Vincent J Pompili

The Ohio State University, Columbus, Ohio, United States

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Publications (33)123.94 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Despite recent advances in cardiovascular medicine, ischemic diseases remain a major cause of morbidity and mortality. Although stem cell-based therapies for the treatment of ischemic diseases show great promise, limited availability of biologically functional stem cells mired the application of stem cell-based therapies. Previously, we reported a PES-nanofiber based ex vivo stem cell expansion technology, which supports expansion of human umbilical cord blood (UCB)-derived CD133(+)/CD34(+) progenitor cells ∼225 fold. Herein, we show that using similar technology and subsequent re-expansion methods, we can achieve ∼5 million-fold yields within 24 days of the initial seeding. Interestingly, stem cell phenotype was preserved during the course of the multiple expansions. The high level of the stem cell homing receptor, CXCR4 was expressed in the primary expansion cells, and was maintained throughout the course of re-expansions. In addition, re-expanded cells preserved their multi-potential differential capabilities in vitro, such as, endothelial and smooth muscle lineages. Moreover, biological functionality of the re-expanded cells was preserved and was confirmed by a murine hind limb ischemia model for revascularization. These cells could also be genetically modified for enhanced vasculogenesis. Immunohistochemical evidences support enhanced expression of angiogenic factors responsible for this enhanced neovascularization. These data further confirms that nanofiber-based ex-vivo expansion technology can generate sufficient numbers of biologically functional stem cells for potential clinical applications.
    Biomaterials 07/2014; · 8.31 Impact Factor
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    ABSTRACT: Many ovarian cancer cells express stress-related molecule MICA/B on their surface that is recognized by Vγ2Vδ2 T cells through their NKG2D receptor, which is transmitted to downstream stress-signaling pathway. However, it is yet to be established how Vγ2Vδ2 T cells-mediated recognition of MICA/B signal is transmitted to downstream stress-related molecules. Identifying targeted molecules would be critical to develop a better therapy for ovarian cancer cells. It is well established that ATM/ATR signal transduction pathways, which is modulated by DNA damage, replication stress, and oxidative stress play central role in stress signaling pathway regulating cell cycle checkpoint and apoptosis. We investigated whether ATM/ATR and its down stream molecules affect Vγ2Vδ2 T cells-mediated cytotoxicity. Herein, we show that ATM/ATR pathway is modulated in ovarian cancer cells in presence of Vγ2Vδ2 T cells. Furthermore, downregulation of ATM pathway resulted downregulation of MICA, and reduced Vγ2Vδ2 T cells-mediated cytotoxicity. Alternately, stimulating ATM pathway enhanced expression of MICA, and sensitized ovarian cancer cells for cytotoxic lysis by Vγ2Vδ2 T cells. We further show that combining currently approved chemotherapeutic drugs, which induced ATM signal transduction, along with Vγ2Vδ2 T cells enhanced cytotoxicity of resistant ovarian cancer cells. These findings indicate that ATM/ATR pathway plays an important role in tumor recognition, and drugs promoting ATM signaling pathway might be considered as a combination therapy together with Vγ2Vδ2 T cells for effectively treating resistant ovarian cancer cells.
    Biochimica et Biophysica Acta 04/2014; · 4.66 Impact Factor
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    ABSTRACT: Background: Intra-aortic balloon pump (IABP) use may be associated with complications; however, in certain patients with ST-elevation myocardial infarction (STEMI) with hemodynamic instability refractory to medical management its use may become necessary. Methods: 36 STEMI patients with IABP placement for hemodynamic instability after percutaneous coronary intervention were studied. IABP duration ranged from one to seven days (median two days). Based on median time, patients were divided into two groups: IABP duration ≤ 2 days (n = 27) or > 2 days (n = 9). Vascular complications and incidence of bleeding were compared. Results: Mean IABP duration was 1.4 ± 0.5 and 4.1 ± 1.3 days in ≤ 2 day and > 2 day groups, respectively (P < 0.01). Glycoprotein IIb/IIIa inhibitor and anti-coagulation use was not significantly different between groups. Mean duration of anti-coagulation was 1.9 ± 1.2 and 4.5 ± 1.3 days in ≤ 2 day and > 2 day groups, respectively (P < 0.05). Complications (vascular, access site bleeding, gastrointestinal bleeding) were significantly greater in > 2 day group (66%) compared to ≤ 2 day group (18%; P < 0.05). Conclusions: When an IABP was used for more than two days complications significantly increased. The clinical implications of the study will be strengthened if the findings are confirmed in a prospective study with a larger number of patients.
