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Mechanism of vascular endothelial growth factor on the prevention of restenosis after angioplasty

Qigong LIU, Honglian ZHOU, Yan ZENG, Shan YE, Jiani LIU, Zaiying LU

《医学前沿（英文）》 2009年 第3卷 第2期   页码 177-180 doi: 10.1007/s11684-009-0021-x

摘要： To evaluate the mechanism of vascular endothelial growth factor (VEGF) on the prevention of restenosis after angioplasty, the recombinant adenovirus vector containing hVEGF cDNA was constructed and transfected into vascular smooth muscle cells (VSMC) . The conditioned medium containing VEGF was collected 72 h after the infection. Then, the VSMC and human umbilical vein endothelial cells (HUVEC) were divided into control group, H O -treated group and H O +VEGF-treated group to observe the proliferation and apoptosis by water soluble tetrazolium (WST-1) method, nick end labeling (TUNEL) and flow cytometry (FCM). Compared with the control and H O +VEGF-treated groups, the absorbance ( ) value of HUVEC was decreased, and apoptosis of HUVEC was significantly increased in H O -treated group. The changes of value and apoptosis of VSMC were contrary to those of HUVEC. H O could stimulate the proliferation of VSMC and induce the apoptosis of HUVEC, inhibit the proliferation of HUVEC and the apoptosis of VSMC and induce restenosis. VEGF could inhibit the effect of H O on HUVEC and VSMC and prevent restenosis. These results offered further theoretical evidence for VEGF on the prevention of restenosis after angioplasty.

关键词： vascular endothelial growth factors     restenosis     reactive oxygen species     endothelial cells     vascular smooth muscle cell    

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Role of nitric oxide in biological effects of vascular endothelial growth factor

Qigong LIU M D , Yan ZENG , Jiani LIU , Shan YE , Yongdong LI , Zaiying LU M D ,

《医学前沿（英文）》 2009年 第3卷 第3期   页码 284-286 doi: 10.1007/s11684-009-0062-1

摘要： To evaluate the role of nitric oxide in the biological effects of vascular endothelial growth factor (VEGF) and the possible mechanism of VEGF, the cultured vascular endothelial cells of rabbit aorta were divided into control group, VEGF-treated group and VEGF+ -nitro-L-arginine methyl ester (L-NAME)-treated group. The absorbance () value of vascular endothelial cells and the levels of prostaglandin (PGI), endothelin-1 (ET-1) and von Willebrand factor (vWF) in the supernatant were observed by water-soluble tetrazolium salt assay, radioimmunoassay and enzyme-linked immunosorbent assay. The values and PGI in VEGF-treated group and VEGF+L-NAME-treated group were higher than those in control group (<0.05 and <0.01). The ET-1 and vWF were significantly decreased in VEGF-treated group and VEGF+L-NAME-treated group compared with the control (<0.05 and <0.01). These results indicate that VEGF could promote the proliferation and secretion of PGI and inhibit the secretion of ET-1 and vWF in vascular endothelial cells and that L-NAME could inhibit the effect of VEGF partially. Nitric oxide is an important mediator in the process of stimulating proliferation and regulating secretion of vascular endothelial cells by VEGF.

关键词： vascular endothelial growth factor     nitric oxide     N-nitro-L-arginine methyl ester     vascular endothelial cells    

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Lymphatic metastasis is related to the epithelial-mesenchymal transition and expressions of VEGF, MMP-9, and COX-2 in breast cancer

