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Fu M.,Chongqing Medical University | Li Z.,Chenzhou First Peoples Hospital | Tan T.,Ohio State University | Guo W.,Guangdong Academy of Medical science | And 5 more authors.
American Journal of Physiology - Heart and Circulatory Physiology

Palmitate (PA) impairs endothelial progenitor cells (EPCs). However, the molecular mechanism underlying the suppressive function of PA remains largely unknown. Ceramide, a free fatty acid metabolite, mediates multiple cellular signals. We hypothesized that ceramide acts as an intermediate molecule to mediate inhibition of EPCs by PA. We first demonstrated that PA could inhibit the attachment, migration, and tube formation of EPCs through suppression of the Akt/endothelial nitric oxide (NO) synthase (eNOS) signaling pathway. In addition, we observed that PA could induce ceramide accumulation in EPCs. To test whether the accumulation of ceramide causes EPC dysfunction, the ceramide synthesis inhibitors myriocin and fumonisin B1 were used. We that found both inhibitors could effectively abolish PA-mediated EPC inhibition. Furthermore, the ceramide deacylation inhibitor N-oleoylethanolamine could augment the inhibitory effect of PA on EPCs, indicating that it is ceramide, not its metabolites, that mediates the suppression of EPCs by PA. We have previously shown that Akt/eNOS phosphorylation was reduced after PA treatment, which, in turn, hampered the normal bioavailability of NO, leading to impaired functions of EPCs. To test the role for ceramide in this process, a clinically used NO donor, sodium nitroprusside, was used. We found that sodium nitroprusside could rescue the suppressive effects of ceramide on EPCs, suggesting that ceramide-mediated EPC inhibition might be through reduction of NO production. Taken together, our findings indicated that ceramide-induced reduction of NO might be the molecular mechanism for PA-mediated EPC inhibition; thus, targeting either ceramide or NO production might be an effective means for improvement of EPC functions in diseases. © 2015 the American Physiological Society. Source

Guo W.,Guangdong Academy of Medical science | Li Z.,Chenzhou First Peoples Hospital | Xie X.,Tongji University | Tan T.,Ohio State University | And 5 more authors.
Biochemical and Biophysical Research Communications

The stromal cell-derived factor-1α/C-X-C chemokine receptor 4 (SDF-1/CXCR4) axis is involved in various aspects of tissue repair, regeneration and development. However, the role of SDF-1/CXCR4 in acute lung injury (ALI) remains largely unknown. The aim of the present investigation is to examine pathological changes in a rabbit model with ALI induced by oleic acid (OA) and to explore the protective effect of SDF-1α on ALI. Intravenous application (i.v.) of oleic acid (0.1 ml/kg/h for 2 h) provoked pulmonary hemorrhage, edema, and protein leakage, resulting in severe ALI. When the rabbit received an infusion of SDF-1α (20 μg/kg/24 h) for 30 min before OA treatment, SDF-1α seemed to significantly improve the pathologies associated with OA-induced ALI. While dissecting the molecular mechanisms underlying the beneficial effects of SDF-1α, we found that SDF-1/CXCR4 is expressed in uninjured lung tissues but is greatly reduced after OA treatment. Interestingly, intravenous delivery of SDF-1α could target an injured lung and rescue expression of CXCR4, which in turn activates anti-apoptotic proteins, Bcl-1 and Bcl-xl, but does not affect pro-apoptotic proteins, such as Bad and Bax. These data suggested that SDF-1α could protect rabbit lungs from AIL. The molecular mechanism might be associated with upregulating anti-apoptosis family expression through CXCR4. Thus, SDF-1/CXCR4 signaling pathway may be a promising target for treatment of patients with ALI. © 2014 Published by Elsevier Inc. Source

Xie N.,Tongji University | Li Z.,Chenzhou First Peoples Hospital | Adesanya T.M.,Ohio State University | Guo W.,Guangdong Academy of Medical science | And 7 more authors.
Journal of Cellular and Molecular Medicine

