• Title, Summary, Keyword: human umbilical vein endothelial cells (HUVECs)

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Inhibitory Activity of Edible Plant Extracts on Proliferation of Human Umbilical Vein Endothelial Cells (HUVECs)

  • Song, Myoung-Chong;Kim, Sung-Hoon;Kwak, Ho-Young;Yang, Hye-Joung;Bang, Myun-Ho;Chung, In-Sik;Lee, Youn-Hyung;Baek, Nam-In
    • Journal of Applied Biological Chemistry
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    • v.50 no.4
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    • pp.249-253
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    • 2007
  • Thirteen edible plants previously reported to show inhibitory activities on farnesyl protein transferase (FPTase) and phosphatase of the regenerating liver-3 (PRL-3) were evaluated for inhibitory activity on the proliferation of human umbilical vein endothelial cells (HUVECs). Four plant extracts, Oenothera erythrosepala, Perilla frutescens, Panicum miliaceum, and Quercus acutissima, significantly inhibited the proliferation of HUVECs induced by the basic fibroblast growth factor (bFGF) without cytotoxicity at 100 ${\mu}g/mL$. Myristica fragrans, Rosmarinus officinalis, and Syringa patula also showed inhibitory activity on the proliferation with only mild cytotoxicity.

Effect of Baechu Kimchi Added Ecklonia cava Extracts on High Glucose-induced Oxidative Stress in Human Umbilical Vein Endothelial Cells

  • Lee, Hyun-Ah;Song, Yeong-Ok;Jang, Mi-Soon;Han, Ji-Sook
    • Preventive Nutrition and Food Science
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    • v.19 no.3
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    • pp.170-177
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    • 2014
  • Endothelial cell dysfunction is considered to be a major cause of vascular complications in diabetes. In the present study, we investigated the protective effect of a baechu kimchi added Ecklonia cava extract (BKE) against high glucose induced oxidative damage in human umbilical vein endothelial cells (HUVECs). Treatment with a high concentration of glucose (30 mM) induced cytotoxicity, whereas treatment with BKE protected HUVECs from high glucose induced damage; by restoring cell viability. In addition, BKE reduced lipid peroxidation, intracellular reactive oxygen species and nitric oxide levels in a dose dependent manner. Treatment with high glucose concentrations also induced the overexpression of inducible nitric oxide synthase, cyclooxygenase-2 and NF-${\kappa}B$ proteins in HUVECs, but BKE treatment significantly reduced the overexpression of these proteins. These findings indicate that BKE may be a valuable treatment against high glucose-induced oxidative stress HUVECs.

Vascular Endothelial Growth Factor Upregulates Follistatin in Human Umbilical Vein Endothelial Cells

  • Oh, In-Suk;Kim, Hwan-Gyu
    • Biotechnology and Bioprocess Engineering:BBE
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    • v.9 no.3
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    • pp.201-206
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    • 2004
  • Vascular endothelial growth factor (VEGF), plays a key role in angiogenesis. Many endogenous factors can affect angiogenesis in endothelial cells. VEGF is known to be a strong migration, sprouting, survival, and proliferation factor for endothelial cells during angiogenesis in endothelial cells. Searching for novel genes involved in VEGF signaling during angiogenesis, we carried out differential display polymerase chain reaction on RNA from VEGF-stimulated human umbilical vein endothelial cells (HUVECs). In this study, follistatin (FS) differentially expressed in VEGF-treated HUVECs, compared with controls. Addition of VEGF (10ng/L) produced an approximately 11.8-fold increase of FS mRNA. F5 or VEGF produced approximately 1.8- or 2.9-fold increases, respectively, in matrix metalloproteinase-2 (MMP-2) secretion for 12h, compared to the addition of a control buffer. We suggest that VEGF may affect the angiogenic effect of HUVECs, through a combination of the direct effects of VEGF itself, and the indirect effects mediated via induction of FS in vitro.

Angiopoietin-1 Is An Radiation-induced Apoptosis Survival Factor for Human Umbilical Vein Endothelial Cells (방사선을 조사한 혈관내피세포에 대한 Angiopoietin-1의 방사선 방어 기작)

