Yangxiao Wu
Third Military Medical University
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Featured researches published by Yangxiao Wu.
Biomaterials | 2012
Wen Zeng; Can Wen; Yangxiao Wu; Li Li; Zhenhua Zhou; Jianhong Mi; Wen Chen; Mingcan Yang; Chunli Hou; Jiansen Sun; Chuhong Zhu
The patency rate of small-diameter tissue-engineered blood vessels is the determinant for their application in coronary artery bypass grafting. The coronary artery is innervated by vagus nerves. The origin of vagus nerves is rich in brain-derived neurotrophic factors (BDNF). We have investigated whether BDNF could improve the patency rate of small-diameter tissue-engineered blood vessels through promoting stem cell homing and paracrine activity. In vitro, we isolated early and late endothelial progenitor cells (EPCs) and found BDNF could promote single clone formation and paracrine function of EPCs, and could also induce the proliferation, migration and differentiation of late EPCs. BDNF could enhance the capturing of EPCs in parallel-plate flow chamber. Flow cytometric analysis and laser-scanning confocal microscope showed BDNF could enhance the mobilization and homing of C57BL/6 mouse EPCs after wire injury. Based on it, BDNF was coupled to the lumen surface of the blood vessel matrix material incubated with collagen through SPDP to construct BDNF-modified small-diameter tissue-engineered blood vessel. The blood vessel patency rate was significantly higher than that of control group 8 weeks after implantation in rats and the endothelialization level was superior to control. These results demonstrate that BDNF can effectively improve patency of small-diameter tissue-engineered blood vessels through stem cell homing and paracrine, and it is expected to play an important role in the construction of substitutes for coronary artery bypass grafting.
Cell Transplantation | 2013
Lei Shen; Wen Zeng; Yangxiao Wu; Chunli Hou; Wen Chen; Mingcan Yang; Li Li; Ya-Fang Zhang; Chuhong Zhu
Angiogenesis is a major obstacle for wound healing in patients with diabetic foot wounds. Mesenchymal stem cells (MSCs) have an important function in wound repair, and neurotrophin-3 (NT-3) can promote nerve regeneration and angiogenesis. We investigated the effect of NT-3 on accelerating wound healing in the diabetic foot by improving human bone marrow MSC (hMSC) activation. In vitro, NT-3 significantly promoted VEGF, NGF, and BDNF secretion in hMSCs. NT-3 improved activation of the hMSC conditioned medium, promoted human umbilical vein endothelial cell (HUVEC) proliferation and migration, and significantly improved the closure rate of HUVEC scratches. In addition, we produced nanofiber mesh biological tissue materials through the electrospinning technique using polylactic acid, mixed silk, and collagen. The hMSCs stimulated by NT-3 were implanted into the material. Compared with the control group, the NT-3-stimulated hMSCs in the biological tissue material significantly promoted angiogenesis in the feet of diabetic C57BL/6J mice and accelerated diabetic foot wound healing. These results suggest that NT-3 significantly promotes hMSC secretion of VEGF, NGF, and other vasoactive factors and that it accelerates wound healing by inducing angiogenesis through improved activation of vascular endothelial cells. The hMSCs stimulated by NT-3 can produce materials that accelerate wound healing in the diabetic foot and other ischemic ulcers.
