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: 3.13

Impact Factor Rankings

2015 Impact Factor Available summer 2016
2014 Impact Factor 3.127
2013 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

Additional details

5-year impact 3.26
Cited half-life 4.60
Immediacy index 0.50
Eigenfactor 0.01
Article influence 0.82
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
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Publications in this journal

  • Cell Transplantation 09/2015; in press.
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    ABSTRACT: This study aimed to enhance the attachment of periodontal ligament stem cells (PDLSCs) onto the decellularized dental root surface using surface coating with fibronectin and/or calcium phosphate (CaP) and to evaluate the activity of PDLSCs attached to a coated dental root surface following tooth replantation. PDLSCs were isolated from five dogs, and the other dental roots were used as a scaffold for carrying PDLSCs and then assigned to one of four groups according to whether their surface was coated with CaP, fibronectin, CaP/fibronectin, or left uncoated (control). Fibronectin increased the adhesion of PDLSCs onto dental root surfaces compared to both the control and CaP-coated groups, and simultaneous surface coating with CaP and fibronectin significantly accelerated and increased PDLSC adhesion compared to the fibronectin-only group. On in vivo tooth replantation, functionally oriented periodontal new attachment was observed on the CaP/fibronectin-coated dental roots to which autologous PDLSCs had adhered, while in the control condition, dental root replantation was associated only with root resorption and ankylosis along the entire root length. CaP and fibronectin synergistically enhanced the attachment of PDLSCs onto dental root surfaces, and autologous PDLSCs could produce de novo periodontal new attachment in an experimental in vivo model.
    Cell Transplantation 09/2015; 24(9):1767-1779. DOI:10.3727/096368914X684628
  • Cell Transplantation 09/2015; 24(9). DOI:10.3727/096368914X683557
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    ABSTRACT: We previously demonstrated that mesenchymal cells from human amniotic membrane (hAMTCs) inhibit the generation and maturation of monocyte-derived dendritic cells (DCs) in vitro. Considering the crucial role of DCs in the immune response and that epithelial cells of the human amniotic membrane (hAECs) share some of the immunoregulatory properties of hAMTCs, we investigated whether hAECs also modulate monocyte-derived DCs. We compared hAECs with hAMTCs in a cell-to-cell contact setting and their secreted factors in modulating DC differentiation and function. First, we demonstrated that primary and expanded hAMTCs strongly inhibited the differentiation of DCs and induced a shift toward M2-like macrophages. This was observed when hAMTCs were cultured in contact (hAMTC-DCcont) or in Transwells (hAMTC-DCtw) with monocytes and even when medium conditioned by hAMTCs was used instead of hAMTCs. hAECs also prevented DC development, but to a lesser extent than hAMTCs. hAECs were more effective when cultured in contact with monocytes (hAEC-DCcont) rather than in Transwells (hAEC-DCtw). The modulatory capacity of hAECs changed during passaging unlike the hAMSCs. The ability to stimulate CD4+ and CD8+ T-cell proliferation was almost completely abolished by hAMTC-DCcont, whereas hAMTC-DCtw and hAEC-DCcont displayed only a reduced ability to stimulate CD8+ T cells. Furthermore, monocytes cocultured with hAMTCs and hAECs showed some similarities, but also differences in cytokine/chemokine secretion. Similarities were observed in the inhibition of IL-12p70 and TNF-α and the increase in IL-10 in supernatants taken from monocyte-DCs cocultured with hAMTCs and hAECs in contact and Transwell settings. The inflammatory factors IL-8, CXCL9, and MIP-1α were significantly lower in hAMTC-DCcont, hAMTC-DCtw, and hAEC-DCcont conditions. In contrast, only hAMTCs (in both contact and Transwell conditions) were able to significantly increase IL-1β and CCL2. Altogether, we demonstrated that hAMTCs and hAECs affect DC differentiation, but that hAMTCs exerted a stronger inhibitory effect, abolished T-cell proliferation, and also induced more changes in cytokine/chemokine production.
