Hai-Xu Chen

Institute for Transfusion Medicine, Pittsburgh, Pennsylvania, United States

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Publications (4)17.54 Total impact

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    ABSTRACT: Radiation-induced intestinal injury is a common complication in radiotherapy for solid organ malignancies in abdomen or pelvis. However, currently there are no approved medical countermeasures for radiation-induced intestinal injury. Therefore, it is urgent to develop new treatments for radiation-induced intestinal injury. In the present study, we demonstrated that bone marrow derived mesenchymal stem cells (MSCs) and overexpression of human manganese superoxide dismutase (MnSOD) could ameliorate radiation-induced intestinal syndrome. NOD/SCID mice received abdominal irradiation at a selected dose of 5 Gy, and then infused intravenously with MnSOD-MSCs. Mice body weight, survival and diarrhea were monitored for 30-days. Colonization and differentiation of MnSOD-MSCs in the irradiated intestine were analyzed by histological and immunohistochemical methods. Consequently, our data demonstrated that intravenous administration of MnSOD-MSCs improved survival, decreased diarrhea occurrence and protected the small intestinal structural integrity of irradiated mice. Moreover, intravenously transplanted MnSOD-MSCs could colonize the irradiated intestine and repair injured sites. These findings suggested that MnSOD-MSCs may be an attractive and potential option for radiation-induced intestinal injury.
    Current Gene Therapy 12/2013; 13(5):305-14. DOI:10.2174/15665232113136660027 · 2.54 Impact Factor
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    ABSTRACT: The study was aimed to investigate the effects and mechanism of manganese superoxide dismutase (MnSOD) on tert-butyl hydroperoxide(t-BHP) induced apoptosis in human bone marrow mesenchymal stem cells (MSCs). The MnSOD gene was cloned from human fetal liver by RT-PCR. The MnSOD recombinant plasmid was transfected into MSCs stably by lentiviral system. The efficiency of virus transfection was identified by expression of enhanced green fluorescence protein (EGFP) analyzed by fluorescence microscope, then MSCs were sorted by fluorescence-activated cell sorting (FACS) according to strong EGFP expression. MnSOD expression was detected by RT-PCR and Western blot. Transfected cells were then treated with different concentration of t-BHP, and the features including cell viability, senescence-associated β-gal activity, and apoptosis were evaluated. Our data demonstrated that overexpression of MnSOD could promote MSCs viability by inhibiting apoptosis or cellular senescence. Furthermore, apoptosis related genes p53 and PUMA were down-regulated. Therefore, these results indicated that overexpression of MnSOD in MSCs could protect against t-BHP induced apoptosis.
    ACTA AGRONOMICA SINICA 06/2013; 40(6):556. DOI:10.3724/SP.J.1206.2012.00576
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    ABSTRACT: Unlabelled: Cancer-associated mesenchymal stem cells (MSCs) play a pivotal role in modulating tumor progression. However, the interactions between liver cancer-associated MSCs (LC-MSCs) and hepatocellular carcinoma (HCC) remain unreported. Here, we identified the presence of MSCs in HCC tissues. We also showed that LC-MSCs significantly enhanced tumor growth in vivo and promoted tumor sphere formation in vitro. LC-MSCs also promoted HCC metastasis in an orthotopic liver transplantation model. Complementary DNA (cDNA) microarray analysis showed that S100A4 expression was significantly higher in LC-MSCs compared with liver normal MSCs (LN-MSCs) from adjacent cancer-free tissues. Importantly, the inhibition of S100A4 led to a reduction of proliferation and invasion of HCC cells, while exogenous S100A4 expression in HCC cells resulted in heavier tumors and more metastasis sites. Our results indicate that S100A4 secreted from LC-MSCs can promote HCC cell proliferation and invasion. We then found the expression of oncogenic microRNA (miR)-155 in HCC cells was significantly up-regulated by coculture with LC-MSCs and by S100A4 ectopic overexpression. The invasion-promoting effects of S100A4 were significantly attenuated by a miR-155 inhibitor. These results suggest that S100A4 exerts its effects through the regulation of miR-155 expression in HCC cells. We demonstrate that S100A4 secreted from LC-MSCs promotes the expression of miR-155, which mediates the down-regulation of suppressor of cytokine signaling 1, leading to the subsequent activation of STAT3 signaling. This promotes the expression of matrix metalloproteinases 9, which results in increased tumor invasiveness. Conclusion: S100A4 secreted from LC-MSCs is involved in the modulation of HCC progression, and may be a potential therapeutic target. (HEPATOLOGY 2013).
    Hepatology 06/2013; 57(6). DOI:10.1002/hep.26257 · 11.06 Impact Factor
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    ABSTRACT: Mesenchymal stem cells (MSCs) play a critical role in promoting cancer progression. However, it is not clear whether MSCs are located in breast cancer tissues and correlated with tumor proliferation. The aim of this study was to investigate the presence of MSCs in breast cancer tissues and evaluate their interactions with cancer cells. We successfully isolated and identified MSCs from primary breast cancer tissues. Breast cancer-associated MSCs (BC-MSCs) showed homogenous immunophenotype, and possessed tri-lineage differentiation potential (osteoblast, adipocyte, and chondrocyte). When co-transplanted with cancer cells in a xenograft model in vivo, BC-MSCs significantly increased the volume and weight of tumors. We observed that BC-MSCs stimulated mammosphere formation in the transwell co-culture system in vitro. This effect was significantly suppressed by the EGF receptor inhibitor. We verified that BC-MSCs could secrete EGF and activate cancer cell's EGF receptors. Furthermore, our data showed that EGF derived from BC-MSCs could promote mammosphere formation via the PI3K/Akt signaling pathway. Our results confirmed the presence of MSC in primary breast cancer tissues, and they could provide a favorable microenvironment for tumor cell growth in vivo, partially enhance mammosphere formation via the EGF/EGFR/Akt pathway.
    Breast Cancer Research and Treatment 05/2011; 132(1):153-64. DOI:10.1007/s10549-011-1577-0 · 3.94 Impact Factor