Biomaterials | 2013
Chunli Hou; Lei Shen; Qiang Huang; Jianhong Mi; Yangxiao Wu; Mingcan Yang; Wen Zeng; Li Li; Wen Chen; Chuhong Zhu
Diabetic ischemic ulcer is an intractable diabetic complication. Bone marrow mesenchymal stem cells (BMSCs) have great potential in variety of tissue repair. In fact, poor cell viability and tolerance limit their ability for tissue repair. In addition, it is difficult for stem cells to home and locate to the lesion. In this study, we explore whether over-expression of heme oxygenase-1 (HO-1) in BMSCs complexed with collagen play an important role in treatment of diabetic ischemic ulcers. In vitro, over-expression of HO-1 promoted the proliferation and paracrine activity of BMSCs and the conditioned medium of BMSCs accelerated HUVECs migration and proliferation. These processes were closely related to Akt signaling pathway and were not dependent on Erk signaling pathway. In vivo, in order to make BMSCs directly act on the wound, we choose a solid collagen as a carrier, BMSCs were planted into it, ischemic wounds of diabetic mice were covered with the complex of BMSCs and collagen. The results indicate that the complex of HO-1-overexpressing BMSCs and collagen biomaterials can significantly promote angiogenesis and wound healing. These preclinical findings open new perspectives for the treatment of diabetic foot ulcers.
Scientific Reports | 2015
Wen Chen; Yangxiao Wu; Li Li; Mingcan Yang; Lei Shen; Ge Liu; Ju Tan; Wen Zeng; Chuhong Zhu
Endothelial progenitor cells (EPCs) seeded on biomaterials can effectively promote diabetic ischemic wound healing. However, the function of transplanted EPCs is negatively affected by a high-glucose and ischemic microenvironment. Our experiments showed that EPC autophagy was inhibited and mitochondrial membrane potential (MMP) was increased in diabetic patients, while adenosine treatment decreased the energy requirements and increased the autophagy levels of EPCs. In animal experiments, we transplanted a biomaterial seeded with EPCs onto the surface of diabetic wounds and found that adenosine-stimulated EPCs effectively promoted wound healing. Increased microvascular genesis and survival of the transplanted cells were also observed in the adenosine-stimulated groups. Interestingly, our study showed that adenosine increased the autophagy of the transplanted EPCs seeded onto the biomaterial and maintained EPC survival at 48 and 96 hours. Moreover, we observed that adenosine induced EPC differentiation through increasing the level of autophagy. In conclusion, our study indicated that adenosine-stimulated EPCs seeded onto a biomaterial significantly improved wound healing in diabetic mice; mechanistically, adenosine might maintain EPC survival and differentiation by increasing high glucose-inhibited EPC autophagy and maintaining cellular energy metabolism.
Tissue Engineering Part A | 2015
Siyi He; Lei Shen; Yangxiao Wu; Li Li; Wen Chen; Chunli Hou; Mingcan Yang; Wen Zeng; Chuhong Zhu
Great challenges in transplantation of mesenchymal stem cells (MSCs) for treating ischemic diabetic ulcers (IDUs) are to find a suitable carrier and create a beneficial microenvironment. Brain-derived neurotrophic factor (BDNF), a member of neurotrophin family, is considered angiogenic and neuroprotective. Given that IDUs are caused by vascular disease and peripheral neuropathy, we used BDNF as a stimulant, and intended to explore the role of new biomaterials complex with MSCs in wound healing. BDNF promoted the proliferation and migration of MSCs using MTT, transwell, and cell scratch assays. The activity of human umbilical vein endothelial cells (HUVECs) was also enhanced by the MSC-conditioned medium in the presence of BDNF, via a vascular endothelial growth factor-independent pathway. Since proliferated HUVECs in the BDNF group made the microenvironment more conducive to endothelial differentiation of MSCs, by establishing co-culture systems with the two cell types, endothelial cells derived from MSCs increased significantly. A new biomaterial made of polylactic acid, silk and collagen was used as the carrier dressing. After transplantation of the BDNF-stimulated MSC/biomaterial complex, the ulcers in hindlimb ischemic mice healed prominently. More blood vessel formation was observed in the wound tissue, and more MSCs were co-stained with some endothelial-specific markers such as cluster of differentiation (CD)31 and von Willebrand Factor (vWF) in the treatment group than in the control group. These results demonstrated that BDNF could improve microenvironment in the new biomaterial, and induce MSCs to differentiate into endothelial cells indirectly, thus accelerating ischemic ulcer healing.
