• Title/Summary/Keyword: adhesion mechanism

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Analysis of common and characteristic actions of Panax ginseng and Panax notoginseng in wound healing based on network pharmacology and meta-analysis

  • Zhen Wang ;Xueheng Xie ;Mengchen Wang ;Meng Ding ;Shengliang Gu ;Xiaoyan Xing;Xiaobo Sun
    • Journal of Ginseng Research
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    • v.47 no.4
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    • pp.493-505
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    • 2023
  • In recent years, an increasing number of reports have explored the wound healing mechanism of these two traditional Chinese herbal medicines- Panax ginseng and Panax notoginseng, but there is no systematic research on the related core functions and different mechanisms in the treatment of wound healing up to now. Based on network pharmacology and meta-analysis, the present work aimed to comprehensively review the commonality and diversity of P. ginseng and P. notoginseng in wound healing. In this study, a wound healing-related "ingredients-targets" network of two herbs was constructed. Thereafter, meta-analysis of the multiple target lists by Metascape showed that these two medicines significantly regulated blood vessel development, responses to cytokines and growth factors and oxygen levels, cell death, cell proliferation and differentiation, and cell adhesion. To better understand the discrepancy between these two herbs, it was found that common signaling pathways including Rap1, PI3K/AKT, MAPK, HIF-1 and Focal adhesion regulated the functions listed above. In parallel, the different pathways including renin-angiotensin system, RNA transport and circadian rhythm, autophagy, and the different metabolic pathways may also explained the discrepancies in the regulation of the above-mentioned functions, consistent with the Traditional Chinese Medicine theory about the effects of P. ginseng and P. notoginseng.

Effect of Prostaglandin F2 Alpha on E-cadherin, N-cadherin and Cell Adhesion in Ovarian Luteal Theca Cells (난소의 황체협막세포에서 E-cadherin, N-cadherin과 세포부착에 미치는 Prostaglandin F2 Alpha의 영향)

  • Lee, Sang-Hee;Jung, Bae Dong;Lee, Seunghyung
    • Korean Journal of Clinical Laboratory Science
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    • v.51 no.3
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    • pp.360-369
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    • 2019
  • Cadherins are essential transmembrane proteins that promote cell-cell adhesion and maintain the corpus luteum structure in the ovary. This study examined the influence of prostaglandin F2 alpha ($PGF2{\alpha}$) on E-cadherin, N-cadherin, and adhesion in luteal theca cells (LTCs). The luteal cells were isolated from the mid-phase corpus luteum, and the LTCs were cultured separately from the luteal heterogeneous cells according to the morphology of the mesenchymal cells and to determine if steroidogenic and endothelial cells of LTCs, 3beta-hydroxysteroid dehydrogenase ($3{\beta}$-HSD), and vascular endothelial growth factor receptor 2 (VEGFR2) mRNA were used. The LTCs were then incubated in the culture medium supplemented with 0.01, 0.1, and 1.0 mM $PGF2{\alpha}$ for 24 h, and the E-cadherin and N-cadherin proteins in the LTCs were detected by confocal laser scanning microscopy. The results revealed $3{\beta}$-HSD mRNA expression in the LTC but no VEGF2R mRNA expression. The E-cadherin and N-cadherin proteins of the LTCs were damaged in the 0.01, 0.1, and 1.0 mM $PGF2{\alpha}$ treatment groups, and the expression of the N-cadherin protein was reduced significantly in 0.01 mM $PGF2{\alpha}$ compared to the 0 mM $PGF2{\alpha}$ treatment groups (P<0.05). In addition, the number of attached LTCs were significantly lower in the 0.01 mM $PGF2{\alpha}$ treatment group than in the 0 mM $PGF2{\alpha}$ treatment group (P<0.05). In conclusion, $PGF2{\alpha}$ affected the disruption of cadherin proteins and cell adhesion in LTCs. These results may help better understand the cadherin and adhesion mechanism during corpus luteum regression in the ovary.

Selection and Mechanism of Anti-Obesity Agents from Natural Products Based on Anti-Angiogenesis (신생혈관형성억제작용을 기반으로 한 항비만제제의 선별 및 작용기전)

  • Shin, Jin-Hyuk;Lee, Jin-Hee;Kang, Kyeong-Wan;Hwang, Jae-Ho;Han, Kyeong-Ho;Shin, Tai-Sun;Kim, Min-Yong;Kim, Jong-Deog
    • KSBB Journal
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    • v.24 no.2
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    • pp.122-130
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    • 2009
  • Anti-angiogenic mechanism was examined for anti-obesity agents with the extract of P.radix, P.semen, S.hebra and C.furctus through anti-cell adhesion effect and western blot. Cell adhesion molecules, VCAM-1 was supressed with the order of P.radix (0.2 ppm, 125%) > P.semen (0.5 ppm, 100%) > S.hebra (5.0 ppm, 114%) > C. furctus (5.0 ppm, 111.8%), ICAM-1 was inhibited by P.radix (0.25 ppm, 130%) > P.semen (0.5 ppm, 100%) > S.hebra (5.0 ppm, 138%) > C. furctus (5.0 ppm, 66.7%), E-Selectin was also supressed P.radix (0.25 ppm, 100%) > P.semen (1.0 ppm, 128%) > S.hebra (5.0 ppm, 120%) > C. furctus (5.0 ppm, 100.7%). And signal molecules, VE-cadherin was supressed by P.radix and S.hebra, ${\beta}$-catenin was inhibited by P.radix, and Akt was supressed all these 4 kinds of natural products. These P.radix, P.semen, S.hebra and C.furctus were showed the possibility of anti-obesity agents based on anti-angiogenesis.

Microarray Analysis of Gene Expression Profile by Treatment of Schizandrae fructus Extract in Inflammation-induced Human Epithelial A549 Cells (염증이 유발된 인간기관지상피세포에서 오미자가 Microarray를 이용한 유전자 발현 분석에 미치는 영향)

  • Jung, Jin-Yong;Jung, Sung-Ki;Jung, Hee-Jae;Rhee, Hyung-Koo
    • The Journal of Internal Korean Medicine
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    • v.29 no.3
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    • pp.543-553
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    • 2008
  • Objective: The goal of this study was to determine the anti-asthma mechanism of SF on TNF-${\alpha}$ induced activation on A549 (human type II-like epithelial) cells. Using oligonucleotide microarray, we sought to establish the molecular mechanism of the protective effects of SF on A549 cells. Material & Methods : Cells were cultured in three different conditions: 1) negative control group was cultured in normal condition of DMEM, 2) positive control group was activated with TNF-${\alpha}$, IL-4. and IL-1${\beta}$, and 3) SF treated group was previously treated with 0.1${\mu}g/ml$ SF after TNF-${\alpha}$, IL-4. and IL-1 activation. Cells of positive control and SF treated groups were cultured for 30 min, 1hr, 3hr and 6hr. Results : The comparative analysis of the gene expression profile revealed that proinflammatory cytokines such as IL1F8, IL1F9, IL1R1. IL1RN, IL1RAPL1, IL8, TNFRSF4, TNFSF10c, TNFSF13, TRAF5, and TRAF7 and inflammation-related genes including MMP2, MMP11, MMP14, MMP15, MMP16, MMP19, MMP25, and MMP27 were down regulated with SF treatment. Cell adhesion molecule genes such as ITGB1, ITGBL1, selectin P ligand, selectin E, ICAM2, ICAM3, VCAM1, PECAM, FCER1G and MMP28 genes were also down-regulated in SF treated A549 cells. Conclusion : These results suggest that the anti-asthmatic effects of SF could be mediated by regulating specific genes related with cell adhesion, proinflammatory cytokine and inflammation-related genes in A549 cells.

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Application of Laser Surface Treatment Technique for Adhesive Bonding of Carbon Fiber Reinforced Composites (탄소복합재 접착공정을 위한 CFRP의 레이저 표면처리 기법의 적용)

  • Hwang, Mun-Young;Kang, Lae-Hyong;Huh, Mongyoung
    • Composites Research
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    • v.33 no.6
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    • pp.371-376
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    • 2020
  • The adhesive strength can be improved through surface treatment. The most common method is to improve physical bonding by varying the surface conditions. This study presents the effect of laser surface treatment on the adhesive strength of CFRP. The surface roughness was patterned using a 1064 nm laser. The effects of the number of laser shots and the direction and length of the pattern on the adhesion of the CFRP/CFRP single joint were investigated through tensile tests. Tests according to ASTM D5868 were performed, and the bonding mechanism was determined by analyzing the damaged surface after a fracture. The optimized number of the laser shots and the optimized depth of the roughness should be required to increase the bonding strength on the CFRP surface. When considering the shear stress in the tensile direction, the roughness pattern in the direction of 45° that increases the length of the fracture path in the adhesive layer resulted in an increase of the adhesive strength. The surface treatment of the bonding surface using a laser is a suitable method to acquire a mechanical bonding mechanism and improve the bonding strength of the CFRP bonding joint. The study on the optimized laser process parameters is required for utilizing the benefits of laser surface processing.

