• Title/Summary/Keyword: Cell adhesion

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Focus on Anti-Oxidative and Free Radical Scavenging Activity of Ganoderma lucidum

  • Lin, Zhi-Bin
    • Biomolecules & Therapeutics
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    • v.12 no.3
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    • pp.133-137
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    • 2004
  • Present review is built on base of research work on Ganoderma lucidum in our laboratory. A great deal of experimental evidence has suggested that the pharmacological activities of Ganoderma lucidum (Lingzhi) are related to anti-oxidative and free radical scavenging activity. The anti-oxidative and free radical scavenging effects of polysaccharides and triterpenoids isolated from Ganoderma lucidum in different oxidative injury models including tert-butylhydroperoxide (tBOOH)- damaged mice peritoneal macrophages, alloxan-induced diabetes, experimental liver injury models induced by carbon tetrachloride (CCl4), D-galactosamine (DGal) and Bacillus Calmette-Guerin (BCG) plus lipopolysaccharides (LPS) were investigated. It is also demonstrated that Lugu lingzhi, one of Ganoderma product, significantly inhibited LDL oxidation mediated by endothelial cells and decreased monocyte adhesion to endothelial cell (EC) induced by Oxidative low-density lipoprotein (ox-LDL) and advanced glycation endproducts (AGE). Lugulingzhi-treated serum could markedly inhibit the expression of intercellular cell adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-l) induced by ox-LDL and AGE.

Focus on anti-oxidative and free radical scavenging activity of Ganoderma lucidum

  • Lin, Zhi-Bin
    • Proceedings of the Korean Society of Applied Pharmacology
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    • 2004.04a
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    • pp.61-77
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    • 2004
  • Present review is built on base of research work on Ganoderma lucidum in our laboratory. A great deal of experimental evidence has suggested that the pharmacological activities of Ganoderma lucidum(Lingzhi) are related to anti-oxidative and free radical scavenging activity. The anti-oxidative and free radical scavenging effects of polysaccharides and triterpenoids isolated from Ganoderma lucidum in different oxidative injury models including tert-butylhydroperoxide (tBOOH)- damaged mice peritoneal macrophages, alloxan-induced diabetes, experimental liver injury models induced by carbon tetrachloride (CC14), D-galactosamine (DGal) and Bacillus Calmette-Guerin(BCG) plus lipopolysaccharides(LPS) were investigated. It is also demonstrated that Lugu lingzhi, one of Ganoderma product, significantly inhibited LDL oxidation mediated by endothelial cells and decreased monocyte adhesion to endothelial cell (EC) induced by Oxidative low-density lipoprotein (ox-LDL) and advanced glycation endproducts(AGE). Lugulingzhi-treated serum could markedly inhibit the expression of intercellular cell adhesion molecule-l (ICAM-1) and vascular cell adhesion molecule-l (VCAM-1) induced by ox-LDL and AGE.

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Expression profiling identified IL-8 as a regulator of homotypic cell-in-cell formation

  • Ruan, Banzhan;Wang, Chenxi;Chen, Ang;Liang, Jianqing;Niu, Zubiao;Zheng, You;Fan, Jie;Gao, Lihua;Huang, Hongyan;Wang, Xiaoning;Sun, Qiang
    • BMB Reports
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    • v.51 no.8
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    • pp.412-417
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    • 2018
  • Homotypic cell-in-cell (CIC) structures forming between cancer cells were proposed to promote tumor evolution via entosis, a nonapoptotic cell death process. However, the mechanisms underlying their formation remained poorly understood. We performed a microarray analysis to identify genes associated with homotypic CIC formation. Cancer cells differing in their ability to form homotypic CIC structures were selected for the study. Association analysis identified 73 probe sets for 62 candidate genes potentially involved in CIC formation. Among them, twenty-one genes were downregulated while 41 genes were upregulated. Pathway analysis identified a gene interaction network centered on IL-8, which was upregulated in high CIC cells. Remarkably, CIC formation was significantly inhibited by IL-8 knockdown and enhanced upon recombinant IL-8 treatment, which correlated with altered cell-cell adhesion and expression of adhesive molecules such as P-cadherin and ${\gamma}$-catenin. Together, our work identified IL-8 as a positive regulator of homotypic CIC formation via enhancing intercellular adhesion.

