Displaying publications 81 - 100 of 150 in total

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  1. Chai WL, Moharamzadeh K, Brook IM, Emanuelsson L, Palmquist A, van Noort R
    J. Periodontol., 2010 Aug;81(8):1187-95.
    PMID: 20450401 DOI: 10.1902/jop.2010.090648
    In dental implant treatment, the long-term prognosis is dependent on the biologic seal formed by the soft tissue around the implant. The in vitro investigation of the implant-soft tissue interface is usually carried out using a monolayer cell-culture model that lacks a polarized-cell phenotype. This study developed a tissue-engineered three-dimensional oral mucosal model (3D OMM) to investigate the implant-soft tissue interface.
    Matched MeSH terms: Cell Adhesion
  2. Khalaf S, Ariffin Z, Husein A, Reza F
    J Prosthodont, 2017 Dec;26(8):664-669.
    PMID: 28177575 DOI: 10.1111/jopr.12460
    PURPOSE: To compare the adhesion of three microorganisms on modified and unmodified silicone elastomer surfaces with different surface roughnesses and porosities.

    MATERIALS AND METHODS: Candida albicans, Streptococcus mutans, and Staphylococcus aureus were incubated with modified and unmodified silicone groups (N = 35) for 30 days at 37°C. The counts of viable microorganisms in the accumulating biofilm layer were determined and converted to cfu/cm2 unit surface area. A scanning electron microscope (SEM) was used to evaluate the microbial adhesion. Statistical analysis was performed using t-test, one-way ANOVA, and post hoc tests as indicated.

    RESULTS: Significant differences in microbial adhesion were observed between modified and unmodified silicone elastomers after the cells were incubated for 30 days (p < 0.001). SEM showed evident differences in microbial adhesion on modified silicone elastomer compared with unmodified silicone elastomer.

    CONCLUSIONS: Surface modification of silicone elastomer yielding a smoother and less porous surface showed lower adhesion of different microorganisms than observed on unmodified surfaces.

    Matched MeSH terms: Cell Adhesion*
  3. Nabil Fikri RM, Norlelawati AT, Nour El-Huda AR, Hanisah MN, Kartini A, Norsidah K, et al.
    J Psychiatr Res, 2017 05;88:28-37.
    PMID: 28086126 DOI: 10.1016/j.jpsychires.2016.12.020
    The epigenetic changes of RELN that are involved in the development of dopaminergic neurons may fit the developmental theory of schizophrenia. However, evidence regarding the association of RELN DNA methylation with schizophrenia is far from sufficient, as studies have only been conducted on a few limited brain samples. As DNA methylation in the peripheral blood may mirror the changes taking place in the brain, the use of peripheral blood for a DNA methylation study in schizophrenia is feasible due to the scarcity of brain samples. Therefore, the aim of our study was to examine the relationship of DNA methylation levels of RELN promoters with schizophrenia using genomic DNA derived from the peripheral blood of patients with the disorder. The case control studies consisted of 110 schizophrenia participants and 122 healthy controls who had been recruited from the same district. After bisufhite conversion, the methylation levels of the DNA samples were calculated based on their differences of the Cq values assayed using the highly sensitive real-time MethyLight TaqMan® procedure. A significantly higher level of methylation of the RELN promoter was found in patients with schizophrenia compared to controls (p = 0.005) and also in males compared with females (p = 0.004). Subsequently, the RELN expression of the methylated group was 25 fold less than that of the non-methylated group. Based upon the assumption of parallel methylation changes in the brain and peripheral blood, we concluded that RELN DNA methylation might contribute to the pathogenesis of schizophrenia. However, the definite effects of methylation on RELN function during development and also in adult life still require further elaboration.
    Matched MeSH terms: Cell Adhesion Molecules, Neuronal/blood*; Cell Adhesion Molecules, Neuronal/genetics*
  4. Chai WL, Brook IM, Palmquist A, van Noort R, Moharamzadeh K
    J R Soc Interface, 2012 Dec 7;9(77):3528-38.
