• Title/Summary/Keyword: endothelial proliferation

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Expression of Vascular Endothelial Growth Factor and Peritumoral Brain Edema in Intracranial Meningiomas (수막종에서 혈관내피성장인자의 발현과 종양주변부 부종)

  • Kim, Tae Young;Park, Jong Tae;Han, Weon Cheol;Moon, Seong Keun
    • Journal of Korean Neurosurgical Society
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    • v.29 no.9
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    • pp.1222-1227
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    • 2000
  • Objective : Vascular endothelial growth factor(VEGF), an endothelial cell specific cytokine, is a potent angiogenic growth factor implicated in the tumor angiogenesis and increases vascular permeability dramatically. Peritumoral brain edema(PTBE) occurs in 40-60% of meningiomas. Many causative factors have been investigated, but the mechanism of PTBE associate with meningioma is unclear. VEGF has been implicated as one of the causative factors of PTBE. This study was designed to determine whether the extent of VEGF expression is correlated with degree of PTBE in meningiomas. Methods : Meningioma tissue samples from 40 patients(7 men and 33 women, mean age $53{\pm}13years$) who underwent surgery were examined retrospectively for the expression of VEGF immunohistochemically. The extent of PTBE was estimated by using preoperative CT or MRI as an edema index(EI). In addition to VEGF, several causative factors including tumor size, location, histologic type, microvasculature(CD31) were compared with EI. Results : Twenty-six meningiomas demonstrated PTBE, and the other 14 did not. Of the 40 patients of meningiomas, 28 were positive(17 were 1+ and 11 were 2+) for VEGF. The EI increased significantly just as VEGF was strongly expressed(p=0.006). Microvascular proliferation was also closely correlated with the extent of peritumoral brain edema(p<0.05). Conclusion : These data suggest that VEGF expression and microvascular proliferation are closely correlated with PTBE in meningioma.

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Gentisyl Alcohol, an Antioxidant from Microbial Metabolite, Induces Angiogenesis In Vitro

  • Kim Hye-Jin;Kim Jin-Hee;Lee Choong-Hwan;Kwon Ho-Jeong
    • Journal of Microbiology and Biotechnology
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    • v.16 no.3
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    • pp.475-479
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    • 2006
  • Gentisyl alcohol isolated from Penicillium sp. has an antioxidative activity, protecting cells from oxidative stresses. From our in vitro angiogenesis assays with bovine aortic endothelial cells (BAECs), gentisyl alcohol was newly identified as a pro-angiogenic small molecule that induces new blood vessel formation of the cells. Gentisyl alcohol stimulated the proliferation of BAECs in a dose-dependent manner. Moreover, it induced in vitro angiogenesis of BAECs such as invasiveness, migration, and tube formation of the endothelial cells. Effects of gentisyl alcohol on invasion and tube formation were also dose-dependent. These results demonstrate that gentisyl alcohol could affect the angiogenic phenotypes of endothelial cells and be developed as a new small molecule with pro-angiogenic activity.

Role of vascular smooth muscle cell in the inflammation of atherosclerosis

  • Lim, Soyeon;Park, Sungha
    • BMB Reports
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    • v.47 no.1
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    • pp.1-7
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    • 2014
  • Atherosclerosis is a pathologic process occurring within the artery, in which many cell types, including T cell, macrophages, endothelial cells, and smooth muscle cells, interact, and cause chronic inflammation, in response to various inner- or outer-cellular stimuli. Atherosclerosis is characterized by a complex interaction of inflammation, lipid deposition, vascular smooth muscle cell proliferation, endothelial dysfunction, and extracellular matrix remodeling, which will result in the formation of an intimal plaque. Although the regulation and function of vascular smooth muscle cells are important in the progression of atherosclerosis, the roles of smooth muscle cells in regulating vascular inflammation are rarely focused upon, compared to those of endothelial cells or inflammatory cells. Therefore, in this review, we will discuss here how smooth muscle cells contribute or regulate the inflammatory reaction in the progression of atherosclerosis, especially in the context of the activation of various membrane receptors, and how they may regulate vascular inflammation.