Curing Behavior and Interfacial Properties of Electrodeposited Carbon Fiber/Epoxy Composites by Electrical Resistivity Measurement under Tensile/Compressive Tests (전기증착된 탄소섬유/에폭시 복합재료의 인장/압축 하중하에서의 전기저항 측정법을 이용한 경화 및 계면특성)

  • Park, Joung-Man;Lee, Sang-Il;Kim, Jin-Won
    • Journal of Adhesion and Interface
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    • v.2 no.1
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    • pp.9-17
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    • 2001
  • Curing behavior and interfacial properties were evaluated using electrical resistance measurement and tensile/compressive fragmentation test. Electrical resistivity difference (${\Delta}R$) during curing process was not observed in a bare carbon fiber. On the other hand, ${\Delta}R$ appeared due to the matrix contraction in single-carbon fiber/epoxy composite. Logarithmic electrical resistivity of the untreated single-carbon fiber composite increased suddenly to the infinity when the fiber fracture occurred under tensile loading, whereas that of the ED composite reached relatively broadly up to the infinity. Comparing to the untreated case, interfacial shear strength (IFSS) of the ED treated composite increased significantly in both tensile fragmentation and compressive Broutman test. Microfailure modes of the untreated and the ED treated fiber composite showed the debonding and the cone shapes in tensile test, respectively. For compressive test, fractures of diagonal slippage were observed in both untreated and the ED treated composite. Sharp-end shape fractures exhibited in the untreated composite, whereas relatively dull fractures showed in the ED Heated composite. It is proved that ED treatments affected differently on the interfacial adhesion and microfailure mechanism under tensile/compressive tests.

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Arsenic Trioxide Induces Apoptosis and Incapacitates Proliferation and Invasive Properties of U87MG Glioblastoma Cells through a Possible NF-κB-Mediated Mechanism

  • Ghaffari, Seyed H.;Yousefi, Meysam;Dizaji, Majid Zaki;Momeny, Majid;Bashash, Davood;Zekri, Ali;Alimoghaddam, Kamran;Ghavamzadeh, Ardeshir
    • Asian Pacific Journal of Cancer Prevention
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    • v.17 no.3
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    • pp.1553-1564
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    • 2016
  • Identification of novel therapeutics in glioblastoma remains crucial due to the devastating and infiltrative capacity of this malignancy. The current study was aimed to appraise effect of arsenic trioxide (ATO) in U87MG cells. The results demonstrated that ATO induced apoptosis and impeded proliferation of U87MG cells in a dose-dependent manner and also inhibited classical NF-${\kappa}B$ signaling pathway. ATO further upregulated expression of Bax as an important proapoptotic target of NF-${\kappa}B$ and also inhibited mRNA expression of survivin, c-Myc and hTERT and suppressed telomerase activity. Moreover, ATO significantly increased adhesion of U87MG cells and also diminished transcription of NF-${\kappa}B$ down-stream targets involved in cell migration and invasion, including cathepsin B, uPA, MMP-2, MMP-9 and MMP-14 and suppressed proteolytic activity of cathepsin B, MMP-2 and MMP-9, demonstrating a possible mechanism of ATO effect on a well-known signaling in glioblastoma dissemination. Taken together, here we suggest that ATO inhibits survival and invasion of U87MG cells possibly through NF-${\kappa}B$-mediated inhibition of survivin and telomerase activity and NF-${\kappa}B$-dependent suppression of cathepsin B, MMP-2 and MMP-9.

Comparative Study of Spiral Oblique Retinacular Ligament Reconstruction Techniques Using Either a Lateral Band or a Tendon Graft

  • Oh, Jae Yun;Kim, Jin Soo;Lee, Dong Chul;Yang, Jae Won;Ki, Sae Hwi;Jeon, Byung Joon;Roh, Si Young
    • Archives of Plastic Surgery
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    • v.40 no.6
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    • pp.773-778
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    • 2013
  • Background In the management of mallet deformities, oblique retinacular ligament (ORL) reconstruction provides a mechanism for automatic distal interphalangeal (DIP) joint extension upon active proximal interphalangeal joint extension. The two variants of ORL reconstruction utilize either the lateral band or a free tendon graft. This study aims to compare these two surgical techniques and to assess any differences in functional outcome. As a secondary measure, the Mitek bone anchor and pull-in suture methods are compared. Methods A single-institutional retrospective review of ORL reconstruction was performed. The standard patient demographics, injury mechanism, type of ORL reconstruction, and pre/postoperative degree of extension lag were collected for the 27 cases identified. The cases were divided into lateral band (group A, n=15) and free tendon graft groups (group B, n=12). Group B was subdivided into the pull-in suture technique (B-I) and the Mitek bone anchor method (B-II). Results Overall, ORL reconstructions had improved the mean DIP extension lag by $10^{\circ}$ (P=0.027). Neither the reconstructive technique choice nor bone fixation method identified any statistically meaningful difference in functional outcome (P=0.51 and P=0.83, respectively). Soft-tissue injury was associated with $30.8^{\circ}$ of improvement in the extension lag. The most common complications were tendon adhesion and rupture. Conclusions The choice of the ORL reconstructive technique or the bone anchor method did not influence the primary functional outcome of extension lag in this study. Both lateral band and free tendon graft ORL reconstructions are valid treatment methods in the management of chronic mallet deformity.