    PMID: 22915635 DOI: 10.1098/rsif.2012.0507
    For dental implants, it is vital that an initial soft tissue seal is achieved as this helps to stabilize and preserve the peri-implant tissues during the restorative stages following placement. The study of the implant-soft tissue interface is usually undertaken in animal models. We have developed an in vitro three-dimensional tissue-engineered oral mucosal model (3D OMM), which lends itself to the study of the implant-soft tissue interface as it has been shown that cells from the three-dimensional OMM attach onto titanium (Ti) surfaces forming a biological seal (BS). This study compares the quality of the BS achieved using the three-dimensional OMM for four types of Ti surfaces: polished, machined, sandblasted and anodized (TiUnite). The BS was evaluated quantitatively by permeability and cell attachment tests. Tritiated water (HTO) was used as the tracing agent for the permeability test. At the end of the permeability test, the Ti discs were removed from the three-dimensional OMM and an Alamar Blue assay was used for the measurement of residual cells attached to the Ti discs. The penetration of the HTO through the BS for the four types of Ti surfaces was not significantly different, and there was no significant difference in the viability of residual cells that attached to the Ti surfaces. The BS of the tissue-engineered oral mucosa around the four types of Ti surface topographies was not significantly different.
    Matched MeSH terms: Cell Adhesion*
  5. Khalajabadi SZ, Abu ABH, Ahmad N, Yajid MAM, Hj Redzuan NB, Nasiri R, et al.
    J Mech Behav Biomed Mater, 2018 Jan;77:360-374.
    PMID: 28985616 DOI: 10.1016/j.jmbbm.2017.09.032
    This study was aimed to improve of the corrosion resistance and mechanical properties of Mg/15TiO2/5HA nanocomposite by silicon and magnesium oxide coatings prepared using a powder metallurgy method. The phase evolution, chemical composition, microstructure and mechanical properties of uncoated and coated samples were characterized. Electrochemical and immersion tests used to investigate the in vitro corrosion behavior of the fabricated samples. The adhesion strength of ~36MPa for MgO and ~32MPa for Si/MgO coatings to substrate was measured by adhesion test. Fabrication a homogenous double layer coating with uniform thicknesses consisting micro-sized particles of Si as outer layer and flake-like particles of MgO as the inner layer on the surface of Mg/15TiO2/5HA nanocomposite caused the corrosion resistance and ductility increased whereas the ultimate compressive stress decreased. However, after immersion in SBF solution, Si/MgO-coated sample indicates the best mechanical properties compared to those of the uncoated and MgO-coated samples. The increase of cell viability percentage of the normal human osteoblast (NHOst) cells indicates the improvement in biocompatibility of Mg/15TiO2/5HA nanocomposite by Si/MgO coating.
    Matched MeSH terms: Cell Adhesion
  6. Aslam Khan MU, Haider A, Abd Razak SI, Abdul Kadir MR, Haider S, Shah SA, et al.
    J Tissue Eng Regen Med, 2021 04;15(4):322-335.
    PMID: 33432773 DOI: 10.1002/term.3168
    The importance of bone scaffolds has increased many folds in the last few years; however, during bone implantation, bacterial infections compromise the implantation and tissue regeneration. This work is focused on this issue while not compromising on the properties of a scaffold for bone regeneration. Biocomposite scaffolds (BS) were fabricated via the freeze-drying technique. The samples were characterized for structural changes, surface morphology, porosity, and mechanical properties through spectroscopic (Fourier transform-infrared [FT-IR]), microscopic (scanning electron microscope [SEM]), X-ray (powder X-ray diffraction and energy-dispersive X-ray), and other analytical (Brunauer-Emmett-Teller, universal testing machine Instron) techniques. Antibacterial, cellular, and hemocompatibility assays were performed using standard protocols. FT-IR confirmed the interactions of all the components. SEM illustrated porous and interconnected porous morphology. The percentage porosity was in the range of 49.75%-67.28%, and the pore size was 215.65-470.87 µm. The pore size was perfect for cellular penetration. Thus, cells showed significant proliferation onto these scaffolds. X-ray studies confirmed the presence of nanohydroxyapatite and graphene oxide (GO). The cell viability was 85%-98% (BS1-BS3), which shows no significant toxicity of the biocomposite. Furthermore, the biocomposites exhibited better antibacterial activity, no effect on the blood clotting (normal in vitro blood clotting), and less than 5% hemolysis. The ultimate compression strength for the biocomposites increased from 4.05 to 7.94 with an increase in the GO content. These exciting results revealed that this material has the potential for possible application in bone tissue engineering.
