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Cell Adhesion - DOAJ

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Last Updated: 10 January 2023

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Activated Leukocyte Cell Adhesion Molecule (ALCAM), a Potential ‘Seed’ and ‘Soil’ Receptor in the Peritoneal Metastasis of Gastrointestinal Cancers

Activated Leukocyte Cell Adhesion Molecule is a cell-u2013cell adhesion protein that promotes heterotypic and homotypic interactions between cells of the same type and those of various species. Specifically, we investigated whether ALCAM acts as both a u2018seedu2019 receptor in these tumor cells and a u2018soilu2019 receptor in peritoneal mesothelial cells during cancer metastasis. Patients with gastric cancer and pancreatic cancer tissues with or without peritoneal metastasis were compared for their ALCAM expressions. Human peritoneal mesothelial cells were also genetically modified to produce cell models with varying degrees of ALCAM expression. Patients with peritoneal metastases had higher ALCAM transcripts than those without. Patients with high ALCAM tumors had a much shorter peritoneal metastasis-free survival than those with poor ALCAM expression. The cells' reduced contact with both gastric cancer cells and pancreatic cancer cells was reduced after the cell line MET5A knockdown by ALCAM. Similary, levels of ALCAM in both human gastric and pancreatic cancer cells were also a determining factor for their adhesiveness to mesothelial cells, a process that was supposed to be responsible for the phosphorylation of the SRC kinase. Both gastric and pancreatic cancer patients with ALCAM are an indicator of peritoneal metastasis. During cancer metastasis, it appears that not only a potential peritoneal 'u2019soil'soil u2019 receptor of tumor seeding but also a u2018soilu2019 receptor in peritoneal mesothelial cells.

Source link: https://doi.org/10.3390/ijms24010876


Selective Polyetheretherketone Implants Combined with Graphene Cause Definitive Cell Adhesion and Osteogenic Differentiation

This study investigated whether graphene-modified PEEK could promote cell adhesion and osteogenic differentiation. Methods: This study looked at whether graphene-modified PEEK could enhance cell adhesion and osteogenic differentiation. The biocompatibility of G-PPEK and the ability to promote cell adhesion and osteogenic differentiation in rabbit bone marrow mesenchymal stem cells were tested using live and dead cell double staining, cell counting kit-8 assay, immunofluorescence, and quantitative real-time PCR. In vivo, G-PEEK demonstrated strong bone formation, as well as promising new implantable scaffolding. Key words: polyetheretheretherketone, graphene, nanocomposites, cell adhesion, osteogenic differentiation, osteogenic differentiation, bone defect restoration In vivo, G-PEEK showed good osteogenesis, according to G-PEEK's bone defect.

Source link: https://doaj.org/article/3db349d1b5ac4eb9a6865838fc1e4f14


Constitutive activation of BMP signalling abrogates experimental metastasis of OVCA429 cells via reduced cell adhesion

Abstract Background: In vitro, initiation of bone morphogenetic protein 4 signalling in human ovarian cancer cells leads to a variety of phenotypic changes, including altered cell morphology, adhesion, motility, and invasion relative to normal human ovarian surface epithelial cells. We hypothesized that active BMP signalling enhances ovarian cancer's metastatic potential. Methods We engineered OVCA429 human ovarian cancer cells with doxycycline-inducible expression of a constitutively-active mutant BMP receptor, ALK3 QD, in vivin a mouse experiment, and transplanted these cells to immunocompromised mice in order to prove this directly. We found that ALK3 QD-expressing cells migrated with long, cytoplasmic projections extending into the wound space using in vitro wound healing assays. The combination of reduced E-cadherin and u03b2-integrin expression in spheroids reduces cell cohesion in spheroids and reduced cell adhesion to the extracellular matrix substrates fibronectin and vitronectin was found in the study.

Source link: https://doi.org/10.1186/1757-2215-3-5


Human recombinant arginase I [HuArgI (Co)-PEG5000]-induced arginine depletion inhibits ovarian cancer cell adhesion and migration through autophagy-mediated inhibition of RhoA

Abstract Ovarian carcinoma is the second most common reproductive system malignancy of the female reproductive system and the leading cause of death from female reproductive system malignancies. The Arginosuccinate synthetase enzyme synthesizes L-arginine, a non-essential amino acid synthesized from L-citrulline. The ovarian cancer cells, SKOV3, are auxotrophic to arginine, and that arginine deprivation by therapy with the genetically engineered human arginase I causes autophagy death of SKOV3 cells. In this article, we investigate the effect of HuArgI-PEG5000 on ovarian cancer cell migration and we dissect the mechanism involved. According to arginine deprivation, 2D random cell migration assays, and cell adhesion testing, it has lowered SKOV3 cell migration and adhesion. This was shown that arginine deprivation prevented cancer cell migration by autophagy, rather than cell death.