Lihui WANG, Lianhong LI, Shen LV, Shujun FAN, Li ZHAN, Bo WANG, Zhong ZHANG

《医学前沿（英文）》 2009年 第3卷 第2期   页码 164-170 doi: 10.1007/s11684-009-0038-1

摘要： The invasion and metastasis of breast cancer are supposed to involve several stages in which epithelial-mesenchymal transition (EMT) is regarded as the mechanistic basis for the behavior of cancer cells. A series of factors related to EMT are apparently involved in such process. The current study aimed to investigate the contributions of EMT and related factors in lymph node metastasis of breast cancer. The expressions of E-cadherin (E-Cad), N-cadherin (N-Cad), vascular endothelial cell growth factor (VEGF), matrix metalloproteinase-9 (MMP-9), cyclooxygenase-2 (COX-2), and CD34 were examined in 74 cases of breast cancer, including 39 cases with lymph node metastasis and 35 cases without lymph node metastasis by immunohistochemistry. Multivariable Cox proportional hazards model was used to analyze the patients’ prognosis. The expressions of N-Cad, VEGF, MMP-9, and COX-2 in cases with lymph node metastasis were significantly higher than those without lymph node metastasis ( <0.05), while the E-Cad level was inversely related to status of lymph node metastasis ( <0.05). The metastasis rate of lymph node in the cases with EMT (lower E-Cad expression and higher N-Cad expression) was 78.3%, while that without EMT (higher E-Cad expression and lower N-Cad expression) was 11.1%. There was a statistical difference in the expression of COX-2 protein between histological grade I and grade II or III, respectively ( <0.05). In the cases with higher grade, the expression of E-Cad was decreased, while that of N-Cad was increased. Higher microvascular density (MVD) was also found to be significantly associated with lymphatic metastasis ( <0.05), and the cases with higher MVD had shorter survival time. This study indicates that EMT and expressions of VEGF, MMP-9 and COX-2, and MVD value are strongly correlated with lymph node metastasis in breast cancer.

关键词： epithelial-mesenchymal transition     vascular endothelial cell growth factor     matrix metalloproteinase-9     cyclooxygenase-2     higher microvascular density     breast cancer    

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糖尿病发作后心脏脂蛋白脂肪酶的变化 Review

Chae Syng Lee, Yajie Zhai, Brian Rodrigues

《工程（英文）》 2023年 第20卷 第1期   页码 19-25 doi: 10.1016/j.eng.2022.06.013

摘要：

由于心脏持续地收缩和舒张，需要大量的能量，其中脂肪酸（FA）是其三磷酸腺苷（ATP）的主要来源。但是，心脏无法制造这种底物，而是从多种来源获得脂肪酸，包括通过脂蛋白脂肪酶（LPL）的作用。脂蛋白脂肪酶在心肌细胞中产生，随后分泌到质膜上的硫酸乙酰肝素蛋白聚糖（HSPG）结合位点。然后为了将脂蛋白脂肪酶转移到内皮细胞管腔，糖基磷脂酰肌醇锚定的高密度脂蛋白结合蛋白1（GPIHBP1）与间质性脂蛋白脂肪酶结合，并将其转移到血管管腔，在那里脂蛋白脂肪酶可将循环中的甘油三酯分解为脂肪酸。内源性-β-葡萄糖醛酸酶乙酰肝素酶（Hpa）的独特之处在于，它是唯一已知的哺乳动物酶，可以裂解硫酸乙酰肝素，从而促进上述脂蛋白脂肪酶从心肌细胞HSPG中释放。在糖尿病中，一直认为心脏产生能量方式的改变是导致糖尿病性心肌病（DCM）的原因。糖尿病发展到中度后，随着葡萄糖利用率的降低，由于Hpa 作用的增强，心脏血管腔内的脂蛋白脂肪酶活性得到增强。虽然这种适应可能有助于补偿心脏对葡萄糖的利用不足，但从长期来看，它是具有毒性的，因为有害的脂质代谢物积聚，以及脂肪酸氧化增强和因此造成的氧化应激，最终导致细胞死亡。这与一种心脏保护生长因子——血管内皮生长因子B（VEGFB）的丧失同时发生。本文探讨了乙酰肝素酶、脂蛋白脂肪酶和血管内皮生长因子B之间的相互联系及其在糖尿病性心肌病中的潜在影响。鉴于缺乏基于机制的DCM治疗，了解这种心肌病的病理，以及脂蛋白脂肪酶的作用，将有助于我们推进其临床治疗。