    Matched MeSH terms: Cell Adhesion/drug effects
  7. Mamidi MK, Singh G, Husin JM, Nathan KG, Sasidharan G, Zakaria Z, et al.
    J Transl Med, 2012;10:229.
    PMID: 23171323 DOI: 10.1186/1479-5876-10-229
    Numerous preclinical and clinical studies have investigated the regenerative potential and the trophic support of mesenchymal stem cells (MSCs) following their injection into a target organ. Clinicians favor the use of smallest bore needles possible for delivering MSCs into vascular organs like heart, liver and spleen. There has been a concern that small needle bore sizes may be detrimental to the health of these cells and reduce the survival and plasticity of MSCs.
    Matched MeSH terms: Cell Adhesion
  8. Tan YJ, Lee YT, Mancera RL, Oon CE
    Life Sci, 2021 Nov 01;284:119747.
    PMID: 34171380 DOI: 10.1016/j.lfs.2021.119747
    BZD9L1 was previously described as a SIRT1/2 inhibitor with anti-cancer activities in colorectal cancer (CRC), either as a standalone chemotherapy or in combination with 5-fluorouracil. BZD9L1 was reported to induce apoptosis in CRC cells; however, the network of intracellular pathways and crosstalk between molecular players mediated by BZD9L1 is not fully understood. This study aimed to uncover the mechanisms involved in BZD9L1-mediated cytotoxicity based on previous and new findings for the prediction and identification of related pathways and key molecular players. BZD9L1-regulated candidate targets (RCTs) were identified using a range of molecular, cell-based and biochemical techniques on the HCT 116 cell line. BZD9L1 regulated major cancer pathways including Notch, p53, cell cycle, NFκB, Myc/MAX, and MAPK/ERK signalling pathways. BZD9L1 also induced reactive oxygen species (ROS), regulated apoptosis-related proteins, and altered cell polarity and adhesion profiles. In silico analyses revealed that most RCTs were interconnected, and were involved in the modulation of catalytic activity, metabolism and transcription regulation, response to cytokines, and apoptosis signalling pathways. These RCTs were implicated in p53-dependent apoptosis pathway. This study provides the first assessment of possible associations of molecular players underlying the cytotoxic activity of BZD9L1, and establishes the links between RCTs and apoptosis through the p53 pathway.
    Matched MeSH terms: Cell Adhesion/drug effects; Cell Adhesion/genetics
  9. Amran AA, Zakaria Z, Othman F, Das S, Al-Mekhlafi HM, Nordin NA
    Lipids Health Dis, 2011 Jan 09;10:2.
    PMID: 21214952 DOI: 10.1186/1476-511X-10-2
    BACKGROUND: Inflammation process plays an important role in the development of atherosclerosis. Hypercholesterolemia is one of the major risk factors for atherosclerosis. The present study aimed to evaluate the effect of aqueous extract of Piper sarmentosum (P.s) on inflammatory markers like vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), and C-reactive protein (CRP).

    METHODS: Forty two male New Zealand white rabbits were divided equally into seven groups; (i) C- control group fed normal rabbit chow (ii) CH- cholesterol diet (1%cholesterol) (iii) X1- 1% cholesterol with water extract of P.s (62.5 mg/kg) (iv) X2- 1% cholesterol with water extract of P.s (125 mg/kg (v) X3- 1% cholesterol with water extract of P.s (250 mg/kg) (vi) X4- 1% cholesterol with water extract of P.s (500 mg/kg) and (vii) SMV group fed with 1% cholesterol supplemented with simvistatin drug (1.2 mg/kg). All animals were treated for 10 weeks. Blood serum was taken for observing the inflammatory markers at the beginning and end of the experiment.

    RESULTS: Rabbits fed with 1% cholesterol diet (CH) showed significant increase in the level of VCAM-1, ICAM-1 and CRP compared to the C group. The levels of VCAM-1, ICAM-1 and CRP in the 1% cholesterol group and supplemented with P.s (500 mg/kg) were significantly reduced compared to the cholesterol group. Similar results were also reported with simvistatin group.

    CONCLUSION: These results suggest that the supplementation of Piper sarmentosum extract could inhibit inflammatory markers which in turn could prevent atherosclerosis.