    Acute Cardiac Care 03/2014;
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    ABSTRACT: Nanofiber-expanded human umbilical cord blood-derived CD34(+) cell therapy has been shown to have potential applications for peripheral and myocardial ischaemic diseases. However, the efficacies of expanded CD34(+) cell therapy for treating cutaneous wounds and its mechanisms of action have yet to be established. Using an excisional wound model in non-obese diabetic/severe combined immune deficient mice, we show herein that CD34(+) cells accelerate the wound-healing process by enhancing collagen synthesis, and increasing fibroblast cell migration within the wound bed. Concomitantly, reduced levels of matrix metalloproteinase (MMPs) such as MMP1, MMP3, MMP9 and MMP13 were detected in the wound beds of animals treated with CD34(+) cells compared with vehicle-treated controls. CD34(+) cells were found to mediate enhanced migration and proliferation of dermal fibroblast cells in vitro. Moreover, CD34(+) cells secrete collagen in a serum-deprived environment. In mechanistic studies, co-culture of CD34(+) cells with primary skin fibroblasts increased the expression of collagen1A1, a component of type 1 collagen, and decreased the expression of MMP1 in fibroblast cells in the presence of a proteasome inhibitor. Finally, CD34(+) cell-mediated functions were transcriptionally regulated by the c-Jun N-terminal kinases pathway. Collectively, these data provide evidence of therapeutic efficacy and a novel mechanism of nanofiber-expanded CD34(+) cell-mediated accelerated wound healing.
    Journal of Cellular and Molecular Medicine 01/2014; · 4.75 Impact Factor
  • Reeva Aggarwal, Vincent J Pompili, Hiranmoy Das
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    ABSTRACT: To evaluate therapeutic efficacy and to investigate involved molecular mechanisms of cell-based therapy in osteoporosis, the generation of a clinically relevant model is critically important. Herein, we describe detailed methods in generation of an immune-deficient osteoporotic murine model, and application of human umbilical cord blood-derived stem cells to assess their therapeutic efficacy.
    Methods in molecular biology (Clifton, N.J.) 01/2014; 1213:209-214. · 1.29 Impact Factor
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    ABSTRACT: Many ovarian cancer cells express stress-related molecule MICA/B on their surface that is recognized by Vγ2Vδ2 T cells through their NKG2D receptor, which is transmitted to downstream stress-signaling pathway. However, it is yet to be established how Vγ2Vδ2 T cell-mediated recognition of MICA/B signal is transmitted to downstream stress-related molecules. Identifying targeted molecules would be critical to develop a better therapy for ovarian cancer cells. It is well established that ATM/ATR signal transduction pathways, which is modulated by DNA damage, replication stress, and oxidative stress play central role in stress signaling pathway regulating cell cycle checkpoint and apoptosis. We investigated whether ATM/ATR and its down stream molecules affect Vγ2Vδ2 T cell-mediated cytotoxicity. Herein, we show that ATM/ATR pathway is modulated in ovarian cancer cells in the presence of Vγ2Vδ2 T cells. Furthermore, downregulation of ATM pathway resulted downregulation of MICA, and reduced Vγ2Vδ2 T cell-mediated cytotoxicity. Alternately, stimulating ATM pathway enhanced expression of MICA, and sensitized ovarian cancer cells for cytotoxic lysis by Vγ2Vδ2 T cells. We further show that combining currently approved chemotherapeutic drugs, which induced ATM signal transduction, along with Vγ2Vδ2 T cells enhanced cytotoxicity of resistant ovarian cancer cells. These findings indicate that ATM/ATR pathway plays an important role in tumor recognition, and drugs promoting ATM signaling pathway might be considered as a combination therapy together with Vγ2Vδ2 T cells for effectively treating resistant ovarian cancer cells.
    Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease 01/2014; · 4.91 Impact Factor
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    ABSTRACT: Nanofiber-expanded human umbilical cord blood-derived CD34+ cell therapy is under consideration for treating peripheral and cardiac ischemia. However, the therapeutic efficacy of nanofiber-expanded human umbilical cord blood-derived (NEHUCB) CD34+ cell therapy for wound healing and its mechanisms are yet to be established. Using an excision wound model in NOD/SCID mice, we show herein that NEHUCB-CD34+ cells home to the wound site and significantly accelerate the wound-healing process compared to vehicle-treated control. Histological analysis reveals that accelerated wound closure is associated with the re-epithelialization and increased angiogenesis. Additionally, NEHUCB-CD34+ cell-therapy decreases expression of pro-inflammatory cytokines, such as TNF-α, IL-1β, IL-6 and NOS2A in the wound bed, and concomitantly increases expression of IL-10 compared to vehicle-treated control. These findings were recapitulated in vitro using primary dermal fibroblasts and NEHUCB-CD34+ cells. Moreover, NEHUCB-CD34+ cells attenuate NF-κB activation and nuclear translocation in dermal fibroblasts through enhanced secretion of IL-10, which is known to bind to NF-κB and suppress transcriptional activity. Collectively, these data provide novel mechanistic evidence of NEHUCB-CD34+ cell-mediated accelerated wound healing.
    Stem Cell Research 11/2013; 12(1):275-288. · 4.47 Impact Factor
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    ABSTRACT: Innate immune system has been known to play an important role in inhibiting the malignant transformation, tumor progression, and invasion. However, the mechanistic basis remains ambiguous. Despite polyclonality of human γδ T cells, Vγ2Vδ2 T cell subset was shown to recognize and limit the growth of various tumors at various degrees. The differential recognition of the tumor cells by Vγ2Vδ2 T cells are yet to be defined. Our current study reveals that γδ T cells limit in vitro growth of most breast tumor cells, such as SkBr7 (HER2+), MCF7 (ER+) and MDA-MB-231 (ER-) by inhibiting their survival and inducing apoptosis, except BrCa-MZ01 (PR+) cells. To investigate detail mechanisms of anti-neoplastic effects, we found that cell death was associated with the surface expression levels of MICA/B and ICAM1. Molecular signaling analysis demonstrated that inhibition of cell growth by γδ T cells was associated with the lower expression levels of cell survival-related molecules such as AKT, ERK and concomitant upregulation of apoptosis-related molecules, such as PARP, cleaved caspase 3, and tumor suppressor genes PTEN and P53. However, opposite molecular signaling was observed in the resistant cell line after co-culture with γδ T cells. In vivo, anti-neoplastic effects of γδ T cells were also documented, where tumor growth was inhibited due to the downregulation of survival signals, strong induction of apoptotic molecules, disruption of microvasculature, and increased infiltration of tumor associated macrophages (TAMs). These findings reveal that a complex molecular signaling is involved in γδ T cell-mediated anti-neoplastic effects. © 2013 Wiley Periodicals, Inc.
    International Journal of Cancer 04/2013; · 6.20 Impact Factor
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    ABSTRACT: Because of their ability for self-renewal and neural differentiation, stem cells are believed to be ideal for cell replacement therapy in Parkinson's disease (PD). Nanofiber-expanded human umbilical cord hematopoietic stem cells (HUHSCs) are advantageous to other stem cells as they provide a source of unlimited stem cell production for clinical application. In this study, we investigated whether 1. nanofiber-expanded HUHSCs are capable of neural differentiation in vitro, and 2. they could improve dopaminergic neuron morphology in the caudate/putamen (CPu) and substantia nigra pars compacta (SNc) of the MPTP-mouse model of PD. When cultured under neural differentiation conditions, nanofiber-expanded HUHSCs were able to undergo neural differentiation in vitro, as determined by gene and protein expression of neural markers such as MAP2, NeuN, HuC, GFAP and Oligo2. Thirty days after a single intracardioventricular injection of HUHSCs to MPTP-mice there was a significant recovery of tyrosine hydroxylase (TH) immunostaining in CPu. There was an increase in the size and staining density of TH+ cells in SNc, while their number was unchanged.
    Frontiers in Bioscience 01/2013; 18:970-81. · 3.29 Impact Factor
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    ABSTRACT: Objective: Compare vascular complications and incidence of bleeding of Impella 2.5 and intra-aortic balloon pump (IABP) in high-risk percutaneous coronary interventions (PCI). Background: Large arterial sheath size for device insertion is associated with vascular and/or bleeding complications; gastrointestinal bleeding may also occur with anti-coagulation use. Methods: Patients with an acute coronary syndrome receiving Impella 2.5 or IABP during high-risk PCI were studied (13 Impella; 62 IABP). Vascular complications and incidence of bleeding were compared. Results: Post-procedure hematocrit was similar between groups. Blood transfusion occurred in 38.4% and 32.2% of patients in the Impella and IABP groups, respectively (P = NS); 65.3%, 30.7% and 3.8% of bleeding were due to vascular access site/procedure related, gastrointestinal and genitourinary, respectively. There was no statistical significant difference in vascular complications between the Impella and IABP groups (15.3% and 6.4% of patients, respectively); mesenteric ischemia (n = 1) and aortic rupture (n = 1) were only in the IABP group. In-hospital and one-year mortality were not statistically significant between groups. Conclusion: Impella can be used as safely as IABP during high-risk PCI with similar vascular and bleeding complications. Importantly, approximately one third of bleeding was from the gastrointestinal system warranting careful prophylactic measures and monitoring.
    Acute Cardiac Care 12/2012; 14(4):120-4.
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    ABSTRACT: Kruppel-like factor 2 (KLF2) plays an important role in the regulation of a variety of immune cells, including monocytes. We have previously shown that KLF2 inhibits proinflammatory activation of monocytes. However, the role of KLF2 in arthritis is yet to be investigated. In the current study, we show that recruitment of significantly greater numbers of inflammatory subset of CD11b(+)F4/80(+)Ly6C+ monocytes to the inflammatory sites in KLF2 hemizygous mice compared to the wild type littermate controls. In parallel, inflammatory mediators, MCP-1, Cox-2 and PAI-1 were significantly up-regulated in bone marrow-derived monocytes isolated from KLF2 hemizygous mice, in comparison to wild-type controls. Methylated-BSA and IL-1β-induced arthritis was more severe in KLF2 hemizygous mice as compared to the littermate wild type controls. Consistent with this observation, monocytes isolated from KLF2 hemizygous mice showed an increased number of cells matured and differentiated towards osteoclastic lineage, potentially contributing to the severity of cartilage and bone damage in induced arthritic mice. The severity of arthritis was associated with the higher expression of proteins such as HSP60, HSP90 and MMP13 and attenuated levels of pPTEN, p21, p38 and HSP25/27 molecules in bone marrow cells of arthritic KLF2 hemizygous mice compared to littermate wild type controls. The data provide new insights and evidences of KLF2-mediated transcriptional regulation of arthritis via modulation of monocyte differentiation and function.
    Current Molecular Medicine 02/2012; 12(2):113-25. · 4.20 Impact Factor
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    ABSTRACT: CD39 (ectonucleoside triphosphate diphosphohydrolase-1; ENTPD-1) rapidly hydrolyzes ATP and ADP to AMP; AMP is hydrolyzed by ecto-5'-nucleotidase (CD73) to adenosine, an anti-thrombotic and cardiovascular protective mediator. While expression of human CD39 in a murine model of myocardial ischemia/reperfusion (I/R) injury confers cardiac protection, the translational therapeutic potential of these findings requires further testing in a large animal model. To determine if transgenic expression of CD39 reduces infarct size in a swine model of myocardial ischemia/reperfusion injury, transgenic pigs expressing human CD39 (hCD39) were generated via somatic cell nuclear transfer and characterized. Expression of hC39 in cardiac tissue was confirmed by immunoblot and immunohistochemistry. Myocardial I/R injury was induced by intracoronary balloon inflation in the left anterior descending (LAD) artery for 60 min followed by 3 hours of reperfusion. The ischemic area was delineated by perfusion with 5% phthalo blue and the myocardial infarct size was determined by triphenyl tetrazolium chloride (TTC) staining. During ischemia, the rate-pressure product was significantly lower in control versus hCD39-Tg swine. Following reperfusion, compared to littermate control swine, hCD39-Tg animals displayed a significant reduction in infarct size (hCD39-Tg: 17.2 ± 4.3% vs. Control: 44.7 ± 5.2%, P=0.0025). Our findings demonstrate for the first time that the findings in transgenic mouse models translate to large animal transgenic models and validate the potential to translate CD39 into the clinical arena to attenuate human myocardial ischemia/reperfusion injury.
    Journal of Molecular and Cellular Cardiology 01/2012; 52(5):958-61. · 5.15 Impact Factor
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    ABSTRACT: Osteoporosis is a bone disorder associated with loss of bone mineral density and micro architecture. A balance of osteoblasts and osteoclasts activities maintains bone homeostasis. Increased bone loss due to increased osteoclast and decreased osteoblast activities is considered as an underlying cause of osteoporosis. The cures for osteoporosis are limited, consequently the potential of CD34+ cell therapies is currently being considered. We developed a nanofiber-based expansion technology to obtain adequate numbers of CD34(+) cells isolated from human umbilical cord blood, for therapeutic applications. Herein, we show that CD34(+) cells could be differentiated into osteoblastic lineage, in vitro. Systemically delivered CD34(+) cells home to the bone marrow and significantly improve bone deposition, bone mineral density and bone micro-architecture in osteoporotic mice. The elevated levels of osteocalcin, IL-10, GM-CSF, and decreased levels of MCP-1 in serum parallel the improvements in bone micro-architecture. Furthermore, CD34(+) cells improved osteoblast activity and concurrently impaired osteoclast differentiation, maturation and functionality. These findings demonstrate a novel approach utilizing nanofiber-expanded CD34(+) cells as a therapeutic application for the treatment of osteoporosis.
    PLoS ONE 01/2012; 7(6):e39365. · 3.53 Impact Factor
  • Jingwei Lu, Reeva Aggarwal, Vincent J. Pompili, Hiranmoy Das
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    ABSTRACT: Ischemia related diseases are on rise worldwide and have been shown to cause irreversible damage to the cells due to the blockage of blood supply to the tissue. Conventional therapies are less effective as they do not consider repair of the damaged tissues. Thus, alternative, stem cell-based therapies are currently under investigation. For example, hematopoietic stem cells (HSCs) were shown to give rise to vascular cells involved in neoangiogenesis; so, they have been tested in variety of animal models and small-scale clinical trials. Improvement in blood flow and tissue functionality was observed and adverse effects were not apparent. However, success of stem cell therapy is limited by the number of functional stem cells for clinical application. Numerous attempts are underway to address this issue via strategies that involve ex vivo expansion of stem cells preserving their stemness. This chapter outlines the mechanism of therapeutic angiogenesis, sources of HSCs, various methods of ex vivo expansion of HSCs via genetic regulators, cytokines and biomaterial scaffolds, and their preclinical and clinical applications. KeywordsHematopoietic stem cells-Ischemia-Angiogenic-Vasculogenesis-Stromal cells-Thrombopoietin
    12/2011: pages 219-229;
  • Jingwei Lu, Vincent J Pompili, Hiranmoy Das
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    ABSTRACT: Vasculogenesis and angiogenesis are the major forms of blood vessel formation. Angiogenesis is the process where new vessels grow from pre-existing blood vessels, and is very important in the functional recovery of pathological conditions, such as wound healing and ischemic heart diseases. The development of better animal model and imaging technologies in past decades has greatly enriched our understanding on vasculogenesis and angiogenesis processes. Hypoxia turned out to be an important driving force for angiogenesis in various ischemic conditions. It stimulates expression of many growth factors like vascular endothelial growth factor, platelet-derived growth factor, insulin-like growth factor, and fibroblast growth factor, which play critical role in induction of angiogenesis. Other cellular components like monocytes, T cells, neutrophils, and platelets also play significant role in induction and regulation of angiogenesis. Various stem/progenitor cells also being recruited to the ischemic sites play crucial role in the angiogenesis process. Pre-clinical studies showed that stem/progenitor cells with/without combination of growth factors induce neovascularization in the ischemic tissues in various animal models. In this review, we will discuss about the fundamental factors that regulate the angiogenesis process and the use of stem cells as therapeutic regime for the treatment of ischemic diseases.
    Cell biochemistry and biophysics 10/2011; · 3.34 Impact Factor
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    R Aggarwal, J Lu, V J Pompili, H Das
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    ABSTRACT: Maintenance of ex vivo hematopoietic stem cells (HSC) pool and its differentiated progeny is regulated by complex network of transcriptional factors, cell cycle proteins, extracellular matrix, and their microenvironment through an orchestrated fashion. Strides have been made to understand the mechanisms regulating in vivo quiescence and proliferation of HSCs to develop strategies for ex vivo expansion. Ex vivo expansion of HSCs is important to procure sufficient number of stem cells and as easily available source for HSC transplants for patients suffering from hematological disorders and malignancies. Our lab has established a nanofiber-based ex vivo expansion strategy for HSCs, while preserving their stem cell characteristics. Ex vivo expanded cells were also found biologically functional in various disease models. However, the therapeutic potential of expanded stem cells at clinical level still needs to be verified. This review outlines transcriptional factors that regulate development of HSCs and their commitment, genes that regulate cell cycle status, studies that attempt to develop an effective and efficient protocol for ex vivo expansion of HSCs and application of HSC in various non-malignant and malignant disorders. Overall the goal of the current review is to deliver an understanding of factors that are critical in resolving the challenges that limit the expansion of HSCs in vivo and ex vivo.