    Cell Transplantation 09/2015; 24(9). DOI:10.3727/096368914X684033
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    ABSTRACT: Bone marrow-derived mesenchymal stem cells (MSCs), which have beneficial effects in acute lung injury (ALI), can serve as a vehicle for gene therapy. Angiotensin-converting enzyme 2 (ACE2), a counterregulatory enzyme of ACE that degrades angiotensin (Ang) II into Ang 1‐7, has a protective role against ALI. Because ACE2 expression is severely reduced in the injured lung, a therapy targeted to improve ACE2 expression in lung might attenuate ALI. We hypothesized that MSCs overexpressing ACE2 would have further benefits in lipopolysaccharide (LPS)-induced ALI mice, when compared with MSCs alone. MSCs were transduced with ACE2 gene (MSC-ACE2) by a lentiviral vector and then infused into wild-type (WT) and ACE2 knockout (ACE2−/y) mice following an LPS-induced intratracheal lung injury. The results demonstrated that the lung injury of ALI mice was alleviated at 24 and 72 h after MSC-ACE2 transplantation. MSC-ACE2 improved the lung histopathology and had additional anti-inflammatory effects when compared with MSCs alone in both WT and ACE2−/y ALI mice. MSC-ACE2 administration also reduced pulmonary vascular permeability, improved endothelial barrier integrity, and normalized lung eNOS expression relative to the MSC group. The beneficial effects of MSC-ACE2 could be attributed to its recruitment into the injured lung and enhanced local expression of ACE2 protein without changing the serum ACE2 levels after MSC-ACE2 transplantation. The biological activity of the increased ACE2 protein decreased the Ang II amount and increased the Ang 1‐7 level in the lung when compared with the ALI and MSC-only groups, thereby inhibiting the detrimental effects of accumulating Ang II. Therefore, compared to MSCs alone, the administration of MSCs overexpressing ACE2 resulted in a further improvement in the inflammatory response and pulmonary endothelial function of LPS-induced ALI mice. These additional benefits could be due to the degradation of Ang II that accompanies the targeted overexpression of ACE2 in the lung.
    Cell Transplantation 09/2015; 24(9):1699-1715. DOI:10.3727/096368914X685087
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    ABSTRACT: The purpose of the study was to further scrutinize the potential of βB2-crystallin in supporting regeneration of injured retinal ganglion cell axons both in vitro and in vivo. Retinal explants obtained from animals after treatment either with lens injury (LI) alone or with combined LI 5 days or 3 days before or simultaneously with an optic nerve crush (ONC) were cultured for 96 h under regenerative conditions, and the regenerating axons were quantified and compared with untreated controls. These measurements were then repeated with LI replaced by intravitreal injections of γ-crystallin and β-crystallin at 5 days before ONC. Finally, βB2-crystallin-overexpressing transfected neural progenitor cells (βB2-crystallin-NPCs) in the eye were studied after crushing the optic nerve in vivo. Regeneration was monitored with the aid of immunoblotting of the retina and optic nerve both distal and proximal to the lesion site, and this was compared with controls that received injections of phosphate buffer only. LI performed 5 days or 3 days before ONC significantly promoted axonal outgrowth in vitro (p < 0.001), while LI performed alone before explantation did not. Intravitreal injections of β-crystallin and γ-crystallin mimicked the effects of LI and significantly increased axonal regeneration in culture at the same time intervals (p < 0.001). Western blot analysis revealed that crystallins were present in the proximal optic nerve stump at the lesion site in ONC, but were neither expressed in the undamaged distal optic nerve nor in uninjured tissue. βB2-crystallin-NPCs supported the regeneration of cut optic nerve axons within the distal optic nerve stump in vivo. The reported data suggest that βB2-crystallin-producing "cell factories" could be used to provide novel therapeutic drugs for central nervous system injuries.
    Cell Transplantation 09/2015; 24(9):1829-1844. DOI:10.3727/096368914X684583
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    ABSTRACT: Dental pulp stem cell (DPSC) subsets mobilized by granulocyte-colony-stimulating factor (G-CSF) are safe and efficacious for complete pulp regeneration. The supply of autologous pulp tissue, however, is very limited in the aged. Therefore, alternative sources of mesenchymal stem/progenitor cells (MSCs) are needed for the cell therapy. In this study, DPSCs, bone marrow (BM), and adipose tissue (AD)-derived stem cells of the same individual dog were isolated using G-CSF-induced mobilization (MDPSCs, MBMSCs, and MADSCs). The positive rates of CXCR4 and G-CSFR in MDPSCs were similar to MADSCs and were significantly higher than those in MBMSCs. Trophic effects of MDPSCs on angiogenesis, neurite extension, migration, and antiapoptosis were higher than those of MBMSCs and MADSCs. Pulp-like loose connective tissues were regenerated in all three MSC transplantations. Significantly higher volume of regenerated pulp and higher density of vascularization and innervation were observed in response to MDPSCs compared to MBMSC and MADSC transplantation. Collagenous matrix containing dentin sialophosphoprotein (DSPP)-positive odontoblast-like cells was the highest in MBMSCs and significantly higher in MADSCs compared to MDPSCs. MBMSCs and MADSCs, therefore, have potential for pulp regeneration, although the volume of regenerated pulp tissue, angiogenesis, and reinnervation, were less. Thus, in conclusion, an alternative cell source for dental pulp/dentin regeneration are stem cells from BM and AD tissue.
