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Netrin-1 works with UNC5B to regulate angiogenesis in diabetic kidney disease

Xiaojing Jiao, Dong Zhang, Quan Hong, Lei Yan, Qiuxia Han, Fengmin Shao, Guangyan Cai, Xiangmei Chen, Hanyu Zhu

《医学前沿（英文）》 2020年第14卷第3期页码 293-304 doi: 10.1007/s11684-019-0715-7

摘要： Netrin-1, an axon guidance factor, and its receptor UNC5B play important roles in axonal development and angiogenesis. This study examined netrin-1 and UNC5B expression in kidneys with diabetic kidney disease (DKD) and investigated their roles in angiogenesis. Netrin-1 and UNC5B were upregulated in streptozotocin-induced DKD Wistar rats, and their expression was compared with that in healthy controls. However, exogenous netrin-1 in UNC5B-depleted human renal glomerular endothelial cells (HRGECs) inhibited cell migration and tubulogenesis. This effect was likely associated with SRC pathway deactivation. Netrin-1 treatment also eliminated the pro-angiogenic effects of exogenous VEGF-165 on UNC5B-silenced HRGECs. These results indicate that UNC5B antagonizes netrin-1 and that UNC5B upregulation contributes partly to enhancing angiogenesis in DKD. Therefore, introducing exogenous netrin-1 and depleting endogenous UNC5B are potential strategies for reducing the incidence of early angiogenesis and mitigating kidney injury in DKD.

关键词： netrin-1 VEGF-165 UNC5B angiogenesis diabetic kidney disease

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Lymphatic metastasis is related to the epithelial-mesenchymal transition and expressions of VEGF, MMP

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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on proliferation and apoptosis of U266 cells and its relationship with the expression variation of VEGF

ZHAN Rong, YU Qinghong, HUANG Haobo

《医学前沿（英文）》 2008年第2卷第4期页码 356-360 doi: 10.1007/s11684-008-0068-0

摘要： The aim of this article is to explore the effect of arsenic trioxide (AsO) on the proliferation and apoptosis of myeloma cell line U266 and its relationship with the expression variation of vascular endothelial growth factor (VEGF). The viability and apoptosis of U266 cells were observed by methylthiazolyl- tetrazolium (MTT) assay and terminal-deoxynucleotidyl transferase mediated nick end labeling (TUNEL). The effect of AsO on the VEGF expression of U266 cells were tested by enzyme linked immunosorbent assay (ELISA) and reverse transcription-polymerase chain reaction (RT-PCR) analysis. We found that AsO could significantly inhibit the growth of U266 cells, and the concentration for 50% growth inhibition (IC) was 2 ?mol/L. After treatment with 2, 5, 10 ?mol/L AsO for 36 hours, dose-dependent apoptosis of U266 cells was observed. After treatment with 2, 5, 10 ?mol/L AsO for 72 hours, a dose-dependent reduction of VEGF in the supernatant of U266 cells culture was found. As far as single cells are concerned, nevertheless, the expression of VEGF mRNA did not vary. So we draw the conclusion that AsO could induce the apoptosis of U266 cells and inhibit their proliferation, decrease the tumor load, and lead to the reduction of VEGF in the culture supernatant, but not change the expression of VEGF in single U266 cells.

关键词： VEGF expression expression variation culture supernatant labeling concentration