    Current Molecular Medicine 10/2011; 12(1):34-49. · 4.20 Impact Factor
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    Suman Kanji, Vincent J Pompili, Hiranmoy Das
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    ABSTRACT: Maintenance of hematopoietic stem cells (HSCs) pool depends on fine balance between self-renewal and differentiation of HSCs. HSCs normally reside within the bone marrow niche of an adult mammal. The embryonic development of HSCs is a complex process that involves the migration of developing HSCs in multiple anatomical sites. Throughout the process, developing HSCs receive internal (transcriptional program) and external (HSC niche) signals, which direct them to maintain balance between self-renewal and differentiation, also to generate a pool of HSCs. In physiological condition HSCs differentiate into all mature cell types present in the blood. However, in pathological condition they may differentiate into non-hematological cells according to the need of the body. It was shown that HSCs can transdifferentiate into cell types that do not belong to the hematopoietic system suggests a complete paradigm shift of the hierarchical hematopoietic tree. This review describes the developmental origins and regulation of HSCs focusing on developmental signals that induce the adult hematopoietic stem cell program, as these informations are very critical for manipulating conditions for expansion of HSCs in ex vivo condition. This review also states clinical application and related patents using HSC.
    Recent patents on biotechnology. 04/2011; 5(1):40-53.
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    ABSTRACT: Mechanisms of human Vγ2Vδ2 T cell-mediated tumor immunity have yet to be fully elucidated. At least some tumor cell recognition is mediated by NKG2D-MICA interactions. Herein, by using MTT assay and PI-BrdU co-staining and Western-blot, we show that these Vγ2Vδ2 T cells can limit the proliferation of ovarian tumor cells by down regulation of apoptosis and cell cycle related molecules in tumor cells. Cell-to-cell contact is critical. γδ T cell-resistant, but not susceptible ovarian tumor cells escape γδ T cell-mediated immune recognition by up-regulating pErk1/2, thereby decreasing surface MICA levels. Erk1/2 inhibitor pretreatment or incubation prevents this MICA decrease, while up-regulating key cell cycle related molecules such as CDK2, CDK4 and Cyclin D1, as well as apoptosis related molecules making resistant tumor cells now vulnerable to γδ T cell-mediated lysis. These findings demonstrate novel effects of γδT cells on ovarian tumor cells.
    PLoS ONE 01/2011; 6(9):e23348. · 3.53 Impact Factor
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    ABSTRACT: The Phase I clinical study was designed to assess the safety and feasibility of a dose escalating intracoronary infusion of autologous bone marrow (BM)-derived CD133+ stem cell therapy to the patients with chronic total occlusion (CTO) and ischemia. Nine patients were received CD133+ cells into epicardial vessels supplying collateral flow to areas of viable ischemic myocardium in the distribution of the CTO. There were no major adverse cardiac events (MACE), revascularization, re-admission to the hospital secondary to angina, or acute myocardial infarction (AMI) for the 24-month period following cellular infusion. In addition, there were no periprocedural infusion-related complications including malignant arrhythmias, loss of normal coronary blood flow or acute neurologic events. Cardiac enzymes were negative in all patients. There was an improvement in the degree of ischemic myocardium, which was accompanied by a trend towards reduction in anginal symptoms. Intracoronary infusion of autologous CD133+ marrow-derived cells is safe and feasible. Cellular therapy with CD133+ cells to reduce anginal symptoms and to improve ischemia in patients with CTO awaits clinical investigation in Phase II/III trials.
    Frontiers in bioscience (Elite edition) 01/2011; 3:506-14.
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    Gregory B Comfort, Melike Bayram, Vincent J Pompili
    Journal of the American College of Cardiology 06/2010; 55(22):2510. · 14.09 Impact Factor

Publication Stats

209 Citations
123.94 Total Impact Points

Institutions

  • 2009–2014
    • The Ohio State University
      • Department of Internal Medicine
      Columbus, Ohio, United States
    • Johns Hopkins University
      Baltimore, Maryland, United States
  • 2011
    • Brigham and Women's Hospital
      • Department of Medicine
      Boston, MA, United States
  • 2006–2008
    • Case Western Reserve University
      • Department of Medicine (University Hospitals Case Medical Center)
      Cleveland, Ohio, United States