Source link: https://doi.org/10.1186/s13048-021-00767-3


Initial Layer Analysis for a Linkage Density in Cell Adhesion Mechanisms★

With respect to u025b, we've got a new initial layer on the asymptotic expansion. In addition, we investigate the convergence of the time derivative of this density and plot how a single term appears when a single term goes to zero. On the first half-axis, we see convergence in the tight topology of measures to the time derivative of the limit solution and a Dirac mass.

Source link: https://doi.org/10.1051/proc/201862108


CD97 expression level and its effect on cell adhesion in Preeclampsia

Methods This prospective research included 20 pregnant women with PE and a control group of 16 healthy pregnant women matched for age, gestational age, gravida, and parity. Conclusions The creatinine, uric acid, and lactate dehydrogenase concentrations from standard blood tests were found to be statistically higher in the PE group. In comparison to the control group, the E-cadherin expression score was statistically higher in the PE group. In the PE group, the N-cadherin expression score was statistically lower than the control group compared to the control group. Conclusions Cellular interactions may be responsible for PE as in cancer.

Source link: https://doi.org/10.1186/s12884-022-05280-z


Investigation of Cell Adhesion and Cell Viability of the Endothelial and Fibroblast Cells on Electrospun PCL, PLGA and Coaxial Scaffolds for Production of Tissue Engineered Blood Vessel

Scaffold morphology was determined by scanning electron microscope and tensile testing to see the scaffold tension resistance as time goes forward. Both cytotoxicity assays and confocal microscopy were carried out in human umbilical vein endothelial cells and human vascular fibroblasts for which cell viability and cell adhesion to the scaffolds were determined by cytotoxicity assays and confocal microscopy, respectively. In particular, PLGA membranes displayed much better adhesion and cell proliferation in comparison to control membranes in the absence of polymers.

Source link: https://doi.org/10.3390/jfb13040282


Different Extracellular β-Amyloid (1-42) Aggregates Differentially Impair Neural Cell Adhesion and Neurite Outgrowth through Differential Induction of Scaffold Palladin

In vivo and vitro, extracellular amyloid u03b2-protein aggregates have been found to be harmful to neural cells. Extracellular A3b242 aggregates had a greater effect on neural cell adhesion and tissue adhesion, with SAu03b242 aggregates reducing cell adhesion and associated live cell adhesion decreasing cell adhesion and associated live cell adhesion more than DAu03b242 aggregates causing higher mortality than DAu03b242 aggregates, although causing more mortality. The decrease in cell adhesion due to extracellular Au03b242 aggregates was accompanied by the reduction in cell adhesion, both in size and number, and in number, and, in contrast, SA 03b242 aggregates impaired neurite growth more severely than DA 3b242 aggregates. Our research, which explores how scaffold palladin responds to extracellular Au3b242 aggregates and is closely associated with cell adhesion and neurite outgrowth, provides new insight into Alzheimer disease's extracellular Au03b242 aggregates.

Source link: https://doi.org/10.3390/biom12121808


Monocytic Cell Adhesion to Oxidised Ligands: Relevance to Cardiovascular Disease

Atherosclerosis, the most common cause of cardiovascular disease, is triggered by an inflammation triggered by blood monocytes' entry into the arterial wall. These cells can be moved by adhesion molecules that bind monocytes to the wall, which allow for cell movement. CD14 is a monocyte surface receptor, a cofactor with TLR4's formation of a complex that binds oxidised phospholipids and causes inflammatory changes in the cells, but results on monocyte adhesion are limited. CD14 and TLR4 are both implicated in monocyte adhesion to oxidised LDL in solid phase oxidised LDL, as well as oxPL and malondialdehyde adducts involved in adhesion to oxLDL in static conditions, as well as the production of oxLDL. Monocytes are linked to heat shock protein 60, but this can be caused by contamination of lipopolysaccharide. Increased endothelial MDA adducts and HSP60 were observed in atherosclerotic human arteries, according to increased endothelial MDA adducts and HSP60, but endothelial oxPL was not detected. Inducing atherosclerosis, monocytes may bind to MDA in endothelial cells, according to Wesley.

Source link: https://doi.org/10.3390/biomedicines10123083


Oligopeptide Sortase Inhibitor Modulates Staphylococcus aureus Cell Adhesion and Biofilm Formation

As a potential way to reduce S. aureus virulence, we wanted to investigate the effects of a peptidic S. aureus A inhibitor's adhesion to eukaryotic cells and biofilm formation. Both microscopic and spectrophotometric methods demonstrated that the incubation of MSSA and MRSA strains with LPRDA resulted in a subsequent decrease in staphylococcal attachment to Vero cells and biofilm formation.

Source link: https://doi.org/10.3390/antibiotics11121836

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions