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Overview of Cell Adhesion Molecules and Their Antagonism
Published in Bruce S. Bochner, Adhesion Molecules in Allergic Disease, 2020
The function of adhesion receptors can be directly inhibited by agents other than mAb. For example, several adhesion molecules have been detected in soluble form. In various in vitro assays, soluble adhesion receptors have been effectively used as competitive inhibitors of adhesion receptor interactions. Moreover, therapeutically administered forms of soluble adhesion receptors have effectively abrogated inflammation in animal models (29). Some constructs of soluble adhesion receptors may ultimately be of use in allergic disease.
Campylobacter
Published in Dongyou Liu, Handbook of Foodborne Diseases, 2018
Hongsheng Huang, Catherine D. Carrillo, Emma Sproston
Adhesion and invasion are dependent on both motility and flagellar expression (90,91). A number of Campylobacter species and strains have been shown to attach to and invade intestinal epithelial cells, including C. jejuni, C. coli, C. concisus, C. fetus, C. rectus, and C. upsaliensis (29,76). Again the processes and factors are still not fully understood due to numerous putative adhesions that will be involved in a complex, interactive adhesion-receptor process. Major components in adhesion include the major outer membrane protein, lipopolysaccharides, CadF and PEB 1 (92).
Integrin Expression in Tumor Progression — Role of Signaling Mechanisms
Published in Róza Ádány, Tumor Matrix Biology, 2017
Tumor cell-endothelial cell interactions are considered as rate-limiting steps of the intra-as well as the extravasation of tumor cells during hematogenous dissemination.83 These interactions are mediated by several adhesion-receptor complexes where the individual role for them is not precisely determined yet. Several similarities can be found between the tumor cell-platelet and tumor cell-endothelial cell interactions. Both interactions involve CAMs as well as integrins. Both host cell types contain intracellularly, in the α-granules or in the Weibel-Palade bodies, respectively, adhesion molecules such as P-selectin, which is released after an appropriate cell-cell contact signal like thrombin, histamin, cytokines, etc. The CAM (P-selectin) would initiate adhesion due to the rapid translocation of the receptor from the cytoplasmic pool to the plasma membrane. The diversity of the selectins expressed by endothelial cells in different organs provides most probably a mechanism for organ-specific tumor cell metastasis.84,85 Both platelets and endothelial cells express cytoadhesins; however, endothelial cells are only characterized by αvβ3 expression, whereas platelets are characterized by αIIbβ3 expression. Tumor cells may express both αvβ3 and αIIbβ3; however, only one of them seems to be functionally predominant at the same time.34,35,86 It seems that these cytoadhesins play equally important roles in tumor cell-platelet as well as tumor cell-endothelial cell interactions — perhaps as stabilizers of the binding.
Inhibition of hypoxia-inducible factor-1 by salidroside in an in vitro model of choroidal neovascularization
Published in Cutaneous and Ocular Toxicology, 2022
Haitao Yang, Qingwu Yang, Linfei Zheng
VEGF is excessively secreted by the RPE layer that forms the outer Blood-Retina Barrier in AMD, and contributes to the stimulation of CNV23,24. Basic fibroblast growth factor (FGF2) was found in the extracellular matrix and in endothelial cells of choroidal neovascular membranes25. In a rat model of laser-induced CNV, increases in FGF2 and VEGF mRNA are seen in RPE-like cells, choroidal vascular endothelial cells, and fibroblast-like cells in the lesions26–28. FGF and VEGF are also present in choroidal neovascular membranes from patients with age-related macular degeneration29. As the target gene of HIF-1, the pro-angiogenic role of FGF in ocular diseases has been widely considered30. Moreover, FGF-2 signalling has been shown to cross-talk with VEGF. Our data demonstrated that endogenous FGF-2 induced the expression of VEGF31. FGF-2 blockage agents have great potential for the treatment of angiogenic disorders. CD31 is an adhesion receptor with several important functions including angiogenesis, transendothelial migration, and integrin activation32. CD31 has been shown to play a pivotal role in the regulation of adhesion-mediated cell growth and the maintenance of vascular permeability as well as integrity33.
All-trans retinoic acid in anticancer therapy: how nanotechnology can enhance its efficacy and resolve its drawbacks
Published in Expert Opinion on Drug Delivery, 2021
Gabriel Silva Marques Borges, Flávia Alves Lima, Guilherme Carneiro, Gisele Assis Castro Goulart, Lucas Antônio Miranda Ferreira
Shimizu et al. (2003) and Takahashi et al. (2003) developed ATRA-loaded liposomes modified with stearylglucoside for active targeting to the liver. Sterylglucoside binds to the asialoglycoprotein receptor present only on the hepatocytes. The researchers found an increase in survival rate of M5076 (sarcoma)-bearing mice, probably due to the diminishing of hepatic metastasis foci caused by the tumor [122,123]. ATRA was also loaded in PLGA polymeric nanoparticles coated with anti-PD-L1 (programmed death-ligand 1) antibody. PD-L1 receptors are highly expressed in some cancer cells and are linked to evasion of the immune system. After intravenous administration in CH3 (sarcoma)-bearing mice, these nanoparticles had higher accumulation in the tumor compared with nanoparticles without anti-PD-L1 antibodies. Moreover, these polymeric nanoparticles protected the animals from liver and kidney injuries caused by free ATRA administration [124]. Li et al. (2018) produced albumin nanoparticles loading ATRA with hyaluronic acid (HA) as active targeting. HA is a ligand for CD44 receptors. CD44 is a cell surface adhesion receptor, being highly expressed in many types of cancer. The HA coating increased the tumor tissue accumulation of the nanoparticles in B16F10 tumor-bearing mice, generating a much higher antitumor activity and reducing lung metastasis foci in the mice. Moreover, the nanoparticles did not evoke any significant toxicity to the animals [125].
Platelets: the point of interconnection among cancer, inflammation and cardiovascular diseases
Published in Expert Review of Hematology, 2021
Massimiliano Camilli, Giulia Iannaccone, Giulia La Vecchia, Luigi Cappannoli, Roberto Scacciavillani, Giorgio Minotti, Massimo Massetti, Filippo Crea, Nadia Aspromonte
The concept of ‘tumor-educated platelets’ has been supported by evidence of a tumor cell-induced platelet aggregation (TCIPA), a product of the interaction between platelets and cancer which offers several advantages to tumor cells such as accelerated growth, immune system evasion and dissemination [32]. Although not easily detected in the peripheral blood, TCIPA may represent a novel diagnostic and prognostic biomarker of cancer disease progression as it has been proven to be associated with worse prognosis and survival [29,33]. Several pathways have been recently elucidated in TCIPA. Tumor cells can induce TCIPA through formation of thrombin, a key enzyme of coagulation cascade which represents also one of the most potent platelet activators [34]. Moreover, cancer cells may express tissue factor (TF), the main activator of the extrinsic coaglative pathway, which ultimately leads to a large burst of thrombin, amplifying platelets activation and TCIPA formation [34]. Once activated, the release of platelet granules content with a pro-aggregatory effect, such as ADP stored in dense granules, sustain the platelet-tumor crosstalk, prompting more ADP secretion in a positive feedback effect [34]. Of note, a large body of evidence suggests that TICPA is also driven by direct contact between platelets and tumor cells. Therefore, poor vessel integrity of the tumor microenvironment, as well as the enhanced expression of adhesion receptor on platelet surface such as GPIb-IX-V, GPIIb/IIIa and P-selectin have been demonstrated to play a crucial role in TCIPA formation [35].