    Matched MeSH terms: Vascular Cell Adhesion Molecule-1/blood*
  10. Zulfahmi Said, Hellen Colley, Craig Murdoch
    MyJurnal
    Introduction: Tissue-engineered oral mucosa (TEOM) is increasingly being used to model oral mucosal diseases and to assess drug toxicity. Current TEOM models are constructed using normal oral fibroblasts (NOF) contained within a hydrogel matrix with normal oral keratinocytes (NOK) cultured on top. NOK are not commercially available and suffer from donor-to-donor variability. Therefore, oral mucosal models based on immortalised keratinocytes may offer advantages over NOK-based models. The objective of this study was to construct and characterise the TEOM developed using TERT2-immortalised oral keratinocyte (FNB6) cells and validate its similarity to normal oral muco-sal tissue. Methods: TEOM were constructed by culturing FNB6 cells on top of a NOF-populated collagen type-1 hydrogel in tissue culture transwell inserts cultured at an air-to-liquid interface and collected at 14 day. TEOM were subjected to morphological (H&E and PAS), ultrastructural (TEM) and immunohistological (Ki-67, cytokeratin 14 and E-cadherin) analysis. Results: Histologically TEOM mimicked native oral mucosa displaying a stratified epithelium, fibroblast-containing connective tissue and basement membrane. Furthermore, TEM confirmed the presence of des-mosomes and hemi-desmosomes in the epithelium. IHC revealed expression of differentiation markers (cytokeratin 14), proliferation (Ki-67), cell adhesion (E-cadherin). Conclusion: FNB6 mucosal models able to mimic native oral mucosa structure. It has potential for drug delivery and toxicity evaluation, and replacing models based on NOK where access to primary cells is limited.
    Matched MeSH terms: Cell Adhesion
  11. Mansouri N, SamiraBagheri
    Mater Sci Eng C Mater Biol Appl, 2016 Apr 1;61:906-21.
    PMID: 26838922 DOI: 10.1016/j.msec.2015.12.094
    The actual in vivo tissue scaffold offers a three-dimensional (3D) structural support along with a nano-textured surfaces consist of a fibrous network in order to deliver cell adhesion and signaling. A scaffold is required, until the tissue is entirely regenerated or restored, to act as a temporary ingrowth template for cell proliferation and extracellular matrix (ECM) deposition. This review depicts some of the most significant three dimensional structure materials used as scaffolds in various tissue engineering application fields currently being employed to mimic in vivo features. Accordingly, some of the researchers' attempts have envisioned utilizing graphene for the fabrication of porous and flexible 3D scaffolds. The main focus of this paper is to evaluate the topographical and topological optimization of scaffolds for tissue engineering applications in order to improve scaffolds' mechanical performances.
    Matched MeSH terms: Cell Adhesion/drug effects
  12. Lim SS, Chai CY, Loh HS
    Mater Sci Eng C Mater Biol Appl, 2017 Jul 01;76:144-152.
    PMID: 28482510 DOI: 10.1016/j.msec.2017.03.075
    Hydrothermally synthesized TiO2nanotubes (TNTs) were first used as a filler for chitosan scaffold for reinforcement purpose. Chitosan-TNTs (CTNTs) scaffolds prepared via direct blending and freeze drying retained cylindrical structure and showed enhanced compressive modulus and reduced degradation rate compared to chitosan membrane which experienced severe shrinkage after rehydration with ethanol. Macroporous interconnectivity with pore size of 70-230μm and porosity of 88% were found in CTNTs scaffolds. Subsequently, the functionalization of CTNTs scaffolds with CaCl2solutions (0.5mM-40.5mM) was conducted at physiological pH. The adsorption isotherm of Ca2+ions onto CTNTs scaffolds fitted well with Freundlich isotherm. CTNTs scaffolds with Ca2+ions showed high biocompatibility by promoting adhesion, proliferation and early differentiation of MG63 in a non-dose dependent manner. CTNTs scaffolds with Ca2+ions can be an alternative for bone regeneration.
    Matched MeSH terms: Cell Adhesion
  13. Chen TF, Siow KS, Ng PY, Majlis BY
    Mater Sci Eng C Mater Biol Appl, 2017 Oct 01;79:613-621.
