scholarly journals The Use of Fiber-Reinforced Scaffolds Cocultured with Schwann Cells and Vascular Endothelial Cells to Repair Rabbit Sciatic Nerve Defect with Vascularization

2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Hongyang Gao ◽  
Yang You ◽  
Guoping Zhang ◽  
Feng Zhao ◽  
Ziyi Sha ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Sciatic Nerve ◽  
Nerve Fiber ◽  
Schwann Cells ◽  
Vascular Endothelial Cells ◽  
Neurological Function ◽  
Control Group ◽  
Vascular Endothelial ◽  
Fiber Reinforced ◽  
3D Scaffolds

To explore the feasibility of biodegradable fiber-reinforced 3D scaffolds with satisfactory mechanical properties for the repair of long-distance sciatic nerve defect in rabbits and effects of vascularized graft in early stage on the recovery of neurological function, Schwann cells and vascular endothelial cells were cocultured in the fiber-reinforced 3D scaffolds. Experiment group which used prevascularized nerve complex for the repair of sciatic nerve defect and control group which only cultured with Schwann cells were set. The animals in both groups underwent electromyography to show the status of the neurological function recovery at 4, 8, and 16 weeks after the surgery. Sciatic nerve regeneration and myelination were observed under the light microscope and electron microscope. Myelin sheath thickness, axonal diameter, and number of myelinated nerve fiber were quantitatively analyzed using image analysis system. The recovery of foot ulcer, the velocity of nerve conduction, the number of regenerating nerve fiber, and the recovery of ultrastructure were increased in the experimental group than those in the control group. Prevascularized tissue engineered fiber-reinforced 3D scaffolds for the repair of sciatic nerve defects in rabbits can effectively promote the recovery of neurological function.

scholarly journals Protective Effects of Oxymatrine on Vascular Endothelial Cells from High-Glucose-Induced Cytotoxicity by Inhibiting the Expression of A2B Receptor

2018 ◽  
Vol 45 (2) ◽  
pp. 558-571 ◽  
Author(s):  
Yun Yi ◽  
Yulin Shen ◽  
Qin Wu ◽  
Jingan Rao ◽  
Shu Guan ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cell Viability ◽  
Western Blotting ◽  
High Glucose ◽  
Vascular Endothelial Cells ◽  
Control Group ◽  
Vascular Endothelial ◽  
A2b Receptor ◽  
High Glucose Group ◽  
Glucose Group

Background/Aims: Diabetes mellitus (DM) has become an increasingly epidemic metabolic disease. Vascular endothelial cells play a key role in developing the cardiovascular complications of DM. The A2B receptor is expressed in vascular endothelial cells, and may help regulate the function of endothelial cells. The aim of this study was to investigate the protective effects of oxymatrine (OMT) on human umbilical vein endothelial cells (HUVECs) from high glucose-induced cytotoxicity. Methods: Homology modeling and molecular docking analysis were used to detect the binding sites between the adenosine A2B receptor and OMT. HUVECs were cultured with control (5.5 mM) or elevated glucose (22.2 mM) in the presence or absence of 3 µM OMT or A2B siRNA for 3 days. The MTS cell viability assay was used to measure the toxicity of high glucose on HUVECs and the protective effect of OMT or A2B siRNA. The expression of the adenosine A2B receptor and CCL5 in HUVECs was detected with real-time quantitative PCR (qPCR) and Western blotting methods in each group. Levels of IL-1β and TNF-α were measured using an enzyme-linked immunosorbent assay (ELISA) kit, and the concentration of NO was detected with the nitrate reductase method. Monocyte chemotactic activity in each group was detected using Transwell chambers. Furthermore, the phosphorylation of p38 and ERK1/2 in each group was observed through the Western blotting method. Results: Homology modeling and molecular docking analysis showed that OMT contains well-fitted binding sites to the A2B receptor. After chronic culture at high glucose, the rate of cell viability was significantly lower than that of the control group. After co-treatment with OMT or A2B siRNA, cell viability was significantly increased compared with the high-glucose group. The results from real-time quantitative RT-PCR (qRT-PCR) and Western blotting indicated that high glucose could increase the expression of A2B receptors in HUVECs, an effect that was inhibited by OMT. In addition, the results revealed that the expression of CCL5, IL-1β and TNF-α was increased in the high-glucose group, and that the NO produced by HUVECs decreased due to hyperglycemia; however, co-culture with OMT or A2B siRNA abolished these effects. Meanwhile, the chemotaxis activity of monocytes to HUVECs cultured in high-glucose medium was enhanced 2.59-fold compared to the control cells. However, the inflammatory reactions in HUVECs were completely relieved by co-treatment with OMT or A2B siRNA. Moreover, the phosphorylation of p38 and ERK1/2 in HUVECs in the high-glucose group was significantly higher than that of the control group; these effects were reversed after co-treatment with OMT or A2B siRNA. Conclusion: OMT may protect the HUVECs from high glucose-induced cytotoxicity through inhibitting the expression of A2B receptor and inflammatory factors as well as decreasing the phosphorylation of p38 and ERK1/2.