  • Lee, Song-Jae;Chang, Chae-Chul
    • The Journal of Korean Society for Radiation Therapy
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    • v.12 no.1
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    • pp.166-173
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    • 2000
  • Angiopoietin-1(Ang-1) is a vasculogenic factor that signals through the endothelial cell-specific Tie2 receptor tyrosine kinase. We examined the effect of angiopoietin-1(Ang-1) on radiation-induced apoptosis in human umbilical vein endothelial cells(HUVECS) and receptor/second messenger signal transduction pathway for Ang-1's effect on HUVECs. The percent of apoptotic cells under control condition(0Gy) was $8.2\%$. Irradiation induced apoptosis was increased in a dose(1, 5, 10, and 15Gy)- and time 12, 24, 48 and 72hr)-dependent manner. The percent of apoptotic cells was approximately $34.9\%$ after 15 Gy of irradiation. Under these conditions, pretreatment with Ang-1's (50, 100, 200, and 400 ng/ml) inhibited irradiation-induced apoptosis in human umbilical vein endothelial cells in a dose-dependent manner. Two hundred ng/ml of Ang-1 inhibited approximately $55-60\%$ of the apoptotic events that occurred in the 10 Gy-irradiated cells. Pre-treatment with soluble Tie2 receptor, but not Tie1 receptor, blocked the Ang-1's antiapoptotic effects. Phosphatidylinositol 3'-kinase (P13-kinase) specific inhibitor, wortmanin and LY294002, blocked the Ang-1-induced antiapoptotic effect. Ang-1 promotes the survival of endothelial cells in irradiation-induced apoptosis through Tie2 receptor binding and P13-kinase activation. Pretreatment of Ang-1 could be beneficial in maintaining normal endothelial cell integrity during irradiation therapy.

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Effects of gintonin on the proliferation, migration, and tube formation of human umbilical-vein endothelial cells: involvement of lysophosphatidic-acid receptors and vascular-endothelial-growth-factor signaling

  • Hwang, Sung-Hee;Lee, Byung-Hwan;Choi, Sun-Hye;Kim, Hyeon-Joong;Won, Kyung Jong;Lee, Hwan Myung;Rhim, Hyewon;Kim, Hyoung-Chun;Nah, Seung-Yeol
    • Journal of Ginseng Research
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    • v.40 no.4
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    • pp.325-333
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    • 2016
  • Background: Ginseng extracts are known to have angiogenic effects. However, to date, only limited information is available on the molecular mechanism underlying the angiogenic effects and the main components of ginseng that exert these effects. Human umbilical-vein endothelial cells (HUVECs) are used as an in vitro model for screening therapeutic agents that promote angiogenesis and wound healing. We recently isolated gintonin, a novel ginseng-derived lysophosphatidic acid (LPA) receptor ligand, from ginseng. LPA plays a key role in angiogenesis and wound healing. Methods: In the present study, we investigated the in vitro effects of gintonin on proliferation, migration, and tube formation of HUVECs, which express endogenous LPA1/3 receptors. Results: Gintonin stimulated proliferation and migration of HUVECs. The LPA1/3 receptor antagonist, Ki16425, short interfering RNA against LPA1 or LPA3 receptor, and the Rho kinase inhibitor, Y-27632, significantly decreased the gintonin-induced proliferation, migration, and tube formation of HUVECs, which indicates the involvement of LPA receptors and Rho kinase activation. Further, gintonin increased the release of vascular endothelial growth factors from HUVECs. The cyclooxygenase-2 inhibitor NS-398, nuclear factor kappa B inhibitor BAY11-7085, and c-Jun N-terminal kinase inhibitor SP600125 blocked the gintonin-induced migration, which shows the involvement of cyclooxygenase-2, nuclear factor kappa B, and c-Jun N-terminal kinase signaling. Conclusion: The gintonin-mediated proliferation, migration, and vascular-endothelial-growth-factor release in HUVECs via LPA-receptor activation may be one of in vitro mechanisms underlying ginsenginduced angiogenic and wound-healing effects.

Protective Effect of Padina arborescens Extract against High Glucose-induced Oxidative Damage in Human Umbilical Vein Endothelial Cells

  • Park, Mi Hwa;Han, Ji Sook
    • Preventive Nutrition and Food Science
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    • v.18 no.1
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    • pp.11-17
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    • 2013
  • Dysfunction of endothelial cells is considered a major cause of vascular complications in diabetes. In the present study, we investigated the protective effect of Padina arborescens extract against high glucose-induced oxidative damage in human umbilical vein endothelial cells (HUVECs). High-concentration of glucose (30 mM) treatment induced cytotoxicity whereas Padina arborescens extract protected the cells from high glucose-induced damage and significantly restored cell viability. In addition, lipid peroxidation, intracellular reactive oxygen species (ROS), and nitric oxide (NO) levels induced by high glucose treatment were effectively inhibited by treatment of Padina arborescens extract in a dose-dependent manner. High glucose treatment also induced the overexpressions of inducible nitric oxide synthase (iNOS), cyclooxygenase- 2 (COX-2) and NF-${\kappa}B$ proteins in HUVECs, but Padina arborescens extract treatment reduced the over-expressions of these proteins. These findings indicate the potential benefits of Padina arborescens extract as a valuable source in reducing the oxidative damage induced by high glucose.