    PMID: 28629060 DOI: 10.1016/j.msec.2017.05.091
    Our studies focused on improving the biocompatibility properties of two microfluidic prototyping substrates i.e. polyurethane methacrylate (PUMA) and off-stoichiometry thiol-ene (OSTE-80) polymer by Ar and N2plasma treatment. The contact angle (CA) measurement showed that both plasma treatments inserted oxygen and nitrogen moieties increased the surface energy and hydrophilicity of PUMA and OSTE-80 polymer which corresponded to an increase of nitrogen to carbon ratios (N/C), as measured by XPS, to provide a conducive environment for cell attachments and proliferation. Under the SEM observation, the surface topography of PUMA and OSTE-80 polymer showed minimal changes after the plasma treatments. Furthermore, ageing studies showed that plasma-treated PUMA and OSTE-80 polymer had stable hydrophilicity and nitrogen composition during storage in ambient air for 15days. After in vitro cell culture of human umbilical vein endothelial cells (HUVECs) on these surfaces for 24h and 72h, both trypan blue and alamar blue assays indicated that PUMA and OSTE-80 polymer treated with N2plasma had the highest viability and proliferation. The polar nitrogen moieties, specifically amide groups, encouraged the HUVECs adhesion on the plasma-treated PUMA and OSTE-80 surfaces. Interestingly, PUMA polymer treated with Ar and N2plasma showed different HUVECs morphology which was spindle and cobblestone-shaped respectively after 72h of incubation. On the contrary, a monolayer of well-spread HUVECs formed on the Ar and N2plasma-treated OSTE-80 polymers. These variable morphologies observed can be ascribed to the adherence HUVECs on the different elastic moduli of these surfaces whereby further investigation might be needed. Overall, Ar and N2plasma treatment had successfully altered the surface properties of PUMA and OSTE-80 polymer by increasing its surface energy, hydrophilicity and chemical functionalities to create a biocompatible surface for HUVECs adhesion and proliferation.
    Matched MeSH terms: Cell Adhesion
  14. Zandi K
    Methods Mol Biol, 2016;1426:255-62.
    PMID: 27233278 DOI: 10.1007/978-1-4939-3618-2_23
    Screening of viral inhibitors through induction of cytopathic effects (CPE) by conventional method has been applied for various viruses including Chikungunya virus (CHIKV), a significant arbovirus. However, it does not provide the information about cytopathic effect from the beginning and throughout the course of virus replication. Conventionally, most of the approaches are constructed on laborious end-point assays which are not capable for detecting minute and rapid changes in cellular morphology. Therefore, we developed a label-free and dynamical method for monitoring the cellular features that comprises cell attachment, proliferation, and viral cytopathogenicity, known as the xCELLigence real-time cell analysis (RTCA). In this chapter, we provide a RTCA protocol for quantitative analysis of CHIKV replication using an infected Vero cell line treated with ribavirin as an in vitro model.
    Matched MeSH terms: Cell Adhesion
  15. Soon CF, Omar WI, Berends RF, Nayan N, Basri H, Tee KS, et al.
    Micron, 2014 Jan;56:73-9.
    PMID: 24231674 DOI: 10.1016/j.micron.2013.10.011
    This study aimed at examining the biophysical characteristics of human derived keratinocytes (HaCaT) cultured on cholesteryl ester liquid crystals (CELC). CELC was previously shown to improve sensitivity in sensing cell contractions. Characteristics of the cell integrin expressions and presence of extracellular matrix (ECM) proteins on the liquid crystals were interrogated using various immunocytochemical techniques. The investigation was followed by characterization of the chemical properties of the liquid crystals (LC) after immersion in cell culture media using Fourier transform infrared spectroscopy (FTIR). The surface morphology of cells adhered to the LC was studied using atomic force microscopy (AFM). Consistent with the expressions of the integrins α2, α3 and β1, extracellular matrix proteins (laminin, collagen type IV and fibronectin) were found secreted by the HaCaT onto CELC and these proteins were also secreted by cells cultured on the glass substrates. FTIR analysis of the LC revealed the existence of spectrum assigned to cholesterol and ester moieties that are essential compounds for the metabolizing activities of keratinocytes. The immunostainings indicated that cell adhesion on the LC is mediated by self-secreted ECM proteins. As revealed by the AFM imaging, the constraint in cell membrane spread on the LC leads to the increase in cell surface roughness and thickness of cell membrane. The biophysical expressions of cells on biocompatible CELC suggested that CELC could be a new class of biological relevant material.