关键词： 心脏代谢     脂蛋白脂肪酶     乙酰肝素酶     血管内皮生长因子     糖尿病性心肌病    

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Expression of PC-cell-derived growth factor in breast cancer

Haiping SONG MD, Lan SHI MD, Chunping LIU MD, Tao HUANG MD,

《医学前沿（英文）》 2009年 第3卷 第4期   页码 426-430 doi: 10.1007/s11684-009-0085-7

摘要： This study is mainly aimed at evaluating the expression of PC-cell-derived growth factor (PCDGF) in breast cancer and breast adenofibroma, and to compare with other commonly used clinical pathological indices, then to investigate the diagnostic and targeted therapeutic purpose of PCDGF in breast cancer tissue. In this study, we detected the expression of PCDGF, p53 and CerbB-2 in breast cancer tissue and the expression of PCDGF in breast adenofibroma tissue by immunohistochemical method, and analyzed the relationship between them. We found that PCDGF was expressed in most breast cancer tissue, but was not in breast adenofibroma tissue, and the expression of PCDGF was related with the tumor’s pathological category and the expression of estrogen receptor (ER) and progesterone receptor (PR) and p53, but there was no statistical dependability between PCDGF and cerbB-2. From this study, we predict that PCDGF may serve as a marker in the secondary diagnosis of breast cancer, and may participate in the generation and differentiation of breast cancer cells, and become an effective target of therapy for breast cancer.

关键词： PC-cell-derived growth factor     breast neoplasms     clinical markers    

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Involvement of p38 mitogen-activated protein kinase in the regulation of platelet-derived growth factor-induced cell migration

GONG Xiaowei, WEI Jie, LI Yusheng, CHENG Weiwei, DENG Peng, JIANG Yong

《医学前沿（英文）》 2007年 第1卷 第3期   页码 248-252 doi: 10.1007/s11684-007-0047-x

摘要： The aim of this study was to investigate the role of p38 mitogen-activated protein kinase (MAPK) in cell migration induced by platelet-derived growth factor (PDGF). Western blot was performed to detect the phosphorylation of p38 in NIH3T3 cells treated with PDGF. A Transwell cell migration system was used to determine the effects of PDGF treatment on the migration of NIH3T3 cells and the influence of deficiency on this process in a gene knockout (p38) mouse embryonic fibroblast cell line. On the stimulation of PDGF, the migration of NIH3T3 cells was significantly increased (〈0.001) compared to the control and p38 MAP kinase was simultaneously phosphorylated. Furthermore, the PDGF-induced cell migration was significantly blocked in gene knockout (p38) mouse embryonic fibroblasts (MEFs) (〈0.001) as compared with the wild type cells (p38). p38 MAPK plays an important role in the regulation of cell migration induced by PDGF.

关键词： control     stimulation     mitogen-activated     growth factor     process    

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lncR-GAS5 upregulates the splicing factor to impair endothelial autophagy, leading to atherogenesis

《医学前沿（英文）》 2023年 第17卷 第2期   页码 317-329 doi: 10.1007/s11684-022-0931-4

摘要： Long noncoding RNAs (lncRNAs) play a critical role in the regulation of atherosclerosis. Here, we investigated the role of the lncRNA growth arrest-specific 5 (lncR-GAS5) in atherogenesis. We found that the enforced expression of lncR-GAS5 contributed to the development of atherosclerosis, which presented as increased plaque size and reduced collagen content. Moreover, impaired autophagy was observed, as shown by a decreased LC3II/LC3I protein ratio and an elevated P62 level in lncR-GAS5-overexpressing human aortic endothelial cells. By contrast, lncR-GAS5 knockdown promoted autophagy. Moreover, serine/arginine-rich splicing factor 10 (SRSF10) knockdown increased the LC3II/LC3I ratio and decreased the P62 level, thus enhancing the formation of autophagic vacuoles, autolysosomes, and autophagosomes. Mechanistically, lncR-GAS5 regulated the downstream splicing factor SRSF10 to impair autophagy in the endothelium, which was reversed by the knockdown of SRSF10. Further results revealed that overexpression of the lncR-GAS5-targeted gene miR-193-5p promoted autophagy and autophagic vacuole accumulation by repressing its direct target gene, SRSF10. Notably, miR-193-5p overexpression decreased plaque size and increased collagen content. Altogether, these findings demonstrate that lncR-GAS5 partially contributes to atherogenesis and plaque instability by impairing endothelial autophagy. In conclusion, lncR-GAS5 overexpression arrested endothelial autophagy through the miR-193-5p/SRSF10 signaling pathway. Thus, miR-193-5p/SRSF10 may serve as a novel treatment target for atherosclerosis.