Biocompatibility study of lithium disilicate and zirconium oxide ceramics for esthetic dental abutments

  • Brunot-Gohin, Celine;Duval, Jean-Luc;Verbeke, Sandra;Belanger, Kayla;Pezron, Isabelle;Kugel, Gerard;Laurent-Maquin, Dominique;Gangloff, Sophie;Egles, Christophe
    • Journal of Periodontal and Implant Science
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    • v.46 no.6
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    • pp.362-371
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    • 2016
  • Purpose: The increasing demand for esthetically pleasing results has contributed to the use of ceramics for dental implant abutments. The aim of this study was to compare the biological response of epithelial tissue cultivated on lithium disilicate ($LS_2$) and zirconium oxide ($ZrO_2$) ceramics. Understanding the relevant physicochemical and mechanical properties of these ceramics will help identify the optimal material for facilitating gingival wound closure. Methods: Both biomaterials were prepared with 2 different surface treatments: raw and polished. Their physicochemical characteristics were analyzed by contact angle measurements, scanning white-light interferometry, and scanning electron microscopy. An organotypic culture was then performed using a chicken epithelium model to simulate peri-implant soft tissue. We measured the contact angle, hydrophobicity, and roughness of the materials as well as the tissue behavior at their surfaces (cell migration and cell adhesion). Results: The best cell migration was observed on $ZrO_2$ ceramic. Cell adhesion was also drastically lower on the polished $ZrO_2$ ceramic than on both the raw and polished $LS_2$. Evaluating various surface topographies of $LS_2$ showed that increasing surface roughness improved cell adhesion, leading to an increase of up to 13%. Conclusions: Our results demonstrate that a biomaterial, here $LS_2$, can be modified using simple surface changes in order to finely modulate soft tissue adhesion. Strong adhesion at the abutment associated with weak migration assists in gingival wound healing. On the same material, polishing can reduce cell adhesion without drastically modifying cell migration. A comparison of $LS_2$ and $ZrO_2$ ceramic showed that $LS_2$ was more conducive to creating varying tissue reactions. Our results can help dental surgeons to choose, especially for esthetic implant abutments, the most appropriate biomaterial as well as the most appropriate surface treatment to use in accordance with specific clinical dental applications.

Platycodin D Induces Apoptosis, and Inhibits Adhesion, Migration and Invasion in HepG2 Hepatocellular Carcinoma Cells

  • Li, Ting;Xu, Wen-Shan;Wu, Guo-Sheng;Chen, Xiu-Ping;Wang, Yi-Tao;Lu, Jin-Jian
    • Asian Pacific Journal of Cancer Prevention
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    • v.15 no.4
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    • pp.1745-1749
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    • 2014
  • Background: Platycodin D (PD), a triterpenoid saponin isolated from the Chinese medicinal herb Platycodonis radix, possesses anti-cancer effects in several cancer cell lines. The aim of this study was to evaluate its anticancer activities in hepatocellular carcinoma cells. Materials and Methods: MTT and colony formation assays were performed to evaluate cell proliferation, along with flow cytometry and Western blotting for apoptosis. Cell adhesion was tested by observing cellular morphology under a microscope, while the transwell assay was employed to investigate the cell migration and invasion. Results: PD concentration-dependently inhibited cell proliferation in both HepG2 and Hep3B cells, and significantly suppressed colony formation and induced apoptosis in HepG2 cells. The protein levels of cleaved poly ADP-ribose polymerase (PARP) and Bax were up-regulated while that of survivin was down-regulated after treatment with PD. Moreover, PD not only obviously suppressed the adhesion of HepG2 cells to Matrigel, but also remarkably depressed their migration and invasion induced by 12-O-tetradecanoylphorbol 13-acetate (TPA). Conclusions: PD presents anti-cancer potential in hepatocellular carcinoma cells via inducing apoptosis, and inhibiting cell adhesion, migration and invasion, indicating promising features as a lead compound for anti-cancer agent development.

Interaction of Fibroblast Cells onto Chloric Acid-treated Poly($\alpha$-hydroxy acid) Polymer Surfaces (염소산 처리된 Poly($\alpha$-hydroxy acid)계 고분자 표면과 섬유아세포의 상호작용)

  • 이상진;강길선;이진호;이영무;이해방
    • Polymer(Korea)
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    • v.24 no.6
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    • pp.877-885
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    • 2000
  • PLA, PGA and PLGA films were treated with chloric acid mixture solution [70% perchloric acid (HClO$_4$)/potassium chlorate (KClO$_3$) aq. saturated solution, 3 : 2] to increase surface wettability and thus cell compatibility. The surface-treated PLA, PGA, and PLGA films were characterized by the measurement of water contact angle, electron spectroscopy for chemical analysis, and scanning electron microscopy. Surface wettability of chloric acid-treated PLA, PGA, and PLGA film surfaces was gradually increased with increase of treatment time. Unlike EtOH pre-treatment, chloric acid-treated polymer films maintain hydrophilic surface after drying. In cell adhesion test, fibroblasts were cultured on the chloric acid-treated film surfaces for 1 and 2 days. As the surface wettability increased, the cell adhesion on the surface were increased. In conclusion, this study demonstrated that the surface wettability of polymer plays an important role for cell adhesion and proliferation behavior.

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The Binding of Aflatoxin $B_1$ Modulates the Adhesion Properties of Lactobacillus casei KCTC 3260 to a HT29 Colon Cancer Cell Line

  • Hwang, Kwon-Tack;Lee, Won-Jae;Kim, Gye-Yeop;Lee, Shin-Kyung;Lee, Jeong-Min;Jun, Woo-Jin
    • Food Science and Biotechnology
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    • v.14 no.6
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    • pp.866-870
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    • 2005
  • The 14 lactic acid bacteria (LAB) have been evaluated to determine the binding capacity to HT29 cell and Aflatoxin $B_1$ ($AFB_1$). The interaction of LAB to HT29 cells has been further investigated to identify the possibility of competing the binding sites with $AFB_1$. Of 14 LAB strains, Lactobacillus casei KCTC 3260 demonstrated the higher adhesiveness to HT29 and $AFB_1$ with the rate of 19.6% and 46.3%, respectively. In competitive analysis for binding sites, the adhesion of L. casei KCTC 3260 to HT29 cells was reduced with 100 nmol $AFB_1$ by 31.2%. The protoplast of L. casei KCTC 3260 showed no binding capacity to HT29 cells with increment of $AFB_1$ concentration, indicating that cell wall components might serve as a critical factor for the binding. To discriminate the major component influencing on L. casei KCTC 3260 binding to HT29 cells and $AFB_1$, four different pre-treatments (lipase, pronase E, sodium m-periodate, and urea) were employed. Of those, sodium m-periodate treatment caused the lower adhesion of L. casei KCTC 3260 to HT29 cells with the increment of $AFB_1$ concentration. These results indicated that carbohydrate moiety on the cell wall of L. casei KCTC 3260 might be the most critical component in binding to both HT29 cells and $AFB_1$.

L1 Cell Adhesion Molecule Suppresses Macrophage-mediated Inflammatory Responses (L1 Cell Adhesion Molecule에 의한 대식세포 매개 염증반응의 억제 기전 분석)

  • Yi, Young-Su
    • YAKHAK HOEJI
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    • v.60 no.3
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    • pp.128-134
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    • 2016
  • L1 cell adhesion molecule (L1CAM) is a cell surface molecule to initiate a variety of cellular responses through interacting with other cell adhesion molecules in a homophilic or heterophilic manner. Although its expression was found to be upregulated in some tumor cells, including cholangiocarcinomas, and ovarian cancers, and many studies have investigated the role of L1CAM in these cancers, its role in inflammatory responses has been poorly understood. In this study, we explored the role of L1CAM in macrophage-mediated inflammatory responses. L1CAM significantly suppressed the production of nitric oxide (NO), but induced cell proliferation in RAW264.7 cells. L1CAM expression was detectable, but its expression was markedly decreased by lipopolysaccharide (LPS) in RAW264.7 cells. In addition, the expression of pro-inflammatory genes, such as tumor necrosis factor (TNF)-${\alpha}$, cyclooxygenase (COX)-2, and inducible nitric oxide synthase (iNOS) induced by LPS was dramatically suppressed by L1CAM in RAW264.7 cells. L1CAM inhibited the transcriptional activities of NF-${\kappa}B$ and AP-1 while its cytoplasmic domain deletion form, $L1{\Delta}CD$ did not suppressed their activities in RAW264.7 cells. Moreover, L1CAM suppressed nuclear translocation of p65 and p50 as well as c-Jun, c-Fos and p-ATF2 which are transcription factors of NF-${\kappa}B$ and AP-1, respectively. In conclusion, L1CAM suppressed inflammatory responses in macrophages through inhibiting NF-${\kappa}B$ and AP-1 pathways.