scholarly journals Involvement of Acid-Sensing Ion Channel 1a Contribute to The Effect of Extracellular Acidosis on Vascular Endothelialcell Damage of Henoch-Schönlein Purpura Patients

2020 ◽  
Author(s):  
Jin-Kun Wang ◽  
Yan Bo ◽  
Qi-lian Zhou ◽  
Li-ping Yuan
Keyword(s):  
Endothelial Cells ◽  
Ion Channel ◽  
Vascular Endothelial Cells ◽  
Binding Activity ◽  
Control Group ◽  
Vascular Endothelial ◽  
Henoch Schonlein Purpura ◽  
Protein Expressions ◽  
Cytoskeleton Protein ◽  
Schonlein Purpura

Abstract Background: Henoch-Schönlein purpura (HSP) is a common kind of systematic vasculitis in children characterized by rash, joint pain,abdominal symptoms and renal disease,the detail pathogenesis of HSP has not been elucidated.Acid-sensing ion channels (ASICs) is a proton-gated sodium selective channel that belongs to Degenerin /epithelial Sodium Channel(DEG/ENaC) superfamily,previous research found the expressions of ASIC1a and ASIC3 in the vascular endothelial cells of HSPThis study aims to investigate the molecular mechanisms of silencing of acid-sensing ion channel 1a(ASIC1a) protects the vascular endothelial cells from Henoch-Schonlein purpura(HSP) patients.Findings:Human dermal microvascular endothelial cells ( HDMVEC) were cultured in vitro, siRNA sequences were designed for the coding region of human ASIC1a gene and HDMVEC cells were transfected with recombinant lentivirus( LV) -sh-ASIC1a. The control group ( NC group) without virus transfection and LV-sh-ASIC1a transfection group ( si-ASIC1a group) were set up. The expression of transfixed ASIC1a gene was detected by RT-PCR. After virus transfection 72 h, serum IgA1from HSP patients and serum IgA1 of normal children were added into HDMVEC cells. ASIC1a and cytoskeleton protein ( sm-α f-actin, MLCK) mRNA and protein expressions were detected by real-time PCR and Western blotting Methods.The binding activity of NF- κB with DNA in HDMVEC was determined by electrophoretic mobility shift assay (EMSA).The whole-cell patch-clamp technique was used to record the current changes and electrophysiological characteristics of ASICs in HDMVEC.Cytoskeleton protein ( sm-α f-actin, MLCK) mRNA and protein expressions in the group of si-ASIC1a group were significantly increased compared with the NC control group( P＜0.01). The HSP serum and silencing of ASIC1a had no significant effect on the binding activity of NF-κB with DNA in HDMVEC. Compared with the NC control group, the ASICS current and calcium overload of the si-ASIC1A group were reduced( P＜0.01) ．Conclusions: Silencing ASIC1a can protect HSP vascular endothelial cell injury by inhibiting ASIC1-related calcium influx and reducing the overload of calcium ,not the NF- κB signaling pathway.

scholarly journals Rat epidermal stem cells promote the angiogenesis of full-thickness wound

2020 ◽  
Author(s):  
Shaobin Huang ◽  
Zhicheng Hu ◽  
Peng Wang ◽  
Yi zhang ◽  
Xiaoling Cao ◽  
...  
Keyword(s):  
Stem Cells ◽  
Wound Healing ◽  
Endothelial Cells ◽  
Cell Suspension ◽  
Vascular Endothelial Cells ◽  
Control Group ◽  
Vascular Endothelial ◽  
Epidermal Stem Cells ◽  
Full Thickness ◽  
Full Thickness Wound