关键词： lncR-GAS5     miR-193-5p     splicing factor SRSF10     autophagy     atherogenesis    

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Endogenous tissue factor pathway inhibitor in vascular smooth muscle cells inhibits arterial thrombosis

null

《医学前沿（英文）》 2017年 第11卷 第3期   页码 403-409 doi: 10.1007/s11684-017-0522-y

摘要：

Tissue factor pathway inhibitor (TFPI) is the main inhibitor of tissue factor-mediated coagulation. TFPI is expressed by endothelial and smooth muscle cells in the vasculature. Endothelium-derived TFPI has been reported to play a regulatory role in arterial thrombosis. However, the role of endogenous TFPI in vascular smooth muscle cells (VSMCs) in thrombosis and vascular disease development has yet to be elucidated. In this TFPIFlox mice crossbred with Sma–Cre mice were utilized to establish TFPI conditional knockout mice and to examine the effects of VSMC-directed TFPI deletion on development, hemostasis, and thrombosis. The mice with deleted TFPI in VSMCs (TFPISma) reproduced viable offspring. Plasma TFPI concentration was reduced 7.2% in the TFPISma mice compared with TFPIFlox littermate controls. Plasma TFPI concentration was also detected in the TFPITie2 (mice deleted TFPI in endothelial cells and cells of hematopoietic origin) mice. Plasma TFPI concentration of the TFPITie2 mice was 80.4% lower (P<0.001) than that of the TFPIFlox mice. No difference in hemostatic measures (PT, APTT, and tail bleeding) was observed between TFPISma and TFPIFlox mice. However, TFPISma mice had increased ferric chloride–induced arterial thrombosis compared with TFPIFlox littermate controls. Taken together, these data indicated that endogenous TFPI from VSMCs inhibited ferric chloride–induced arterial thrombosis without causing hemostatic effects.

关键词： arterial thrombosis     conditional knockout mice     tissue factor pathway inhibitor     vascular smooth muscle cells    

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Study on the action of resistin-induced human umbilical vein endothelial cell dysfunction

LI Zhizhen, LI Fangping, YAN Li, LI Feng, LI Yan, CHENG Hua, FU Zuzhi

《医学前沿（英文）》 2007年 第1卷 第2期   页码 196-199 doi: 10.1007/s11684-007-0037-z

摘要： The aim of this paper was to investigate the effects of resistin on human umbilical vein endothelial cells (HUVECs), and to explore its role and mechanism of action in atherosclerosis. HUVECs were incubated with recombinant human resistin (0, 50, 100 ng/mL) for 24 h. ICAM-1, VCAM-1 and reactive oxygen species (ROS) were assayed by flow cytometer. ET-1, eNOS and iNOS mRNA expression were measured by semi-quantitative RT-PCR. Incubation of HUVECs with resistin resulted in an increase in ICAM-1 expression and ET-1 mRNA expression. However, resistin had no effect on VCAM-1 expression and ROS release. eNOS and iNOS mRNA expression were not altered by resistin stimulation. Adipokine resistin exerted a direct effect in promoting HUVEC dysfunction by promoting ICAM-1 and ET-1 expression. These data suggest that adipocyteendothelium cross-talk might play an important role in the pathogenesis of cardiovascular disease in diabetes mellitus.