Ginsenoside Rg2 Inhibits Lipopolysaccharide-Induced Adhesion Molecule Expression in Human Umbilical Vein Endothelial Cell

  • Cho, Young-Suk;Kim, Chan Hyung;Ha, Tae-Sun;Lee, Sang Jin;Ahn, Hee Yul
    • The Korean Journal of Physiology and Pharmacology
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    • v.17 no.2
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    • pp.133-137
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    • 2013
  • Vascular cell adhesion molecule 1 (VCAM-1), intercellular adhesion molecule 1 (ICAM-1), P- and E-selectin play a pivotal role for initiation of atherosclerosis. Ginsenoside, a class of steroid glycosides, is abundant in Panax ginseng root, which has been used for prevention of illness in Korea. In this study, we investigated the mechanism(s) by which ginsenoside Rg2 may inhibit VCAM-1 and ICAM-1 expressions stimulated with lipopolysaccharide (LPS) in human umbilical vein endothelial cell (HUVEC). LPS increased VCAM-1 and ICAM-1 expression. Ginsenoside Rg2 prevented LPS-mediated increase of VCAM-1 and ICAM-1 expression. On the other hand, JSH, a nuclear factor kappa B (NF-${\kappa}B$) inhibitor, reduced both VCAM-1 and ICAM-1 expression stimulated with LPS. SB202190, inhibitor of p38 mitogen-activated protein kinase (p38 MAPK), and wortmannin, phosphatidylinositol 3-kinase (PI3-kinase) inhibitor, reduced LPS-mediated VCAM-1 but not ICAM-1 expression. PD98059, inhibitor of mitogen-activated protein kinase kinase/extracellular signal-regulated kinase (MEK/ERK) did not affect VCAM-1 and ICAM-1 expression stimulated with LPS. SP600125, inhibitor of c-Jun N-terminal kinase (JNK), reduced LPS-mediated ICAM-1 but not VCAM-1 expression. LPS reduced IkappaB${\alpha}$ ($I{\kappa}B{\alpha}$) expression, in a time-dependent manner within 1 hr. Ginsenoside Rg2 prevented the decrease of $I{\kappa}B{\alpha}$ expression stimulated with LPS. Moreover, ginsenoside Rg2 reduced LPS-mediated THP-1 monocyte adhesion to HUVEC, in a concentration-dependent manner. These data provide a novel mechanism where the ginsenoside Rg2 may provide direct vascular benefits with inhibition of leukocyte adhesion into vascular wall thereby providing protection against vascular inflammatory disease.

MC3T3-E1 osteoblast adhesion to laser induced hydroxyapatite coating on Ti alloy

  • Huang, Lu;Goddard, Samuel C.;Soundarapandian, Santhanakrishnan;Cao, Yu;Dahotre, Narendra B.;He, Wei
    • Biomaterials and Biomechanics in Bioengineering
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    • v.1 no.2
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    • pp.81-93
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    • 2014
  • An in vitro cell study evaluating cell adhesion to hydroxyapatite (HA) coated prosthetic Ti-6Al-4V alloy via laser treatment is presented in comparison with uncoated alloy. Based on our previous in vitro biocompatibility study, which demonstrated higher cell attachment and proliferation with MC3T3-E1 preosteoblast cells, the present investigation aims to reveal the effect of laser coating Ti alloy with HA on the adhesion strength of bone-forming cells against centrifugal forces. Remaining cells on different substrates after centrifugation were visualized using fluorescent staining. Semi-quantifications on the numbers of cells were conducted based on fluorescent images, which demonstrated higher numbers of cells retained on HA laser treated substrates post centrifugation. The results indicate potential increase in the normalized maximum force required to displace cells from HA coated surfaces versus uncoated control surface. The possible mechanisms that govern the enhancing effect were discussed, including surface roughness, chemistry, wettability, and protein adsorption. The improvement in cell adhesion through laser treatment with a biomimetic coating could be useful in reducing tissue damage at the prosthetic to bone junction and minimizing the loosening of prosthetics over time.