• 대한의생명과학회지
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• 제10권3호
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• pp.269-273
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• 2004

This study was designed to investigate the effect of ferulic acid on cell viability and cell adhesion activity in normal human gingival fibroblasts. The cell viability and cell adhesion activity of ferulic acid was measured by MTT assay or XTT assay, respectively, after normal human gingival fibroblasts were treated with or without ferulic acid for 48 hours. The cell viability of ferolic acid on normal human gingival fibroblasts did not show any decreasement by MTT assay and also, cell adhesion activity did not decreased by XTT assay, respectively, compared with control after cells were treated with various concentrations of ferolic acid for 48 hours. MTT/sub 50/ and XTT/sub 50/ were 2,130.0 μM and 1,773.7 μM ferolic acid, respectively. These results suggest that ferolic acid is non-toxic to normal human gingival fibroblasts by showing no significant differences in the cell viability and the adhesion activity compared with control by colorimetric assay.

• Journal of Ginseng Research
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• 제33권4호
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• pp.324-329
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• 2009

G-Rh1에 의한 단핵구 세포주인 U937 세포의 유착조절 능을 조사하여 다음과 같은 결론을 얻었다. 1. G-Rh1은 CD29 항체 (MEM101A) 처리에 의해 유도된 세포-세포간 유착현상을 유의적으로 억제하였다. 2. G-Rh1은 fibronectin처리에 의해 유도된 U937 세포-fibronectin간 유착현상을 유의적으로 억제하였다. 3. G-Rh1은 CD29의 세포표면 발현 수준을 유의적으로 감소시켰다. 최근 활발히 G-Rh1의 약리작용 연구들이 진행되고 있다. 특별히, 본 화합물은 항알러지, 피부염증질환 치료효과, 항암효과 및 여성호르몬 유사기능 등이 있는 것으로 보고된 바있다. CD29-매개성 세포유착과정이 다양한 염증과정, 알러지 반응 및 암세포의 이동 및 전이성과 관련이 있다는 관점에서 볼 때 본 연구결과는 이들 약물이 갖는 치료기전의 하나가 CD29 기능저해에서 비롯될 수 있음을 제시한다고 하겠다. 이후 G-Rh1의 억제 기능에 관한 기전 이해를 위해 세포유착 유도 신호전달 단백질의 활성을 포함한 다양한 분자적 수준에서의 추가적인 실험들을 진행하고 한다.

• BMB Reports
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• 제39권2호
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• pp.132-139
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• 2006

Vascular endothelial cadherin (VE-cadherin), which belongs to the classical cadherin family, is localized at adherens junctions exclusively in vascular endothelial cells. Biochemical and biomechanical cues regulate the VE-cadherin adhesive potential by triggering the intracellular signals. VE-cadherin-mediated cell adhesion is required for cell survival and endothelial cell deadhesion is required for vascular development. It is therefore crucial to understand how VE-cadherin-based cell adhesion is controlled. This review summarizes the inter-endothelial cell adhesions and introduces our recent advance in Rap1-regulated VE-cadherin adhesion. A further analysis of the VE-cadherin recycling system will aid the understanding of cell adhesion/deadhesion mechanisms mediated by VE-cadherin in response to extracellular stimuli during development and angiogenesis.

• 한국생물공학회:학술대회논문집
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• 한국생물공학회 2005년도 생물공학의 동향(XVII)
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• pp.406-411
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• 2005

Fermented materials with enterobacteria isolated from fusiform fish, have strong anti-angiogenesis effect and anti-cell adhesion effect. PLM-f74 got from 74th fraction of size exclusion chromatography from fermented material, showed strong anti-cell adhesion effect between HUVECs and U937 monocytic cell. Adhesion of U937 cell to HUVEC stimulated with IL-1b was clearly inhibited by PLM-f74 in a dose-dependent manner by 12.1, 21.2, 50.9, and 78.2%, when U937 cells treated with each of the PLM-f74 and stimulated with PMA (100 mg/L) was added onto untreated and unstimulated HUVECs, adhesion was observed by 15.8, 31.9, 70.8, and 102%, when both cell types were pretreated with PLM-f74, the adhesion was prominently decreased by 83.7, 99.2, 110, and 120.8%, with 0.74, 3.7, 7.4, and 18.5ug/mL of PLM-f74, respectively. PLM-f74, also, reduced IL-1-stimulated HUVEC expression of adhesion molecules, VCAM-1, ICAM-1, and E-selectin dose-dependently by ELISA method.