Abstract Background: Full-thickness wounds are a serious problem which badly affects patients’ life quality and also become the difficult problem for clinicians. Stem cells have great prospects in the treatment of wounds. Our previous experiments proved that autologous basal cell suspension can promote wound healing, and there are epidermal stem cells (ESCs) in basal cell suspension. We then conducted experiments to explore the effect of ESCs on full-thickness wound. Methods: In our study, the rat ESCs were isolated and expanded, and transfected with lentivirus to stably express EGFP. Experimental rats were randomly divided into 2 groups, in the ESCs group, the rat ESCs were sprayed on the Full-thickness wounds of the rats, while in control group, sprayed the PBS on the wound. Wound healing and neovascularization were then evaluated. Colonization, division and differentiation of ESCs on the wound were discovered by immunofluorescence.Results: The result suggested that rat ESCs can colonize, divide and proliferate in the wound. What’s more, the rat ESCs around blood vessels can differentiate into vascular endothelial cells and form a lumen-like structure. Compared with the control group, spraying the rat ESCs on the wound bed can promote angiogenesis and accelerate wound healing. Conclusions: Our study proved that rat ESCs were safe and effective for treating full-thickness wounds, and under certain conditions, ESCs can differentiate into vascular endothelial cells to promote angiogenesis and wound healing.

scholarly journals Effects of IL-1β and TNF-α on the Expression of P311 in Vascular Endothelial Cells and Wound Healing in Mice

2020 ◽  
Vol 11 ◽  
Author(s):  
Daijun Zhou ◽  
Tengfei Liu ◽  
Song Wang ◽  
Weifeng He ◽  
Wei Qian ◽  
...  
Keyword(s):  
Wound Healing ◽  
Endothelial Cells ◽  
Cell Migration ◽  
Protein Expression ◽  
Vascular Endothelial Cells ◽  
Control Group ◽  
Vascular Endothelial ◽  
Expression Levels ◽  
Relative Expression ◽  
Tnf Α

ObjectiveThis study aimed to define the role of interleukine-1β (IL-1β) and tumor necrosis factor-α (TNF-α) in the expression of P311 in vascular endothelial cells (VECs) and in wound healing.MethodsDAPI staining, a CCK-8 assay, cell migration assay, and an angiogenesis assay were used to assess the effects exerted by TNF-α and IL-1β at various concentrations on morphology, proliferation, migration, and angiogenesis of VECs. Western blot (WB) and reverse transcription-polymerase chain reaction (RT-PCR) models were employed to observe the effects exerted by proteins related to the nuclear factor-kappa B (NF-κB) signaling pathway and P311 mRNA expression. Bioinformatics analysis was performed on the binding sites of P311 and NF-κB. Finally, to investigate the effects of IL-1β and TNF-α on wound healing and the length of new epithelium in mice, we established a full-thickness wound defect model in mice. Immunohistochemistry was used to measure changes in P311, proliferating cell nuclear antigen (PCNA), vascular endothelial growth factor (VEGF), CD31 (platelet endothelial cell adhesion molecule-1, PECAM-1/CD31), as well as other related proteins.ResultsWhen levels of TNF-α and IL-1β were both 20 ng/ml, their effects on cell proliferation, cytoskeleton protein expression, cell migration, and angiogenesis were the greatest (P < 0.05). IL-1β and TNF-α at moderate concentrations effectively promoted P311 mRNA and p-NF-κB protein expression (P < 0.05), while p-NF-K b protein expression was decreased (P < 0.05). Luciferase assays showed that P311 expression was also relatively greater when stimulated at moderate concentrations (P < 0.05), while relative expression was significantly lower when the p-NF-K b inhibitor CAPE was added (P < 0.05). On 7-day wound healing rate comparison, the control, IL-1β, IL-1βab, TNF-α, and TNF-αab groups were 18, 37, 35, 39, and 36%, respectively, while control group + P311 siRNA was 31% (P < 0.05). New epithelial length, granulation tissue thickness, and number of blood vessels trends were also the same. In the control group, P311 showed lower relative expression levels than the others (P < 0.05). P311 relative expression levels trended as follows: control group > IL-1βab > IL-1β > TNF-αab > TNF-α (P < 0.05).ConclusionWhen IL-1β and TNF-α concentrations are moderate, they effectively promote the proliferation, expression, migration, and angiogenesis of VECs, possibly by promoting the expression of the NF-K b pathway and thereby promoting the expression of P311. In vitro experiments on mice suggest that P311 effectively promotes wound healing, and its mechanism may be closely related to PCNA, CD31, and VEGF.