    Matched MeSH terms: Cell Adhesion
  16. Mohtar MA, Hernychova L, O'Neill JR, Lawrence ML, Murray E, Vojtesek B, et al.
    Mol Cell Proteomics, 2018 04;17(4):737-763.
    PMID: 29339412 DOI: 10.1074/mcp.RA118.000573
    AGR2 is an oncogenic endoplasmic reticulum (ER)-resident protein disulfide isomerase. AGR2 protein has a relatively unique property for a chaperone in that it can bind sequence-specifically to a specific peptide motif (TTIYY). A synthetic TTIYY-containing peptide column was used to affinity-purify AGR2 from crude lysates highlighting peptide selectivity in complex mixtures. Hydrogen-deuterium exchange mass spectrometry localized the dominant region in AGR2 that interacts with the TTIYY peptide to within a structural loop from amino acids 131-135 (VDPSL). A peptide binding site consensus of Tx[IL][YF][YF] was developed for AGR2 by measuring its activity against a mutant peptide library. Screening the human proteome for proteins harboring this motif revealed an enrichment in transmembrane proteins and we focused on validating EpCAM as a potential AGR2-interacting protein. AGR2 and EpCAM proteins formed a dose-dependent protein-protein interaction in vitro Proximity ligation assays demonstrated that endogenous AGR2 and EpCAM protein associate in cells. Introducing a single alanine mutation in EpCAM at Tyr251 attenuated its binding to AGR2 in vitro and in cells. Hydrogen-deuterium exchange mass spectrometry was used to identify a stable binding site for AGR2 on EpCAM, adjacent to the TLIYY motif and surrounding EpCAM's detergent binding site. These data define a dominant site on AGR2 that mediates its specific peptide-binding function. EpCAM forms a model client protein for AGR2 to study how an ER-resident chaperone can dock specifically to a peptide motif and regulate the trafficking a protein destined for the secretory pathway.
    Matched MeSH terms: Epithelial Cell Adhesion Molecule/genetics; Epithelial Cell Adhesion Molecule/metabolism*
  17. Ziganshin RH, Ivanova OM, Lomakin YA, Belogurov AA, Kovalchuk SI, Azarkin IV, et al.
    Mol Cell Proteomics, 2016 Jul;15(7):2366-78.
    PMID: 27143409 DOI: 10.1074/mcp.M115.056036
    Acute inflammatory demyelinating polyneuropathy (AIDP) - the main form of Guillain-Barre syndrome-is a rare and severe disorder of the peripheral nervous system with an unknown etiology. One of the hallmarks of the AIDP pathogenesis is a significantly elevated cerebrospinal fluid (CSF) protein level. In this paper CSF peptidome and proteome in AIDP were analyzed and compared with multiple sclerosis and control patients. A total protein concentration increase was shown to be because of even changes in all proteins rather than some specific response, supporting the hypothesis of protein leakage from blood through the blood-nerve barrier. The elevated CSF protein level in AIDP was complemented by activization of protein degradation and much higher peptidome diversity. Because of the studies of the acute motor axonal form, Guillain-Barre syndrome as a whole is thought to be associated with autoimmune response against neurospecific molecules. Thus, in AIDP, autoantibodies against cell adhesion proteins localized at Ranvier's nodes were suggested as possible targets in AIDP. Indeed, AIDP CSF peptidome analysis revealed cell adhesion proteins degradation, however no reliable dependence on the corresponding autoantibodies levels was found. Proteome analysis revealed overrepresentation of Gene Ontology groups related to responses to bacteria and virus infections, which were earlier suggested as possible AIDP triggers. Immunoglobulin blood serum analysis against most common neuronal viruses did not reveal any specific pathogen; however, AIDP patients were more immunopositive in average and often had polyinfections. Cytokine analysis of both AIDP CSF and blood did not show a systemic adaptive immune response or general inflammation, whereas innate immunity cytokines were up-regulated. To supplement the widely-accepted though still unproven autoimmunity-based AIDP mechanism we propose a hypothesis of the primary peripheral nervous system damaging initiated as an innate immunity-associated local inflammation following neurotropic viruses egress, whereas the autoantibody production might be an optional complementary secondary process.
    Matched MeSH terms: Cell Adhesion
  18. Baker EJ, Yusof MH, Yaqoob P, Miles EA, Calder PC
    Mol Aspects Med, 2018 12;64:169-181.