• 한국동물학회:학술대회논문집
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• 한국동물학회 2001년도 한국생물과학협회 학술발표대회
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• pp.184.3-185
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• 2001

No Abstract, See Full Text

• BMB Reports
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• 제46권4호
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• pp.230-235
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• 2013

Nephrin, a structural molecule, is also a signaling molecule after phosphorylation. Inhibition of nephrin phosphorylation is correlated with podocyte injury. The PINCH-1-ILK-${\alpha}$-parvin (PIP) complex plays a crucial role in cell adhesion and cytoskeleton formation. We hypothesized that nephrin phosphorylation influenced cytoskeleton and cell adhesion in podocytes by regulating the PIP complex. The nephrin phosphorylation, PIP complex formation, and F-actin in Wistar rats intraperitoneally injected with puromycin aminonucleoside were gradually decreased but increased with time, coinciding with the recovery from glomerular/podocyte injury and proteinuria. In cultured podocytes, PIP complex knockdown resulted in cytoskeleton reorganization and decreased cell adhesion and spreading. Nephrin and its phosphorylation were unaffected after PIP complex knockdown. Furthermore, inhibition of nephrin phosphorylation suppressed PIP complex expression, disorganized podocyte cytoskeleton, and decreased cell adhesion and spreading. These findings indicate that alterations in nephrin phosphorylation disorganize podocyte cytoskeleton and decrease cell adhesion through a PIP complex-dependent mechanism.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• 제33권5호
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• pp.445-454
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• 2007

Background: Phosphatidic acid(PA), an important second messenger, is involved in inflammation. Notably, cell-cell interactions via adhesion molecules playa central role in inflammation. This thesis show that PA induces expression of intercellular adhesion molecule-1(ICAM-1) on macrophages and describe the signaling pathways. Materials and methods: Macrophages were cultured in the presence of 10% FBS and assayed cell to cell adhesion using HUVEC. For the gene and protein analysis, RT-PCR, Western blot and flow cytometry were performed. In addition, overexpressed cell lines for dominant negative PKC-${\delta}$ mutant established and tested their effect on the promoter activity and expression of ICAM-1 protein by PA. Results: PA-activated macrophages significantly increased adhering to human umbilical vein endothelial cell and this adhesion was mediated by ICAM-1. Pretreatment with rottlerin(PKC-${\delta}$ inhibitor) or expression of a dominant negative PKC-${\delta}$ mutant, but not Go6976(classical PKC-${\alpha}$ inhibitor) and myristoylated PKC-${\xi}$ inhibitor, attenuated PA-induced ICAM-1 expression. The p38 mitogen-activated protein kinase(MAPK) inhibitor blocked PA-induced ICAM-1 expression in contrast, ERK upstream inhibitor didn't block ICAM-1. Conclusion: These data suggest that PA-induced ICAM-1 expression and cell-cell adhesion in macrophages requires PKC-${\delta}$ activation and that PKC-${\delta}$ activation is triggers to sequential activation of p38 MAPK.

• The Korean Journal of Physiology and Pharmacology
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• 제20권5호
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• pp.515-523
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• 2016

Adhesion events of monocytes represent an important step in inflammatory responses induced by chemokines. The ${\beta}1$-integrin CD29 is a major adhesion molecule regulating leukocyte migration and extravasation. Although several adhesion molecules have been known as regulators of CD29, the molecular interactions between CD29 and its regulatory adhesion molecules (such as CD98 and CD147) have not been fully elucidated. Therefore, in this study, we examined whether these molecules are functionally, biochemically, and cell-biologically associated using monocytic U937 cells treated with aggregation-stimulating and blocking antibodies, as well as enzyme inhibitors. The surface levels of CD29, CD98, and CD147 (but not CD43, CD44, and CD82) were increased. The activation of CD29, CD98, and CD147 by ligation of them with aggregation-activating antibodies triggered the induction of cell-cell adhesion, and sensitivity to various enzyme inhibitors and aggregation-blocking antibodies was similar for CD29-, CD98-, and CD147-induced U937 cell aggregation. Molecular association between these molecules and the actin cytoskeleton was confirmed by confocal microscopy and immunoprecipitation. These results strongly suggest that CD29 might be modulated by its biochemical and cellular regulators, including CD98 and CD147, via the actin cytoskeleton.