scholarly journals Early Intervention of Didang Decoction on MLCK Signaling Pathways in Vascular Endothelial Cells of Type 2 Diabetic Rats

2016 ◽  
Vol 2016 ◽  
pp. 1-7 ◽  
Author(s):  
Shoujiao Ye ◽  
Zhenqiang Song ◽  
Jing Li ◽  
Chunshen Li ◽  
Juhong Yang ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Protein Kinase ◽  
Early Phase ◽  
Vascular Endothelial Cells ◽  
Late Phase ◽  
Intervention Group ◽  
Control Group ◽  
Vascular Endothelial ◽  
Type 2 Diabetic

In the study, type 2 diabetic rat model was established using streptozotocin (STZ) combined with a high-fat diet, and the rats were divided into control and diabetic groups. Diabetic groups were further divided into nonintervening, simvastatin, Didang Decoction (DDD) early-phase intervening, DDD mid-phase intervening, and DDD late-phase intervening groups. The expression level of MLCK was detected using Western Blot analysis, and the levels of cyclic adenosine monophosphate (cAMP), protein kinase C (PKC), and protein kinase A (PKA) were examined using Real Time PCR. Under the electron microscope, the cells in the early-DDD-intervention group and the simvastatin group were significantly more continuous and compact than those in the diabetic group. Compared with the control group, the expression of cAMP-1 and PKA was decreased in all diabetic groups, whereas the expression of MLCK and PKC was increased in early- and mid-phase DDD-intervening groups (P<0.05); compared with the late-phase DDD-intervening group, the expression of cAMP-1 and PKA was higher, but the level of MLCK and PKC was lower in early-phase DDD-intervening group (P<0.05). In conclusion, the early use of DDD improves the permeability of vascular endothelial cells by regulating the MLCK signaling pathway.

scholarly journals Blood–Nerve Barrier (BNB) Pathology in Diabetic Peripheral Neuropathy and In Vitro Human BNB Model

2020 ◽  
Vol 22 (1) ◽  
pp. 62
Author(s):  
Yukio Takeshita ◽  
Ryota Sato ◽  
Takashi Kanda
Keyword(s):  
Endothelial Cells ◽  
Peripheral Neuropathy ◽  
Schwann Cells ◽  
Cell Lines ◽  
Diabetic Peripheral Neuropathy ◽  
Peripheral Nerves ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Immortalized Cell

In diabetic peripheral neuropathy (DPN), metabolic disorder by hyperglycemia progresses in peripheral nerves. In addition to the direct damage to peripheral neural axons, the homeostatic mechanism of peripheral nerves is disrupted by dysfunction of the blood–nerve barrier (BNB) and Schwann cells. The disruption of the BNB, which is a crucial factor in DPN development and exacerbation, causes axonal degeneration via various pathways. Although many reports revealed that hyperglycemia and other important factors, such as dyslipidemia-induced dysfunction of Schwann cells, contributed to DPN, the molecular mechanisms underlying BNB disruption have not been sufficiently elucidated, mainly because of the lack of in vitro studies owing to difficulties in establishing human cell lines from vascular endothelial cells and pericytes that form the BNB. We have developed, for the first time, temperature-sensitive immortalized cell lines of vascular endothelial cells and pericytes originating from the BNB of human sciatic nerves, and we have elucidated the disruption to the BNB mainly in response to advanced glycation end products in DPN. Recently, we succeeded in developing an in vitro BNB model to reflect the anatomical characteristics of the BNB using cell sheet engineering, and we established immortalized cell lines originating from the human BNB. In this article, we review the pathologic evidence of the pathology of DPN in terms of BNB disruption, and we introduce the current in vitro BNB models.

scholarly journals Study on Damage Mechanism and Repair of Vascular Endothelial Cells Based on Ultrasound Technology

2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Shuhao Deng ◽  
Quan Jiang ◽  
Xin Lu ◽  
Yuan Zhang
Keyword(s):  
Endothelial Cells ◽  
Endothelial Function ◽  
Relaxation Function ◽  
Vascular Endothelial Cells ◽  
Early Stage ◽  
Gradient Centrifugation ◽  
Control Group ◽  
Dependent Manner ◽  
Vascular Endothelial ◽  
Vascular Endothelial Function