    Cell Transplantation 09/2015; 24(9). DOI:10.3727/096368914X683502
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    ABSTRACT: Previous studies have indicated a neuroprotective effect of remote limb ischemic preconditioning. The aim of the present study was to assess whether upper arm ischemic preconditioning is feasible and safe in patients with unilateral middle cerebral artery (MCA) stenosis compared to healthy volunteers. Ten patients with unilateral MCA stenosis and 24 healthy volunteers underwent limb ischemic preconditioning, consisting of five cycles of 5-min inflations of a blood pressure cuff to 200 mmHg around an upper limb followed by 5 min of reperfusion. Limb ischemic preconditioning has no significant effect on the heart rate, oxygenation index, or mean flow velocity in patients with unilateral MCA stenosis or healthy volunteers. However, healthy volunteers showed a reduction in blood pressure 30 min following reperfusion of the last cycle. Limb ischemic preconditioning was found to be safe and well tolerated in both patients and healthy volunteers. We highlight the potential of limb ischemic preconditioning as an adjunct to neuroprotective treatment.
    Cell Transplantation 09/2015; 24(9). DOI:10.3727/096368914X683520
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    ABSTRACT: Unlabelled: The aim of this study was to investigate the effects of elevated donor HbA1c levels (type 2 diabetes, T2D) on the islet yield and functionality postisolation. In this retrospective analysis, donors for islet isolations were classified into two groups: T2D group (HbA1c ≥ 6.5%, n = 18) and normal group (HbA1c < 6.5%, n = 308). Optimum pancreas digestion time (switch time) was significantly higher in the T2D group compared to the normal group (13.7 ± 1.2 vs. 11.7 ± 0.1 min, respectively, p = 0.005). Islet yields were significantly lower in the T2D group compared to the control (T2D vs. control): islet equivalent (IEQ)/g (prepurification 2,318 ± 195 vs. 3,713 ± 114, p = 0.003; postpurification 1,735 ± 175 vs. 2,663 ± 89, p = 0.013) and islet particle number (IPN)/g (prepurification, 2,519 ± 336 vs. 4,433 ± 143, p = 0.001; postpurification, 1,760 ± 229 vs. 2,715 ± 85, p = 0.007). Islets from T2D pancreata had significantly lower viability (T2D vs. Control: 91.9 ± 1.6 vs. 94.4 ± 0.3%, p = 0.004) and decreased oxygen consumption rate (ΔOCR) (T2D vs. Control: 0.09 ± 0.01 and 0.21 ± 0.03 nmol O2 100 islets(-1) min(-1), p = 0.049). The islets isolated from T2D donor pancreata reversed diabetes in NOD-SCID mice in 9% (2/22) compared to islets from control donor pancreata, which reversed diabetes in 67% (175/260, p < 0.001). In conclusion, this study demonstrates that elevated HbA1c (≥6.5%) is associated with impairment of islet function and lower islet yield; however, these islets could not be suitable for clinical applications.
    Cell Transplantation 09/2015; 24(9). DOI:10.3727/096368914X683548
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    ABSTRACT: X-linked myotubular myopathy (XLMTM) is an isogenic muscle disease characterized by progressive wasting of skeletal muscle, weakness, and premature death of affected male offspring. Recently, the XLMTM gene knock-in mouse, Mtm1 p.R69C, was found to have a similar phenotype as the Mtm1 gene mutation in humans (e.g., central nucleation of small myofibers, attenuated muscle strength, and motor unit potentials). Using this rodent model, we investigated whether syngeneic cell therapy could mitigate muscle weakness. Donor skeletal muscle-derived myoblasts were isolated from C57BL6 wild-type (WT) and Mtm1 p.R69C (KI) mice for transplantation into the gastrocnemius muscle of recipient KI mice. Initial experiments demonstrated that donor skeletal muscle-derived myoblasts from WT and KI mice remained in the gastrocnemius muscle of the recipient KI mouse for up to 4 weeks posttransplantation. KI mice receiving syngeneic skeletal muscle-derived myoblasts displayed an increase in skeletal muscle mass, augmented force generation, and increased nerve-evoked skeletal muscle action potential amplitude. Taken together, these results support our hypothesis that syngeneic cell therapy may potentially be used to ameliorate muscle weakness and delay the progression of XLMTM, as application expands to other muscles.
