• Biotechnology and Bioprocess Engineering:BBE
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• 제8권4호
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• pp.246-251
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• 2003

The blood-brain barrier (BBB) is composed of the brain capillaries, which are lined by endothelial cells displaying extremely tight intercellular junctions. Several attempts at creating an in vitro model of the BBB have been met with moderate success as brain capillary endothelial cells lose their barrier properties when isolated in cell culture. This may be due to a lack of recreation of the in vivo endothelial cellular environment in these models, including nearly constant contact with astrocyte foot processes. This work is motivated by the hypothesis that growing endothelial cells on one side of an ultra-thin, highly porous membrane and differentiating astrocyte or astrogliomal cells on the opposite side will lead to a higher degree of interaction between the two cell types and therefore to an improved model. Here we describe our initial efforts towards testing this hypothesis including a procedure for membrane fabrication and methods for culturing endothelial cells on these membranes. We have fabricated a 1 $\mu\textrm{m}$ thick, 2.0 $\mu\textrm{m}$ pore size, and 55% porous membrane with a very narrow pore size distribution from low-stress silicon nitride (SiN) utilizing techniques from the microelectronics industry. We have developed a base, acid, autoclave routine that prepares the membranes for cell culture both by cleaning residual fabrication chemicals from the surface and by increasing the hydrophilicity of the membranes (confirmed by contact angle measurements). Gelatin, fibronectin, and a 50/50 mixture of the two proteins were evaluated as potential basement membrane protein treatments prior to membrane cell seeding. All three treatments support adequate attachment and growth on the membranes compared to the control.

• 대한기계학회:학술대회논문집
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• 대한기계학회 2000년도 춘계학술대회논문집B
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• pp.531-534
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• 2000

The objective of this investigation is to find effects of the pulsatile flow on the morphological changes of the endothelial cell(E.C.) in blood vessel. The shear flow experiment system is used to get the morphological changes of the E.C. The shapes of E.C. are simulated by the cosine curves and computer simulation is used to calculate the pressure and shear stress fields on the E.C. The inlet boundary condition is given from the measured velocity data of femoral artery. The endothelial cells reduce their heights in the flow field so as to reduce the pressure and wall shear stress on the surface. As the exposed time increases, the shear stress and pressure on the E.C. are reduced under the pulsatile flow. The shear stresses on the cell surface show the minimum values during the deceleration phase.

• Reproductive and Developmental Biology
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• 제39권1호
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• pp.1-6
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• 2015

Luteolysis is a cyclical regression of the corpus luteum in many non-primate mammalian species. Prostaglandin $F_2{\alpha}$($PGF_2{\alpha}$) from the uterus and ovary induces functional and structural luteolysis in bovine. The action of $PGF_2{\alpha}$ is mediated by $PGF_2{\alpha}$ receptor located on the luteal steroidogenic and endothelial cell membranes. $PGF_2{\alpha}$ plays an important role in regulating nitric oxide production in endothelial cells of the bovine corpus luteum. Nitric oxide production and nitric oxide synthase activity are stimulated and induced by $PGF_2{\alpha}$ in luteal endothelial cells. Moreover, the reactive oxygen species inhibits progesterone secretion in bovine luteal cells and induces apoptosis. Thus, the interaction between $PGF_2{\alpha}$ and reactive oxygen species provides important aspects in physiology of the corpus luteum forfunctional and structural luteolysis.

• 대한약학회:학술대회논문집
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• 대한약학회 2002년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.2
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• pp.337.2-337.2
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• 2002

Conjugated linoleic acid (CLA) is a potent inhibitor of mammary carcinogenesis. Cancer cells produce various angiogenic factors which stimulate host vascular endothelial cell mitogenesis and chemotaxis for their growth and metastasis. Basic fibroblast growth factor (bFGF) is a potent angiogenic factor that is expressed in many tumors. In this study. we found that CLA decreased bFGF-induced endothelial cell proliferation and DNA synthesis in a dose-dependent manner. However, CLA did not inhibit endothelial cell migration. Furthermore CLA showed a potent inhibitory effect on embryonic vasculogenesis and bF GF-induced angiogenesis in vivo. Collectively. these results suggest that CLA selectively inhibis the active proliferating endothelial edll induced by bFGF. which may explain its anti-carcinogenix properties in vivo.

• Archives of Plastic Surgery
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• 제33권1호
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• pp.5-12
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• 2006

Protein tyrosine kinase(PTK), protein kinase C(PKC), oxidase, as a mediator, take a significant role in signal transduction pathway of angiogenesis. The authors utilized the inhibitors, targeting the formation of three co-enzyme in signal transduction pathway in order to quantify the suppression of abnormal vascular endothelial cell proliferation induced by DMH, to compare the level suppression in each up-regulated growth factors, CTGF, CYR61, $ITG{\beta}1$, FHL2, and to identify the relationship between abnormal cell proliferation and signal transduction pathway. Five groups were established; Control group, Group of DMH, Group of DMH-mixed Herbimycin, inhibitor of protein tyrosine kinase, Group of DMH-mixed Calphostin C, inhibitor of protein kinase C, Group Of Dmh-Mixed 10U Catalase, Inhibitor Of oxidase. The rise of vascular endothelial cell was compared by MTT assay, and four growth factors were analysed with RT-PCR method, at pre-administration, 4, 8, 12, and 24 hours after administration. In comparison of abnormal proliferation of vascular endothelial cell induced by DMH, suppression was noticed in Herbimycin and Calphostin C group, and Calphostin C group revealed higher suppression effect. Nevertheless, Catalase group did not have any suppression. In manifestation of four growth factors, Herbimycin and Calphostin C group presented similar manifestation with control group, except in $ITG{\beta}$. Catalse group had similar manifestation with DMH group in all four growth factors. Abnormal proliferation of vascular endothelial cell induced by DMH have a direct relationship with PTK and PKC, more specifically to PKC. Oxidase was confirmed not to have any relevance.