Objective. To detect the endothelial function of external iliac artery in rats with different stages of atherosclerosis by high-resolution ultrasound, so as to provide experimental methodological basis for evaluating the function of vascular endothelial cells by ultrasound. Methods. The animals were randomly divided into the control group ( n = 6 ) and the atherosclerosis model group ( n = 15 ). The atherosclerosis group was further divided into 4-week group, 8-week group, and 12-week group, with 5 animals in each group. After separating and grinding rat spleen, the obtained cells were cultured by density gradient centrifugation. After the cells adhered, the morphology of the cells was observed under a microscope and identified by DiI-Ac-LDL and FITC-UEA-I double staining. The activities of LDH and SOD, the contents of MDA and GSH, and the contents of NO in plasma were detected by biochemical methods. Results. The protective effect of rosanilin on brain injury in rats with acute hypobaric hypoxia and its regulation on the expression of pAkt protein; ox-LDL inhibited the proliferation activity of EPCs in a concentration-dependent manner. The expression of KLF2 and S1PR1 in HAEC can be knocked down by small interfering RNA, and knocking down KLF2 can not only downregulate the expression of S1PR1 but also downregulate HAVEN. With the development of atherosclerosis, the endothelium-dependent relaxation function and endothelium-independent relaxation function of the control group and the atherosclerosis model at 4, 8, and 12 weeks were damaged in different degrees and gradually aggravated. Conclusion. Atherosclerosis is a disease with both morphological and functional damage, and vascular endothelial function is damaged in the early stage with corresponding pathological changes. Ultrasound is an effective method to evaluate vascular endothelial function.

scholarly journals IMMUNOHISTOCHEMICAL MARKERS AND HISTOLOGICAL AND MORPHOLOGICAL CHANGES IN THE PLACENTA OF WOMEN, WHO GAVE BIRTH TO CHILDREN WITH ANENCEPHALY

2020 ◽  
Vol 22 (1) ◽  
pp. 22-27
Author(s):  
Veronika Melnikova V ◽  
◽  
Munavvara Dodkhoeva ◽  
Keyword(s):  
Endothelial Cells ◽  
Vascular Endothelial Cells ◽  
Morphological Changes ◽  
Inverse Correlation ◽  
Control Group ◽  
Healthy Children ◽  
Vascular Endothelial ◽  
Morphological Examination ◽  
Immunohistochemical Markers ◽  
Definition Of

Objective: To study immunohystochemical markers and features of histological and morphological changes in the placenta of women who have given birth to children with anencephaly. Methods: 15 women with anencephaly in the fetus (the main group) and 20 women, who gave birth to practically healthy children (control group), were examined. All women were tested for tumor marker alpha-fetoprotein (AFP) and human chorionic gonadotropin (HCG), morphological examination of placenta and levels of apoptosis, definition expression Nkx-2.2 in vascular endothelial cells of the villous chorion of the placenta of women in norm, and with congenital malformation (CM) of the central nervous system (CNS), in particular – anencephaly in the fetus. Results: A feature of the histochemical characteristics of placenta in women who have given birth to children with anencephaly is the predominance of chronic compensated deficiency with manifestations of dyscirculatory disorders. Statistically significant reduction of Nkx-2.2 expression levels in the vascular endothelial cells of the villous chorion placenta of women who gave birth to children with anencephaly, confirms the role of this factor in the differentiation of nervous structures. An inverse correlation between the level of Nkx-2.2 expression in the placenta and the level of AFP in the blood serum of pregnant women at the beginning of the second trimester of pregnancy determines the level of AFP as the most significant marker of the development of anencephaly in the fetus. Conclusions: Based on the conducted studies it is possible to assume the participation of the placenta in the formation of abnormalities of the CNS of fetuses and newborns. Consequently, properly organized antenatal surveillance with mandatory definition of AFP level at 14 weeks of pregnancy will improve the quality of care for women at risk development of CM of the CNS of the fetus, in particular – anencephaly. Keywords: Immunohistochemical markers, diagnostics of anencephaly, expression of Nkx-2.2 in the placenta, degree of apoptosis in the placenta

scholarly journals P53/DRAM/ autophagy - a new target for improving the therapeutic effect of anti-VEGF on intraocular neovascularization