Mesenchymal stem cell-based therapy has emerged as a promising approach for the treatment of peripheral arterial disease. The purpose of this study was to examine the potential effects of human placenta-derived mesenchymal stem cells (PMSCs) on mouse hindlimb ischemia. PMSCs were isolated from human placenta tissue and characterized by flow cytometry. An in vivo surgical ligation-induced murine limb ischemia model was generated with fluorescent dye (CM-DiI) labelled PMSCs delivered via intramuscular injection. Our data show that PMSCs treatment significantly enhanced microvessel density, improved blood perfusion and diminished pathologies in ischemic mouse hindlimbs as compared to those in the control group. Further immunostaining studies suggested that injected PMSCs can incorporate into the vasculature and differentiate into endothelial and smooth muscle cells to enhance angiogenesis in ischemic hind limbs. This may in part explain the beneficial effects of PMSCs treatment. Taken together, we found that PMSCs treatment might be an effective treatment modality for treatment of ischemia-induced injury to mouse hind limbs by enhancement of angiogenesis. © 2016 John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine. Source

To compare the difference between muscle-tension-balance acupuncture and conventional acupuncture in the impacts on motor function and living ability of patients with drop foot and strephenopodia after stroke. Seventy cases were randomly divided into a muscle-tension-balance acupuncture group (group A) and a conventional acupuncture group (group B), 35 cases in each one. In group A, firstly the acupuncture of weakening technique was applied to Sanyinjiao (SP 6) and Taixi (KI 3) on the musculus extensor side; secondly, the strengthening technique was adopted at Jiexi (ST 41), Shenmai (BL 62) and Yanglingquan (GB 34) on musculus flexor side. In group B, the conventional needling technique was applied to Zusanli (ST 36), Sanyinjiao (SP 6), Xuanzhong (GB 39), etc. The treatment was given once every day in either group, 10 treatments made one session and 3 sessions of treatment were required. The score of Fugl-Meyer motor function of the lower limb on the affected side and Barthel index score were assessed before and after treatment in two groups. After treated for 3 sessions, Fugle-Meyer motor function score and Barthel index score of the patients all increased in two groups (all P < 0.01). The results in group A were better than those in group B (both P < 0.05). The improvements were apparent in the 2nd session of treatment in group A (both P < 0.01), which were superior to those in group B (both P < 0.05). Either acupuncture therapy can improve the motor function and living ability of patients with drop foot and strephenopodia after stroke. The muscle-tension-balance acupuncture achieves the efficacy quickly and its efficacy is much better. Source

Chen F.,Shaoxing University | Li J.,Chenzhou First Peoples Hospital | Zhang L.,University of South China | Wang Q.,Shaoxing University
Chinese Journal of Gastroenterology

Background: Vascular endothelial growth factor-C (VEGF-C) can induce lymphangiogenesis via activation of VEGFR-3 localized on the surface of lymphatic endothelial cells. PPARγ ligand rosiglitazone (ROS) has been verified to have inhibitory effect on VEGF-C expression and lymphangiogenesis of human gastric cancer cells in vitro. Aims: To investigate whether ROS could inhibit growth and lymphangiogenesis of gastric cancer in vivo. Methods: Nude mice bearing transplantation tumor were established by subcutaneous injection of human gastric cancer cell line SGC7901. The model mice were randomly divided into four groups: model group and three ROS groups administered intragastrically with 50, 75 and 100 mg·kg-1·2 d-1 ROS, respectively, for 42 days. Then all model mice were sacrificed, the volume of transplantation tumor was measured; lymphatic microvessel density (LMVD) were evaluated by immunohistochemical staining with D2-40 monoclonal antibody, a selective marker for lymphatic endothelium; RT-PCR and Western blotting were used to detect the mRNA and protein expressions of VEGF-C. Results: Volume of transplantation tumor, intratumoral LMVD counting and VEGF-C mRNA and protein expressions in ROS groups were decreased in a concentration-dependent manner (100 mg/kg group < 75 mg/kg group < 50 mg/kg group, P<0.05). All these parameters in ROS groups were significantly lower than those in model group (P<0.05). Conclusions: ROS inhibits the growth and lymphangiogenesis of human gastric cancer cell transplantation tumor in nude mice in a concentration-dependent manner. Its effect on tumor lymphangiogenesis is exerted through down-regulating VEGF-C expression. Source

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