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Exosomes in Cancer Disease, Progression, and Drug Resistance
Published in Vladimir Torchilin, Handbook of Materials for Nanomedicine, 2020
Taraka Sai Pavan Grandhi, Rajeshwar Nitiyanandan, Kaushal Rege
Cancer cell–derived exosomes can also significantly impact the endothelial cells in the tumor vicinity [63]. Schillaci et al. [64] showed that the exosomes derived from highly metastatic colon cancer cells (SW620Exos) were able to induce higher endothelial hyperpermeability compared to a non-metastatic colon cancer cell line (SW480Exos). Higher hyperpermeability could aid in metastatic progression of the cells due to improper tight junctions. Compared to exosomes derived from a non-metastatic cell line, those derived from the metastatic cancer cells induced significantly higher hyperpermeability in a confluent HUVEC cell layer in vitro as determined using FITC-Dextran. Exosomes derived from the metastatic cell line caused cytosolic delocalization of the cell surface tight junction protein VE-cadherin, and other adherens junction (AJ) proteins, β-catenin and p120-catenin. Proteomic analyses showed ~ 150 proteins that were significantly different between the exosomes derived from SW480Exos and SW620Exos cells. Exosomes derived from the metastatic cell line were enriched in proteins related to cytoskeletal transformation, actin and microtubule remodeling. Exosomes were enriched in thrombin, a RhoA activator responsible for cytoskeletal changes in the target cells, and treating the monolayer of endothelial cells with thrombin resulted in similar levels of hyperpermeability as observed with the SW620Exos cells [64].
Adaptation 2
Published in James E. Ferrell, Systems Biology of Cell Signaling, 2021
The second protein to be recruited to the autophosphorylated EGFR is the GTPase-activating protein p120 GAP, which causes Ras to hydrolyze its bound GTP to GDP. This hydrolysis allows Ras to flip back to its inactive conformation (Figure 13.1). The actions of Sos and GAP on Ras constitute a cycle of activation and inactivation that is roughly analogous to a phosphorylation–dephosphorylation cycle, except that the “marks” that distinguish active from inactive Ras are non-covalently bound GTP vs. GDP molecules rather than covalently bound phosphate vs. hydroxyl groups on amino acid side chains.
Histopathologic and physiologic effect of overlapping vs single coronary stents: impact of stent evolution
Published in Expert Review of Medical Devices, 2018
Atsushi Sakamoto, Sho Torii, Hiroyuki Jinnouchi, Renu Virmani, Aloke V. Finn
Endothelial cells play a pivotal role in the regulation of permeability by cell-to-cell adhesions and also maintaining vascular homeostasis by liberating both antithrombotic and prothrombotic molecules (Figure 5(c and d)). The importance of a sustained balance between these functions has been shown in the initiation and progression of atherosclerosis. Vascular endothelial cadherin (VE-cad)-based adherens junction regulates vascular permeability via interaction with intracellular protein p120 catenin. Our group previously reported that DES-loaded sirolimus is primarily the cause of increased endothelial permeability at implanted segment by activation of protein kinase C-α and downstream disruption of the p120/VE-cad interaction in vascular endothelium [63]. Although direct correlation between vascular permeability and subsequent neoatherosclerotic formation at the site of DES implantation has not been proven, we propose that the anatomic integrity and functional recovery of endothelial cells govern the early development of neoatherosclesosis. To achieve functional integrity of endothelial cells may be related to drug continuing to leach from permanent polymer for a longer period as compared to bioabsorbable-polymer DES because the drug is impregnated into the polymer, and therefore, when the polymer is fully degraded, the drug is no longer available, and the endothelial cells proliferate and able to be fully functional.