2020 ◽  
Author(s):  
Yi Wang ◽  
Yao Yang ◽  
Rong Li ◽  
Binghui Wu ◽  
Huiqin Lu ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cell Migration ◽  
Therapeutic Effect ◽  
Vascular Endothelial Cells ◽  
Tube Formation ◽  
Control Group ◽  
Vascular Endothelial ◽  
Autophagy Inhibitor ◽  
Anti Vegf ◽  
Autophagy Inhibition

Abstract Backgroud Recurrence of intraocular neovascularization is a major clinical problem. Anti-VEGF drugs are the main treatment for intraocular neovascularization currently. However, anti-VEGF drugs can activate endothelial autophagy and weaken the therapeutic effect. This study aims to elucidate the effect and mechanism of anti-VEGF drugs on autophagy of vascular endothelial cells. Methods RF/6A cells were randomly divided into five groups: The control group, hypoxia group (1% O2、5% CO2、94% N2), anti-VEGF group(group1:Ranibizumab 100ug/ml; group2: Aflibercept, 400ug/ml; group3: Conbercept, 100ug/ml) and autophagy inhibition group(3-MA or CQ) which was corresponding to anti-VEGF group. Autophagy-related proteins were examined by Western blot. RFP-GFP-LC3 was used to detect autophagy and autophagic flow. CCK-8 assay was used to detect cell proliferation. Flow cytometry and Tunel was used to detect cell apoptosis. Cell migration and tube formation were assessed by wound assay and matrix method, respectively. Results Ranibizumab and Conbercept can triger autophagy in hypoxia condition in RF/6A cells, while Aflibercept can inhibit autophagy. Conbercept combined with autophagy inhibitor (3-MA or CQ) could inhibit cell migration and tube formation of RF/6A cells more effectively in hypoxia condition. For mechanism, p53 and DRAM proteins paly an important role in Conbercept induced autophagy. Inhibition of P53 can suppressed the autophagy induced by Conbercept. Conclusion Ranibizumab and Conbercept can triger the autophagy of vascular endothelial cells while Aflibercept can inhibit it. The combination of ranibizumab/ Concept and autophagy inhibitor can significantly inhibit the formation of angiogenesis in vitro. The mechanism of autophagy activation is related to the activation of p53 / DRAM pathway.

scholarly journals Rat epidermal stem cells promote the angiogenesis of full-thickness wound

2020 ◽  
Author(s):  
Shaobin Huang ◽  
Zhicheng Hu ◽  
Peng Wang ◽  
Yi zhang ◽  
Xiaoling Cao ◽  
...  
Keyword(s):  
Stem Cells ◽  
Wound Healing ◽  
Endothelial Cells ◽  
Cell Suspension ◽  
Basal Cell ◽  
Vascular Endothelial Cells ◽  
Control Group ◽  
Vascular Endothelial ◽  
Epidermal Stem Cells ◽  
Full Thickness

Abstract Background: Full-thickness wounds severely affect patients’ life quality and become challenging problems for clinicians. Stem cells have great prospects in the treatment of wounds. Our previous study confirmed that autologous basal cell suspension could promote wound healing, and epidermal stem cells (ESCs) were detected in the basal cell suspension. Herein, this study aimed to explore the effect of ESCs on full-thickness wounds. Methods: Rat ESCs were isolated and expanded, and then were transfected with lentivirus to stably express enhanced green fluorescent protein. The experimental rats were randomly divided into 2 groups: in the ESC group, the rat ESCs were sprayed on the full-thickness wounds of rats; in the control group, phosphate-buffered saline was sprayed the on the wounds. Next, wound healing and neovascularization were evaluated. Colonization, division and differentiation of ESCs on the wound were analyzed by immunofluorescence. Results: The rat ESCs colonized, divided and proliferated in the wound. Additionally, rat ESCs around blood vessels differentiated into vascular endothelial cells and formed a lumen-like structure. Compared with the control group, the ESC group showed enhanced angiogenesis and accelerated wound healing. Conclusions: Our study confirmed that rat ESCs are safe and effective for treating full-thickness wounds . Additionally, under certain conditions, ESCs can differentiate into vascular endothelial cells to promote angiogenesis and wound healing.

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