    Cell Transplantation 09/2015; 24(9). DOI:10.3727/096368914X683494
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    ABSTRACT: Articular cartilage damage and osteoarthritis are the most common joint diseases. Joints are prone to damage caused by sports injuries or aging, and such damage regularly progresses to more serious joint disorders, including osteoarthritis, which is a degenerative disease characterized by the thinning and eventual wearing out of articular cartilage, ultimately leading to joint destruction. Osteoarthritis affects millions of people worldwide. Current approaches to repair of articular cartilage damage include mosaicplasty, microfracture, and injection of autologous chondrocytes. These treatments relieve pain and improve joint function, but the long-term results are unsatisfactory. The long-term success of cartilage repair depends on development of regenerative methodologies that restore articular cartilage to a near-native state. Two promising approaches are (i) implantation of engineered constructs of mesenchymal stem cell (MSC)-seeded scaffolds, and (ii) delivery of an appropriate population of MSCs by direct intra-articular injection. MSCs may be used as trophic producers of bioactive factors initiating regenerative activities in a defective joint. Current challenges in MSC therapy are the need to overcome current limitations in cartilage cell purity and to in vitro engineer tissue structures exhibiting the required biomechanical properties. This review outlines the current status of MSCs used in cartilage tissue engineering and in cell therapy seeking to repair articular cartilage defects and related problems. MSC-based technologies show promise when used to repair cartilage defects in joints.
    Cell Transplantation 09/2015; 24(9). DOI:10.3727/096368914X683485
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    ABSTRACT: In murine allogeneic transplantation models, ICOS gene-transduced bone marrow-derived mesenchymal stem cells (MSCsICOS-EGFP) were evaluated for their effects on GvHD severity and long-term survival. Lethally irradiated BALB/c or first filial generation of BALB/c and C57BL/6 (CB6F1) mice were transplanted with bone marrow cells and splenocytes from C57BL/6 mice to establish acute GvHD models. Recipient mice were injected with MSCsICOS-EGFP, MSCs, MSCsEGFP, ICOS-Ig fusion protein, MSCs + ICOS-Ig, or PBS (control group). Long-term survival, GvHD rates and severity, CD4+ T-cell apoptosis and proliferation, and Th1/Th2/Th17 effecter cell polarization were evaluated. In the C57BL/6 → CB6F1 HSCT model, the long-term survival in the MSCICOS-EGFP group was higher than that in the GvHD group (74.29 ± 7.39% vs. 0, p p = 0.004; 48.57 ± 8.45%, p = 0.03; or 50.43 ± 8.45% p = 0.04, respectively). The survival advantages of MSCICOS-EGFP-treated group were confirmed in the C57BL/6 → BALB/c HSCT model. In both HSCT models, the low mortality in the MSCICOS-EGFP group was associated with lower incidence and severity of acute GvHD. Treatment with MSCsICOS-EGFP induced more CD4+ T-cell apoptosis compared with that in the GvHD group. The effect on CD4+ T cells was shown as early as day 2 and maintained until day 14 (p ICOS-EGFP were able to suppress Th1 and Th17 polarization and promote Th2 polarization on both protein expression and gene transcription levels. Higher serum levels of IL-4, IL-10, and lower levels of IFN-γ, IL-2, IL-12, and IL-17A were detected in the MSCICOS-EGFP group. The MSCsICOS-EGFP could also induce GATA-3, STAT6 expression and inhibit T-bet, STAT4, ROR-γt expression. Our results showed that injection of MSCsICOS-EGFP is a promising strategy for acute GvHD prevention and treatment. It provides synergistic benefits of MSC immune modulation and ICOS-B7h pathway blockage.
    Cell Transplantation 09/2015; 24(9). DOI:10.3727/096368914X684592
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    ABSTRACT: Autologous engineered skin substitutes (ESS) have been shown to close excised, full-thickness burns, but are consistently hypopigmented due to depletion of human melanocytes (hM) during culture of keratinocytes. Hypothetically, addition of hM to ESS may restore uniform pigmentation, but may also promote neoplasia and tumor formation. To evaluate this risk, 16 strains of hM were isolated and propagated in selective culture medium, then injected subcutaneously into athymic mice (1 × 107 hM/animal; n = 6/strain) and followed for 24 weeks. Human melanoma cells (SK-Mel-2, SK-Mel-5) served as positive controls. No detectable tumors formed from hM strains derived from normal skin. In contrast, SK-Mel-2 formed tumors in 50% of mice, and SK-Mel-5 formed tumors in 83% of mice. Histopathology confirmed the tumorigenic anatomy of the controls and the presence of hM that were not tumorigenic in the test groups. These results support the safety of cultured hM for transplantation to restore uniform skin pigmentation in wounds closed with ESS.
    Cell Transplantation 08/2015; 24(8). DOI:10.3727/096368914X683052
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    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