Advanced Healthcare Materials | 2015
Wen Chen; Fangjuan Wang; Wen Zeng; Jun Sun; Li Li; Mingcan Yang; Jiansen Sun; Yangxiao Wu; Xiaohui Zhao; Chuhong Zhu
Regulation of cellular response pattern to phosphorus ion (PI) is a new target for the design of tissue-engineered materials. Changing cellular response pattern to high PI can maintain monocyte/macrophage survival in TEBV and the signal of increasing PI can be converted by klotho to the adenosine signals through the regulation of energy metabolism in monocytes/macrophages.
Tissue Engineering Part A | 2015
Yangxiao Wu; Li Li; Wen Chen; Wen Zeng; Lingqin Zeng; Can Wen; Chuhong Zhu
Small-diameter tissue-engineered blood vessels (TEBVs) have been associated with low, long-term patency rates primarily because of acute thrombosis in early stages and an inability to achieve early endothelialization. Platelets and endothelial progenitor cells (EPCs) play a key role in these processes. A nano delayed-release 5-aminoimidazole-4-carboxamide 1-β-D-ribofuranoside (AICAR)-bound TEBV was implanted in rat carotid arteries for 3 months. AICAR-bound TEBVs had a high patency rate compared with control TEBVs after 3 months. We found that AICAR maintained moderate platelet aggregation in vivo. In vitro data indicated that AICAR inhibits the release of 5-hydroxytryptamine and thromboxane A2 in activating platelets to reduce platelet aggregation. Then, we confirmed that AICAR strengthens the EPC energy state, which results in earlier endothelialization. The homing, migration, and paracrine function of EPCs were enhanced by AICAR in vitro. Besides, AICAR can contribute to the migration of endothelial cells near the anastomosis. The cellularization of TEBVs at different time points was observed too. In conclusion, our study suggests that the application of nanodelivery material containing AICAR can effectively improve small-diameter TEBVs by maintaining moderate platelet aggregation and improving metabolism of EPCs.
Journal of Biomedical Materials Research Part B | 2017
Yangxiao Wu; Ge Liu; Wen Chen; Mingcan Yang; Chuhong Zhu
Intimal hyperplasia (IH) is the cause of clinical failure in patients with vascular transplants and intravascular stents. The proliferation and phenotype switching of vascular smooth muscle cells (VSMCs) play important roles in IH. Inhibiting the proliferation of VSMCs and maintaining the differentiated phenotype of VSMCs is one way to reduce IH. In this article, 5-aminoimidazole-4-carboxamide 1-β-D-ribofuranoside (AICAR) was used in experiments after drug screening. We found that the metabolism, autophagy, and differentiation of VSMCs were enhanced which were important to the normal function of VSMCs, but the secretion of VSMCs was reduced after AICAR treatment. AICAR induces G1 phase arrest and inhibits the proliferation of VSMCs using the MTT and EdU assays and cell cycle analysis. Then, the rat carotid artery vessel transplantation model was used to evaluate the function of AICAR in vivo. AICAR-modified tissue-engineered blood vessels (TEBVs) had a higher patency rate and less IH than the control TEBVs. In conclusion, AICAR can improve the normal function of VSMCs by increasing the metabolism and autophagy of VSMCs but inhibit the proliferation, paracrine, and phenotypes switching of VSMCs, further contribute the reducing of IH in TEBVs.
ACS Nano | 2015
Wen Chen; Wen Zeng; Jiansen Sun; Mingcan Yang; Li Li; Jingting Zhou; Yangxiao Wu; Jun Sun; Ge Liu; Rui Tang; Ju Tan; Chuhong Zhu
Advanced Healthcare Materials | 2014
Wen Chen; Wen Zeng; Yangxiao Wu; Can Wen; Li Li; Ge Liu; Lei Shen; Mingcan Yang; Ju Tan; Chuhong Zhu