Effect of Polyopes lancifolia Extract on Oxidative Stress in Human Umbilical Vein Endothelial Cells Induced by High Glucose

  • Min, Seong Won;Han, Ji Sook
    • Preventive Nutrition and Food Science
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    • v.18 no.1
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    • pp.38-44
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    • 2013
  • The protective effect of Polyopes lancifolia extract on high glucose-induced oxidative stress was investigated using human umbilical vein endothelial cells (HUVECs). High concentration of glucose (30 mM) treatment induced HUVECs cell death, but Polyopes lancifolia extract, at concentrations of 25, 50, and $100{\mu}g/mL$, protected cells from high glucose-induced damage. Furthermore, thiobarbituric acid reactive substances, intracellular reactive oxygen species, and nitric oxide levels increased by high glucose treatment were effectively decreased by treatment with Polyopes lancifolia extract in a dose-dependent manner. Also, Polyopes lancifolia extract treatment reduced the overexpressions of inducible nitric oxide synthase, cyclooxygenase-2, and nuclear factor-kappa B proteins activation that was induced by high glucose in HUVECs. These results indicate that Polyopes lancifolia extract is a potential therapeutic material that will reduce the damage caused by high glucose-induced-oxidative stress associated with diabetes.

Effect of Fibroblast Growth Factor-2 on Migration and Proteinases Secretion of Human Umbilical Vein Endothelial Cells

  • Oh, In-Suk;Kim, Hwan-Gyu
    • Journal of Microbiology and Biotechnology
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    • v.14 no.2
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    • pp.379-384
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    • 2004
  • Fibroblast growth factor-2 (FGF-2) is known to modulate numerous cellular functions in various cell types, including cell proliferation, differentiation, survival, adhesion, migration, and motility, and also in processes such as wound healing, angiogenesis, and vasculogenesis. FGF-2 regulates the expression of several molecules thought to mediate critical steps during angiogenesis. This study examines the mechanisms underlying FGF-2-induced cell migration, using human umbilical vein endothelial cells (HUVECs). FGF-2 induced the nondirectional and directional migration of endothelial cells, which are inhibited by MMPs and plasmin inhibitors, and induced the secretion of matrix metalloproteinase-3 (MMP3) and MMP-9, but not MMP-l and MMP-2. FGF-2 also induced the secretion of the tissue inhibitor of metalloproteinase-l (TIMP-I), but not of TIMP- 2. Also, the pan-PKC inhibitor inhibited FGF-2-induced MMP-9 secretion. It is, therefore, suggested that FGF-2 induces the migration of cultured endothelial cells by means of increased MMPs and plasmin secretion. Furthermore, FGF-2 may increase MMP-9 secretion by activating the PKC pathway.

Zerumbone, Sesquiterpene Photochemical from Ginger, Inhibits Angiogenesis

  • Park, Ju-Hyung;Park, Geun Mook;Kim, Jin-Kyung
    • The Korean Journal of Physiology and Pharmacology
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    • v.19 no.4
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    • pp.335-340
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    • 2015
  • Here, we investigated the role of zerumbone, a natural cyclic sesquiterpene of Zingiber zerumbet Smith, on angiogenesis using human umbilical vein endothelial cells (HUVECs). Zerumbone inhibited HUVECs proliferation, migration and tubule formation, as well as angiogenic activity by rat aorta explants. In particular, zerumbone inhibited phosphorylation of vascular endothelial growth factor receptor-2 and fibroblast growth factor receptor-1, which are key regulators of endothelial cell function and angiogenesis. In vivo matrigel plug assay in mice demonstrated significant decrease in vascularization and hemoglobin content in the plugs from zerumbone-treated mice, compared with control mice. Overall, these results suggest that zerumbone inhibits various attributes of angiogenesis, which might contribute to its reported antitumor effects.

Growth Inhibition and Apoptosis Induction of Human Umbilical Vein Endothelial Cells by Apogossypolone

  • Zhan, Yong-Hua;Huang, Xiao-Feng;Hu, Xing-Bin;An, Qun-Xing;Liu, Zhi-Xin;Zhang, Xian-Qing
    • Asian Pacific Journal of Cancer Prevention
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    • v.14 no.3
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    • pp.1791-1795
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    • 2013
  • Aims and Background: Prostate cancer is one of the most common malignant tumors in the male reproductive system, which causes the second most cancer deaths of males, and control of angiogenesis in prostate lesions is of obvious importance. This study assessed the effect of apogossypolone (ApoG2) on proliferation and apoptosis of human umbilical vein endothelial cells (HUVECs). Subjects and Methods: HUVECs were treated with different concentrations of ApoG2. The survival rate of HUVECs were determined by MTT assay. Utrastructural changes of HUVECs were assessed with transmission electron microscopy. Apoptosis in HUVECs was analyzed by flow cytometry and cell migration by Boyden chamber assay. Matrigel assays were used to quantify the development of tube-like networks. Results: ApoG2 significantly inhibited HUVEC growth even at 24 h (P<0.05). The inhibitory effect of ApoG2 is more obvious as the concentration and the culture time increased (P<0.05). These results indicate that ApoG2 inhibits the proliferation of HUVECs in a time- and concentration-dependent manner with increase of the apoptosis rate. Besides, ApoG2 reduced the formation of total pseudotubule length and network branches of HUVECs. Conclusions: The results suggest that ApoG2 inhibits angiogenesis of HUVECs by growth inhibition and apoptosis induction.