关键词： endothelial     resistin stimulation     Incubation     pathogenesis     dysfunction    

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Relative expression of PTTG and bFGF in oral squamous cell carcinoma and Tca8113

Yumei DING BM , Lili CHEN MD , Bo CHENG PhD , Handong ZHANG MM ,

《医学前沿（英文）》 2009年 第3卷 第3期   页码 357-362 doi: 10.1007/s11684-009-0046-1

摘要： The purpose of this study was to investigate the expression of pituitary tumor transforming gene (PTTG) and basic fibroblast growth factor (bFGF) in oral squamous cell carcinoma (OSCC) and tongue cancer cell line Tca8113, as well as their effects on each other. We detected PTTG protein and bFGF in OSCC tissues from 56 cases using the streptavidin-biotin peroxidase (S-P) method; additionally, after being treated with different concentrations of anti bFGF or PTTG antibody, PTTG or bFGF expression in Tca8113 was examined by immunocytochemistry. The results were as follows: (1) Positive rates of PTTG protein and bFGF were 78.2% and 67.3% in OSCC, respectively, which were significantly higher than those in normal mucosal tissues (<0.05). PTTG protein was significantly up-regulated in poorly and moderately differentiated tumors compared to well differentiated tumors (<0.05), and there was also a significant difference between tumors with lymph node metastasis and tumors without lymph node metastasis (<0.05). PTTG protein expression was positively correlated with bFGF ( = 0.382, <0.05); (2) PTTG protein emitted strong fluorescence in Tca8113, and it decreased after being treated with anti-bFGF antibody. Anti-PTTG antibody also had an inhibitive effect on bFGF expression. In summary, the overexpression of PTTG protein is closely related with OSCC differentiation and lymph node metastasis. PTTG protein expression conforms to bFGF in OSCC tissues and Tca8113 cells. Detection of both PTTG and bFGF may help to judge the degree of malignancy and prognosis of patients with OSCC.

关键词： carcinoma     squamous cell     pituitary tumor transforming gene (PTTG) protein     basic fibroblast growth factor    

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The relationship between platelet-derived growth factor expression and angiogenesis/lymphangiogenesis

Guocheng LIU MD, Shouhua YANG MD, Zehua WANG MD,

《医学前沿（英文）》 2009年 第3卷 第4期   页码 447-451 doi: 10.1007/s11684-009-0082-x

摘要： This paper is aimed to examine if changes in platelet-derived growth factor (PDGF) expression at different stages of cervical cancer are related to the variation in blood vessel density (BVD) and lymphatic vessel density (LVD) to evaluate the relationship between PDGF expression and stages and metastasis of cervical cancer. Polymerase chain reaction (PCR) and RT-PCR were used to detect the expression levels of PDGF in 45 cervical cancer tissue samples (the experimental group). The samples were immunohistochemically stained with monoclonal antibodies D2-40 and CD34, and BVD and LVD were measured. The expressions of PDGF-A, -B, and- D were all higher in the experimental group than in the control group (<0.05); no significant difference was found in the expression of PDGF-C between the experimental group and the control group (>0.05). PDGF-A and -B expression was positively related with BVD and LVD (<0.01, R= 0.49, 0.527, 0.327, 0.68). The expression levels of PDGF-C and -D were not significantly related with BVD and LVD. At the early stage of cervical cancer, BVD and LVD were significantly higher than in the controls (<0.01). The BVD and LVD in tissues in the surrounding areas of cervical cancer were significantly higher than in tissues at cancer center, and LVD was related to lymph node metastasis (<0.001). BVD and LVD were not associated with the differentiation and pathological stages of cervical cancer. The expressions of PDGF-A, -B, and -D in cervical cancer were closely related with the clinical stages of cervical cancer. PDGF-A and -B were intimately associated with the lymph node metastasis and prognosis of cervical cancer.