A Numerical Study of a Hemodynamical Model for Tumor Angiogenesis (종양혈관생성의 혈류역학 모델에 대한 수치해석 연구)

  • Ko H. J.;Shim E. B.;Cho K. H.;Jung G. S.
    • Proceedings of the KSME Conference
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    • 2002.08a
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    • pp.711-712
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    • 2002
  • A numerical study of a hemodynamical model for the tumor angiogenesis is carried out. The tumor angiogenesis process is comprised of a sequence of events; secretion of tumor angiogenesis factor(TAF) from the solid tumor, degradation of the basement membrane of nearby blood vessels, migration and proliferation of the endothelial cells. The model takes into account the effect of TAF concentration and endothelial cell density, and their conservation equations are represented as a set of one-dimensional initial boundary value problems. These equations are discretized by using a finite difference method in which the second order schemes both in time and in space are used. The effects of the parameters contained in the model are Investigated extensively through the numerical simulation of the discretized model. The result for the typical case compares very well with the known result.

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EFFECTS OF UNIFORM SHEAR STRESS ON THE MIGRATION OF VASCULAR ENDOTHELIAL CELL (균일한 전단응력에 의한 혈관내피세포의 운동성 변화)

  • Shin, Jennifer H.;Song, Suk-Hyun
    • Proceedings of the KSME Conference
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    • 2008.11a
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    • pp.1404-1408
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    • 2008
  • The migration and proliferation of vascular endothelial cells (VEC), which play an important role in vascular remodeling, are known to be regulated by hemodynamic forces in the blood vessels. When shear stresses of 2, 6, 15 dynes/$cm^2$ are applied on mouse micro-VEC in vitro, cells surprisingly migrate against the flow direction at all conditions. While higher flow rate imposes more resistance against the cells, reducing their migration speed, the horizontal component of the velocity parallel to the flow increases with the flow rate, indicating the higher alignment of cells in the direction parallel to the flow at a higher shear stress. In addition, cells exhibit substrate stiffness and calcium dependent migration behavior, which can be explained by polarized remodeling in the mechanosensitive pathway under shear stress.

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Effect of Silk in Silk/PLGA Hybrid Films on Attachment and Proliferation of Human Aortic Endothelial Cells (실크/PLGA 하이브리드 필름에서 실크가 인간 대동맥 내피세포의 부착과 증식에 미치는 효과)

  • Lee, Jihye;Lee, Sojin;Kim, Seulji;Kim, Kyounghee;Kim, Younglae;Song, Jeongeun;Lee, Dongwon;Khang, Gilson
    • Polymer(Korea)
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    • v.37 no.2
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    • pp.127-134
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    • 2013
  • The vascular endothelial cells are the inner layers of blood vessels. It regulates the function of blood vessels and proliferation of vascular smooth muscle cells. Poly(lactide-co-glycolic acid) (PLGA) is a biodegradable synthetic polymer with a well-controlled degradation rate and an acceptable mechanical strength. It can be easily fabricated into many shapes. Silk consists of 18 amino acids. It found important for attaching cells cultured in vitro, and maintaining cell functions. In this study, we fabricated silk/PLGA biomaterial hybrid films of 0, 10, 20, 40 and 80 wt% silk. We performed MTT, SEM, ELISA, and immunocytochemistry analyses. We confirmed the adhesion and the proliferation of HAECs on silk/PLGA according to the content of silk, and 40 wt% silk/PLGA hybrid films have superior adhesion and proliferation properties. These results demonstrate that silk/PLGA hybrid films provide suitable surfaces for HAECs, and there is the effect of silk on cell growth and proliferation.

