRACT: Irisflorentin is an isoflavone component derived from the roots of Belamcanda chinensis (L.) DC. In traditional Chinese medicine, this herb has pharmacological properties to treat inflammatory disorders. Dendritic cells (DCs) are crucial modulators for the development of optimal T-cell immunity and maintenance of tolerance. Aberrant activation of DCs can induce harmful immune responses, and so agents that effectively improve DC properties have great clinical value. We herein investigated the effects of irisflorentin on lipopolysaccharide (LPS)-stimulated maturation of mouse bone marrow-derived DCs in vitro and in the contact hypersensitivity response (CHSR) in vivo. Our results demonstrated that treatment with up to 40 μM irisflorentin does not cause cellular toxicity. Irisflorentin significantly lessened the pro-inflammatory cytokine production (tumor necrosis factor-α, interleukin-6, and interleukin-12p70) by LPS-stimulated DCs. Irisflorentin also inhibited the expression of LPS-induced major histocompatibility complex class II and co-stimulatory molecules (CD40 and CD86) on LPS-stimulated DCs. In addition, irisflorentin diminished LPS-stimulated DC-elicited allogeneic T-cell proliferation. Furthermore, irisflorentin significantly interfered with LPS-induced activation of IκB kinase, c-Jun N-terminal kinase, and p38, as well as the nuclear translocation of NF-κB p65. Subsequently, treatment with irisflorentin obviously weakened 2,4-dinitro-1-fluorobenzene-induced delayed-type hypersensitivity. These findings suggest new insights into the role of irisflorentin as an immunotherapeutic adjuvant through its capability to modulate the properties of DCs.
    Cell Transplantation 02/2015; 24(3). DOI:10.3727/096368915X687002
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    ABSTRACT: Cardiovascular diseases are related to many risk factors, such as diabetes, high blood pressure, smoking, and obesity. Myocardial infarction (MI), a cardiovascular disease, is the most common cause of cardiomyocyte death. In MI, hypoxia induces cardiomyocyte apoptosis; in particular, diabetes combined with MI has a synergistic effect that exacerbates cardiomyocyte death. The hypoxia-inducible factor-1α (HIF1α) transcriptional factor and a BH-3 only protein, Bcl-2 adenovirus E1B 19 kDa interacting protein 3 (BNIP3), are known to play fundamental roles in both adaptive and cell-death processes in response to hypoxia. In addition, most cardioprotective studies used H9c2 cells that were not beating so H9c2 cells may not be the best model for testing cardioprotective effects. Embryonic stem cells (ESCs) are pluripotent stem cells that are able to differentiate into several types of cells, including cardiomyocytes. In this study, we reveal a simple method to differentiate ESCs into cardiomyocytes by using poly-D-lysine coated plates combined with ITS and N2 containing medium and characterized the ESC-derived cardiomyocytes by cardiomyocyte marker staining. The ESC-derived cardiomyocytes were used to investigate the protective effect of salvianolic acid B (Sal-B) in high glucose combined with hypoxic conditions to mimic diabetes patients with ischemia. The results of MTT and TUNEL assays indicate that Sal-B suppresses the apoptotic effect of treatment with high glucose combined with hypoxia in ESC-derived cardiomyocytes. In particular, Sal-B inhibited HIF1α, BNIP3, and cleavage-caspase 3 expression levels, thereby suppressing apoptosis. This is the first study to mention the correlation between BNIP3 and Sal-B for cardioprotective effects. In conclusion, we suggest that Sal-B may be suitable for use as a future cardioprotective medicine.
    Cell Transplantation 02/2015; 24(3). DOI:10.3727/096368915X686995
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    ABSTRACT: MicroRNAs (miRNAs) are critically important in both normal neuronal development and neurological diseases. Although cerebral ischemia has been shown to alter the miRNA profiles of rats, the role of miRNA in the cornu ammonis 1 (CA1) region of the gerbil hippocampus under ischemic tolerance has not been studied. In the present study, Mongolian gerbils were subjected to one or three times the nonlethal dose of 2 min-transient common carotid artery occlusion (tCCAO). miRNA microarray technology detected 251 miRNAs, and the expression of seven of these in terms of ischemic tolerance. They were compared at different time points: 1 day (d), 7 d, 1 month (M) and 6 M. Mmu-miR-15a-5p, related to neurogenesis, showed increased expression after one dose of 2 min-tCCAO and was much higher after three doses. An increase in sha-miR-24 and oan-let-7b-3p, related to transactivation response DNA-binding protein (TDP43), was observed after one dose of 2 min-tCCAO, but the peak was accelerated to an earlier period of reperfusion after three doses. In contrast, mmu-miR-125b-5p and mmu-miR-132-5p, related to fused in sarcoma/translocated in liposarcoma (FUS/TLS), showed similar increases at both doses. Mmu-miR-181c-5p and mmu-miR-378a-5p, related to heat shock protein 70 (HSP70), also showed accelerated expression after three doses. This data set provides new insight about miRNA expression during neurogenesis, and related to TDP43, FUS/TLS, and HSP70, which may be useful when pursuing further studies on the possible use of miRNAs as biomarkers in cerebral ischemic tolerance and neuroregeneration.
    Cell Transplantation 02/2015; 24(3). DOI:10.3727/096368915X686869
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    ABSTRACT: Enhancer of zeste homolog 2 (EZH2), a catalytic component of polycomb repressive complex 2 (PRC2), serves as a histone methyltransferase toward histone H3K27 tri-methylation and also recruits DNA methyltransferases to regulate gene expression and chromatin structure. Accumulating evidence indicates the critical roles of EZH2 in stem cell maintenance and cell fate decision in differentiation into specific cell lineages. In this article, we retrospect the updated progress in the field and the potential application of EZH2 in regenerative medicine including nervous system, muscle, pancreas, and dental pulp regeneration.
    Cell Transplantation 02/2015; 24(3). DOI:10.3727/096368915X686823