关键词： cervical cancer     lymphatic vessel density     blood vessel density     platelet-derived growth factor    

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Fibroblast growth factor 21: a novel metabolic regulator from pharmacology to physiology

null

《医学前沿（英文）》 2013年 第7卷 第1期   页码 25-30 doi: 10.1007/s11684-013-0244-8

摘要：

Fibroblast growth factor 21 (FGF21) is a member of the fibroblast growth factor family. It actually functions as endocrine hormones but does not regulate cell growth and differentiation. It is demonstrated that FGF21 acts on multiple tissue to coordinate carbohydrate and lipid metabolism, including enhancing insulin sensitivity, decreasing triglyceride concentrations, causing weight loss, ameliorating obesity-associated hyperglycemia and hyperlipidemia. Moreover, FGF21 also plays important roles in some physiological processes, such as fasting and feeding, growth hormone axis and thermogenic function of brown adipose tissue. Clinical relevance of FGF21 in humans is still unclear, and the basis and consequences of increased FGF21 in metabolic disease remain to be determined. Both the pharmacological actions and physiological roles make FGF21 attractive drug candidates for treating metabolic disease, but some questions remain to be answered. This article concentrates on recent advances in our understanding of FGF21.

关键词： FGF21     metabolism     pharmacology     physiology     clinical relevance    

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Current advances for bone regeneration based on tissue engineering strategies

Rui Shi, Yuelong Huang, Chi Ma, Chengai Wu, Wei Tian

《医学前沿（英文）》 2019年 第13卷 第2期   页码 160-188 doi: 10.1007/s11684-018-0629-9

摘要： Bone tissue engineering (BTE) is a rapidly developing strategy for repairing critical-sized bone defects to address the unmet need for bone augmentation and skeletal repair. Effective therapies for bone regeneration primarily require the coordinated combination of innovative scaffolds, seed cells, and biological factors. However, current techniques in bone tissue engineering have not yet reached valid translation into clinical applications because of several limitations, such as weaker osteogenic differentiation, inadequate vascularization of scaffolds, and inefficient growth factor delivery. Therefore, further standardized protocols and innovative measures are required to overcome these shortcomings and facilitate the clinical application of these techniques to enhance bone regeneration. Given the deficiency of comprehensive studies in the development in BTE, our review systematically introduces the new types of biomimetic and bifunctional scaffolds. We describe the cell sources, biology of seed cells, growth factors, vascular development, and the interactions of relevant molecules. Furthermore, we discuss the challenges and perspectives that may propel the direction of future clinical delivery in bone regeneration.

关键词： bone tissue engineering     stem cell     bone scaffold     growth factor     bone regeneration    

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sulfate promotes the formation of atherosclerotic lesions and induces plaque instability by targeting vascular

null

《医学前沿（英文）》 2016年 第10卷 第3期   页码 320-329 doi: 10.1007/s11684-016-0463-x

摘要：

Coronary atherosclerosis is a major complication of chronic kidney disease. This condition contributes to the increased mortality in dialysis patients. p-Cresyl sulfate (PCS) is a prototype of protein-bound uremic toxins that cannot be efficiently removed through routine dialysis procedures. In the present study, ApoE−/− mice that underwent 5/6 nephrectomy were randomly divided into two groups, namely, vehicle-treated group (n = 20) and PCS-treated group (n = 20). Mice were sacrificed for en face and immunohistological analyses after 8 or 24 weeks of high-fat diet. Rat aortic vascular smooth muscle cells (VSMCs) were treated with phosphate buffer solution or 500 µmol/L PCS for in vitro evaluation. PCS-treated mice were observed to suffer increased atherosclerotic lesions after eight weeks of PCS administration. Moreover, 24 weeks of PCS administration also markedly increased the vulnerability index of aortic plaques. PCS was also observed to facilitate the migration and proliferation of VSMCs during the progression of the disease. Moreover, PCS disturbed the balance between matrix metalloproteinases and tissue inhibitor of metalloproteinases within the plaques. Thus, PCS played a vital role in promoting atherogenesis and disturbing the stability of formed plaques probably by targeting VSMCs.