Analysis of Fatty Acid Composition and Effects of Pumpkin Seed Oil on Human Umbilical Vein Endothelial Cells (호박씨유의 지방산 성분 분석 및 Human Umbilical Vein Endothelial Cell에 미치는 영향 연구)

  • Kim, Kyoung Kon;Kang, Yun Hwan;Kim, Dae Jung;Kim, Tae Woo;Lee, Jeong Il;Choe, Myeon
    • Journal of the East Asian Society of Dietary Life
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    • v.24 no.3
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    • pp.351-358
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    • 2014
  • Pumpkin seed oil (PSO) was investigated for its parasite elimination activity and efficacy in treating disorders of the prostate gland and urinary bladder. We confirmed the composition of PSO and identified its ability to improve vessels. Gas chromatography coupled with mass spectrometric (GC-MS) system was used for PSO composition analysis. Cytotoxicity and cell proliferation were confirmed by Cell Counting Kit-8 (CCK-8) assay. Nitric oxide(NO) production was measured with Griess reagent, and intercellular adhesion molecule (ICAM)-1 and vascular cell adhesion molecule (VCAM)-1 mRNA expression levels were measured by reverse transcription polymerase chain reaction (RT-PCR). As a result, PSO revealed the presence of several components such as linoleic acid, oleic acid, palmitic acid and stearic acid. Cytotoxic effects of PSO were not observed, and PSO increased nitric oxide production in human umbilical vein endothelial cells (HUVEC). Additionally, TNF-${\alpha}$-induced cell proliferation and ICAM-1 expression in HUVEC were inhibited by PSO treatment, whereas VCAM-1 expression was not significantly reduced. Taken together, these results show that PSO is worthy of study as a candidate food material for improvement of vascular disease.

MicroRNA let-7c inhibits Bcl-xl expression and regulates ox-LDL-induced endothelial apoptosis

  • Qin, Bing;Xiao, Bo;Liang, Desheng;Li, Ye;Jiang, Ting;Yang, Huan
    • BMB Reports
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    • v.45 no.8
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    • pp.464-469
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    • 2012
  • Endothelial cells (ECs) apoptosis induced by oxidized low-density lipoprotein (ox-LDL) is thought to play a critical role in atherosclerosis. MicroRNAs (miRNAs) are a class of noncoding RNAs that posttranscriptionally regulate the expression of genes involved in diverse cell functions, including differentiation, growth, proliferation, and apoptosis. MiRNA let-7 family is known to be involved in the regulation of cell apoptosis. However, the function of let-7 in ox-LDL induced ECs apoptosis and atherosclerosis is still unknown. Here, we show that let-7c expression was markedly up-regulated in ox-LDL induced apoptotic human umbilical cord vein endothelial cells (HUVECs). Let-7c over-expression enhanced apoptosis in ECs whereas inhibition of let-7c could partly alleviate apoptotic cell death mediated by ox-LDL. Searching for how let-7c affected apoptosis, we discovered that antiapoptotic protein Bcl-xl was a direct target of let-7c in ECs. Our data suggest that let-7c contributes to endothelial apoptosis through suppression of Bcl-xl.

Antiangiogenic Effects of Gold Nanoparticles VEGF-induced Vascular Endothelial Cells (금 나노입자의 VEGF에 의해 유발된 혈관 내피세포의 신생혈관형성 억제 효과)

  • Choi, Seung-Hyun;Ryu, Geun-Chang;Kim, In-Suk;Chae, Soo-Chul
    • Korean Journal of Environmental Biology
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    • v.28 no.1
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    • pp.14-19
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    • 2010
  • Angiogenesis is an important event involved in cell growth and wound healing process. However, the imbalance of growth factors causes diseases, such as ocular, inflammatory diseases. One of treatment of these diseases is to suppress the formation of blood vessels. Function and mechanism of gold nanoparticles (AuNPs) in the formation of blood vessels is not yet proved. Pigment epithelium derived factor (PEDF) is currently being offered anti-angiogenic materials. In this study, we postulated that AuNPs might have the ability to inhibit angiogenesis, the pivotal step in tumor growth, invasion and metastasis. We have demonstrated that AuNPs could inhibit vascular endothelial growth factor (VEGF) induced cell proliferation, angiogenesis in bovine retinal endothelial cells.

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.