• Journal of Ginseng Research
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• 제33권4호
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• pp.330-336
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• 2009

G-Rb1에 의한 단핵구 세포주인 U937 세포와 대식세포주인 RAW264.7 세포의 유착조절 능, 세포표면 단백질 발현율 및 세포모양 변화능 조절효과를 조사하여 다음과 같은 결론을 얻었다. 1. G-Rb1은 CD29항체 (MEM101A) 및 CD43 항체(161-46) 처리에 의해 유도된 세포-세포간 유착현상을 20%에서 35%까지 유의적으로 상승하였다. 2. G-Rb1은 fibronectin처리에 의해 유도된 U937 세포-fibronectin간 유착현상을 상승시켰다. 3. G-Rb1은 CD29 및 CD43의 세포표면 발현 수준을 유의적으로 증가시켰으나 CD82의 발현은 억제시켰다. 4. G-Rb1은 PMA에 의해 유도된 형태변화는 촉진경향을 반면에 LPS에 의한 변화는 억제경향을 나타내었다. 인삼의 주요사포닌 성분인 G-Rb1의 약리작용이 활발히 연구되고 있다. 특별히, 본 화합물이 갖는 면역증강 및 항암 효능은 인삼이 갖는 이들 효과를 대신하는 것으로 보고 되어져 있다. 그러나, 세포유착과정이 다양한 염증과정, 알러지 반응 및 암세포의 이동과 전이성 등에 관련이 있다는 관점에서 볼 때 본 연구결과는 이들 약물이 갖는 치료기전을 설명하기에는 충분하지 않는 것으로 판단된다. 오히려, 본 결과는 G-Rb1이 특정 농도 ($25-50\;{\mu}M$ 수준)에서 세포의 활성을 촉진할 수 있다는 가능성을 시사한다고 하겠다. 특별히, G-Rb1의 세포유착 촉진 기능에 관한 기전 이해를 위해, 이후, 세포유착 유도 신호전달 단백질의 활성을 포함한 다양한 분자적 수준에서의 추가적인 실험들을 진행하고 한다.

• Journal of Microbiology and Biotechnology
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• 제11권6호
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• pp.922-927
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• 2001

In an effort to regulate the mammalian cell behavior in entrapment with a gel, we have functionalized hydrogels with the putative cell-binding (-Arg-Gly-Asp-)(RGD) domain. An adhesion molecule of Gly-Arg-Gly-Asp-Ser (GRGDS) peptides, a cell recognition ligand, was induced into thermo-reversible hydrogels, composed of N-isopropylacrylamide with small amounts of acrylic acid (typically 2-5 $mol\%$ in feed), as a biomimetic extracellular matrix (ECM). The GRGDS containing a p(NiPAAm-co-AAc) copolymer gel was studied in vitro for its ability to promote the spreading and viability of cells by introducing a GRGDS sequence. Hydrogel with no adhesion molecule was a poor ECM for adhesion, permiting spreading of only $3\%$ of the seeded cells for 36h. By immobilizing the peptide linkage into the hydrogel, the conjugation of RGD promoted $50\%$ of proliferation for 36h. However, the GREDS sequence, nonadhesive peptide linkage, conjugated hydrogel showed only $5\%$ of the seeded cell for the same time period. In addition, with the serum-free medium, only GRGDS peptides conjugated to hydrogel was able to promotecell spreading, while there was no cell proliferation in the hydrogel without GRGDS. Thus, the GRGDS peptide-conjugated thermo-reversible hydrogel specifically mediated the cell spreading. This result suggests that utilization of peptide sequences conjugating with the cell-adhesive motifs can enhance the degree of cell surface interaction and influence the long-term formation of ECM in vitro.