关键词： p-cresyl sulfate     atherosclerosis     plaque stability     vascular smooth muscle cell    

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An investigation on prevalent strategies for XFEM-based numerical modeling of crack growth in porous

《结构与土木工程前沿（英文）》 2021年 第15卷 第4期   页码 914-936 doi: 10.1007/s11709-021-0750-8

摘要： Crack growth modeling has always been one of the major challenges in fracture mechanics. Among all numerical methods, the extended finite element method (XFEM) has recently attracted much attention due to its ability to estimate the discontinuous deformation field. However, XFEM modeling does not directly lead to reliable results, and choosing a strategy of implementation is inevitable, especially in porous media. In this study, two prevalent XFEM strategies are evaluated: a) applying reduced Young’s modulus to pores and b) using different partitions to the model and enriching each part individually. We mention the advantages and limitations of each strategy via both analytical and experimental validations. Finally, the crack growth is modeled in a natural porous media (Fontainebleau sandstone). Our investigations proved that although both strategies can identically predict the stress distribution in the sample, the first strategy simulates only the initial crack propagation, while the second strategy could model multiple cracks growths. Both strategies are reliable and highly accurate in calculating the stress intensity factor, but the second strategy can compute a more reliable reaction force. Experimental tests showed that the second strategy is a more accurate strategy in predicting the preferred crack growth path and determining the maximum strength of the sample.

关键词： numerical modeling     extended finite element method     porous media     crack growth     stress intensity factor    

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标题 作者 时间 类型 操作

Mechanism of vascular endothelial growth factor on the prevention of restenosis after angioplasty

Qigong LIU, Honglian ZHOU, Yan ZENG, Shan YE, Jiani LIU, Zaiying LU

期刊论文

Role of nitric oxide in biological effects of vascular endothelial growth factor

Qigong LIU M D , Yan ZENG , Jiani LIU , Shan YE , Yongdong LI , Zaiying LU M D ,

期刊论文

Lymphatic metastasis is related to the epithelial-mesenchymal transition and expressions of VEGF, MMP-9, and COX-2 in breast cancer

Lihui WANG, Lianhong LI, Shen LV, Shujun FAN, Li ZHAN, Bo WANG, Zhong ZHANG

期刊论文

糖尿病发作后心脏脂蛋白脂肪酶的变化

Chae Syng Lee, Yajie Zhai, Brian Rodrigues

期刊论文

Expression of PC-cell-derived growth factor in breast cancer

Haiping SONG MD, Lan SHI MD, Chunping LIU MD, Tao HUANG MD,

期刊论文

Involvement of p38 mitogen-activated protein kinase in the regulation of platelet-derived growth factor-induced cell migration

GONG Xiaowei, WEI Jie, LI Yusheng, CHENG Weiwei, DENG Peng, JIANG Yong

期刊论文

lncR-GAS5 upregulates the splicing factor to impair endothelial autophagy, leading to atherogenesis

期刊论文

Endogenous tissue factor pathway inhibitor in vascular smooth muscle cells inhibits arterial thrombosis

null

期刊论文

Study on the action of resistin-induced human umbilical vein endothelial cell dysfunction

LI Zhizhen, LI Fangping, YAN Li, LI Feng, LI Yan, CHENG Hua, FU Zuzhi

期刊论文

Relative expression of PTTG and bFGF in oral squamous cell carcinoma and Tca8113

Yumei DING BM , Lili CHEN MD , Bo CHENG PhD , Handong ZHANG MM ,

期刊论文

The relationship between platelet-derived growth factor expression and angiogenesis/lymphangiogenesis

Guocheng LIU MD, Shouhua YANG MD, Zehua WANG MD,

期刊论文

Fibroblast growth factor 21: a novel metabolic regulator from pharmacology to physiology

null

期刊论文

Current advances for bone regeneration based on tissue engineering strategies

Rui Shi, Yuelong Huang, Chi Ma, Chengai Wu, Wei Tian

期刊论文

sulfate promotes the formation of atherosclerotic lesions and induces plaque instability by targeting vascular

null

期刊论文

An investigation on prevalent strategies for XFEM-based numerical modeling of crack growth in porous

期刊论文