Gene Expression Profiling of Doxifluridine Treated Liver, Small and Large Intestine in Cynomolgus (Macaca fascicularis) Monkeys

  • Jeong, Sun-Young;Park, Han-Jin;Oh, Jung-Hwa;Kim, Choong-Yong;Yoon, Seok-Joo
    • Molecular & Cellular Toxicology
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    • v.3 no.2
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    • pp.137-144
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    • 2007
  • The mechanism of cytotoxicity of doxifluridine, a prodrug fluorouracil (5-FU), has been ascribed to the misincorporation of fluoropyrimidine into RNA and DNA and to the inhibition of the nucleotide synthetic enzyme thymidylate synthase. Increased understanding of the mechanism of 5-FU has led to the development of strategies that increases its anticancer activity or predicts its sensitivity to patients. Using GeneChip?? Rhesus Macaque Genome arrays, we analyzed gene expression profiles of doxifluridine after two weeks repeated administration in cynomolgus monkey. Kegg pathway analysis suggested that cytoskeletal rearrangement and cell adhesion remodeling were commonly occurred in colon, jejunum, and liver. However, expression of genes encoding extracellular matrix was distinguished colon from others. In colon, COL6A2, COL18A1, ELN, and LAMA5 were over-expressed. In contrast, genes included in same category were down-regulated in jejunum and liver. Interestingly, MMP7 and TIMP1, the key enzymes responsible for ECM regulation, were overexpressed in colon. Several studies were reported that both gene reduced cell sensitivity to chemotherapy-induced apoptosis. Therefore, we suggest they have potential as target for modulation of 5-FU action. In addition, the expression of genes which have been previously known to involve in 5-FU pathway, were examined in three organs. Particularly, there were more remarkable changes in colon than in others. In colon, ECGF1, DYPD, TYMS, DHFR, FPGS, DUT, BCL2, BAX, and BAK1 except CAD were expressed in the direction that was good response to doxifluridine. These results may provide that colon is a prominent target of doxifluridine and transcriptional profiling is useful to find new targets affecting the response to the drug.

Regulation of IL-6 signaling by miR-125a and let-7e in endothelial cells controls vasculogenic mimicry formation of breast cancer cells

  • Park, Youngsook;Kim, Jongmin
    • BMB Reports
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    • v.52 no.3
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    • pp.214-219
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    • 2019
  • The role of tumor-proximal factors in tumor plasticity during chemoresistance and metastasis following chemotherapy is well studied. However, the role of endothelial cell (EC) derived paracrine factors in tumor plasticity, their effect on chemotherapeutic outcome, and the mechanism by which these paracrine factors modulate the tumor microenvironment are not well understood. In this study, we report a novel mechanism by which endothelial miR-125a and let-7e-mediated regulation of interleukin-6 (IL-6) signaling can manipulate vasculogenic mimicry (VM) formation of MDA-MB-231 breast cancer cells. We found that endothelial IL-6 levels were significantly higher in response to cisplatin treatment, whereas levels of IL-6 upon cisplatin exposure remained unchanged in MDA-MB-231 breast cancer cells. We additionally found an inverse correlation between IL-6 and miR-125a/let-7e expression levels in cisplatin treated ECs. Interestingly, IL-6, IL-6 receptor (IL-6R), and signal transducer and activator of transcription 3 (STAT3) genes in the IL-6 pathway are closely regulated by miR-125a and let-7e, which directly target its 3' untranslated region. Functional analyses revealed that endothelial miR-125a and let-7e inhibit IL-6-induced adhesion of monocytes to ECs. Furthermore, conditioned medium from cisplatin treated ECs induced a significantly higher formation of VM in MDA-MB-231 breast cancer cells as compared to that from intact ECs; this effect of cisplatin treatment was abrogated by concurrent overexpression of miR-125a and let-7e. Overall, this study reveals a novel EC-tumor cell crosstalk mediated by the endothelial miR-125a/let-7e-IL-6 signaling axis, which might improve chemosensitivity and provide potential therapeutic targets for the treatment of cancer.