• Biotechnology and Bioprocess Engineering:BBE
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• 제11권5호
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• pp.402-407
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• 2006

Vascular endothelial cells release proteinases that degrade the extracellular matrix (ECM), thus enabling cell migration during angiogenesis and vasculogenesis. Sildenafil citrate stimulates the nitric oxide-cyclic guanosine monophosphate pathway through inhibition of phosphodiesterase type V (PDE5). In this report, we examined the mechanisms underlying sildenafil citrate-induced cell migration using cultured mouse aortic endothelial cells (MAECs). Sildenafil citrate induced migration and proteinase secretion by murine endothelial cells. Sildenafil citrate induced the secretion of matrix metalloproteinase-2 (MMP-2) and MMP-9, which is inhibited by $NF-{\kappa}B$ inhibitors. Sildenafil citrate also induced the secretion of plasmin, which is inhibited by PI 3'-kinase inhibitors. It is suggested that sildenafil citrate-induced migrating activity in endothelial cells may be accomplished by increased secretion of proteinases.

• Biomolecules & Therapeutics
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• 제12권3호
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• pp.145-150
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• 2004

Inflammation is a frequent radiation-induced reaction following therapeutic irradiation. Treatment of human umbilical endothelial cells (HUVEC) with ${\gamma}$-irradiation (${\gamma}$IR) induces the expression of adhesion proteins such as intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and E-selectin. Since the upregulation of these proteins on endothelial cell Surface has been known to be associated with inflammation, interfering with the expression of adhesion molecules is an important therapeutic target. In the present study, we demonstrate that vitamin C inhibits ${\gamma}$IR induced expression of ICAM-1, VCAM-1, and E-selectin on HUVEC in a dose- and time dependent manner. Vitamin C a1so inhibited the production of Nitric oxide (NO) induced by ${\gamma}$IR. These data suggest that vitamin C has therapeutic potential for the treatment of various inflammatory disorder associated with an increase of endothelial leukocyte adhesion molecules.

• BMB Reports
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• 제52권2호
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• pp.111-112
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• 2019

Although many studies have reported that the breakdown of the blood-brain barrier (BBB) represents one of the major pathological changes in aging, the mechanism underlying this process remains relatively unexplored. In this study, we described that acid sphingomyelinase (ASM) derived from endothelial cells plays a critical role in BBB disruption in aging. ASM levels were elevated in the brain endothelium and plasma of aged humans and mice, resulting in BBB leakage through an increase in caveolae-mediated transcytosis. Moreover, ASM caused damage to the caveolae-cytoskeleton via protein phosphatase 1-mediated ezrin/radixin/moesin dephosphorylation in primary mouse brain endothelial cells. Mice overexpressing brain endothelial cell-specific ASM exhibited acceleration of BBB impairment and neuronal dysfunction. However, genetic inhibition and endothelial specific knock-down of ASM in mice improved BBB disruption and neurocognitive impairment during aging. Results of this study revealed a novel role of ASM in the regulation of BBB integrity and neuronal function in aging, thus highlighting the potential of ASM as a new therapeutic target for anti-aging.

• BMB Reports
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• 제47권1호
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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.

• 대한의용생체공학회:의공학회지
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• 제16권4호
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• pp.463-470
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• 1995

사람의 내피세포는 동물내피세포에 비해 배양증식이 어려운 것으로 알려져 있어 이를 효율적으로 배양증식 시키기 위해서 배양액에 내피세포성장인자를 헤파린과 함께 첨가하는 방법이 많이 사용되어 오고 있다. 한편 최근에는 세포내 cyclic adenosine monophosphate(cAMP)을 증가시키는 물질들인 콜레라독소와 아이소부틸메틸산틴(isobutlmethylxanthine, IBMX)을 세포배양액에 첨가하여 내피세포 증식을 향상시킨 실험결과가 보고된바 있다. 이런 연구결과들을 토대로 할때 내피세포 배양액에 내피세포성장인자 및 헤파린과 함께 cAMP 증가물질을 같이 첨가하여 주면 내피세포의 성장증식을 보다 향상시킬수 있을 것이라는 가설이 가능할 것이다. 본 실험에서는 이와같은 가설을 검증하기 위해 사람의 대망 미세혈관(omental microvessel)으로부터 내피세포를 분리배양한뒤 내피세포성장인자 및 헤파린과 cAMP 증가물질들의 첨가가 내피세포의 증식에 미치는 영향을 분석하고, 궁극적으로는 사람 내피세포의 최적 배양증식 조건을 확립하고자 하였다. 실험 결과 사람의 대망 미세조직에서 내피세포를 분리하여 이를 효과적으로 배양증식하기 위해서는 내피세포성장인자와 헤파린을 첨가한 배지를 사용하거나, 또는 내피세포성장인자를 사용하지 않는 경우 콜레라독소와 IBMX를 병합 첨가하는 것이 좋은 것으로 관찰되었으며, 내피세포성장인자와 콜레라독소 및 IBMX를 동시에 병합 첨가하는 것은 효과가 없는 것으로 밝혀졌다.