    PMID: 30102930 DOI: 10.1016/j.mam.2018.08.002
    Endothelial cells (ECs) play a role in the optimal function of blood vessels. When endothelial function becomes dysregulated, the risk of developing atherosclerosis increases. Specifically, upregulation of adhesion molecule expression on ECs promotes the movement of leukocytes, particularly monocytes, into the vessel wall. Here, monocytes differentiate into macrophages and may become foam cells, contributing to the initiation and progression of an atherosclerotic plaque. The ability of omega-3 (n-3) polyunsaturated fatty acids (PUFAs) to influence the expression of adhesion molecules by ECs and to modulate leukocyte-endothelial adhesion has been studied in cell culture using various types of ECs, in animal feeding studies and in human trials; the latter have tended to evaluate soluble forms of adhesion molecules that circulate in the bloodstream. These studies indicate that n-3 PUFAs (both eicosapentaenoic acid and docosahexaenoic acid) can decrease the expression of key adhesion molecules, such as vascular cell adhesion molecule 1, by ECs and that this results in decreased adhesive interactions between leukocytes and ECs. These findings suggest that n-3 PUFAs may lower leukocyte infiltration into the vascular wall, which could contribute to reduced atherosclerosis and lowered risk of cardiovascular disease.
    Matched MeSH terms: Cell Adhesion Molecules; Vascular Cell Adhesion Molecule-1
  19. Tan KL, Chia WC, How CW, Tor YS, Show PL, Looi QHD, et al.
    Mol Biotechnol, 2021 Sep;63(9):780-791.
    PMID: 34061307 DOI: 10.1007/s12033-021-00339-2
    The objective of this study is to develop a simple protocol to isolate and characterise small extracellular vesicles (sEVs) from human umbilical cord-derived MSCs (hUC-MSCs). hUC-MSCs were characterised through analysis of morphology, immunophenotyping and multidifferentiation ability. SEVs were successfully isolated by ultrafiltration from the conditioned medium of hUC-MSCs. The sEVs' size distribution, intensity within a specific surface marker population were measured with zetasizer or nanoparticle tracking analysis. The expression of surface and internal markers of sEVs was also assessed by western blotting. Morphology of hUC-MSCs displayed as spindle-shaped, fibroblast-like adherent cells. Phenotypic analysis by flow cytometry revealed that hUC-MSCs expressed MSC surface marker, including CD90, CD73, CD105, CD44 and exhibited the capacity for osteogenic, adipogenic and chondrogenic differentiation. Populations of sEVs with CD9, CD63 and CD81 positive were detected with size distribution in the diameter of 63.2 to 162.5 nm. Typical sEVs biomarkers such as CD9, CD63, CD81, HSP70 and TSG101 were also detected with western blotting. Our study showed that sEVs from hUC-MSCs conditioned medium were successfully isolated and characterised. Downstream application of hUC-MSCs-sEVs will be further explored.
    Matched MeSH terms: Cell Adhesion
  20. Gee HY, Sadowski CE, Aggarwal PK, Porath JD, Yakulov TA, Schueler M, et al.
    Nat Commun, 2016 Feb 24;7:10822.
    PMID: 26905694 DOI: 10.1038/ncomms10822
    Steroid-resistant nephrotic syndrome (SRNS) causes 15% of chronic kidney disease (CKD). Here we show that recessive mutations in FAT1 cause a distinct renal disease entity in four families with a combination of SRNS, tubular ectasia, haematuria and facultative neurological involvement. Loss of FAT1 results in decreased cell adhesion and migration in fibroblasts and podocytes and the decreased migration is partially reversed by a RAC1/CDC42 activator. Podocyte-specific deletion of Fat1 in mice induces abnormal glomerular filtration barrier development, leading to podocyte foot process effacement. Knockdown of Fat1 in renal tubular cells reduces migration, decreases active RAC1 and CDC42, and induces defects in lumen formation. Knockdown of fat1 in zebrafish causes pronephric cysts, which is partially rescued by RAC1/CDC42 activators, confirming a role of the two small GTPases in the pathogenesis. These findings provide new insights into the pathogenesis of SRNS and tubulopathy, linking FAT1 and RAC1/CDC42 to podocyte and tubular cell function.
    Matched MeSH terms: Cell Adhesion/genetics*
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