Explore chapters and articles related to this topic
Introduction to Cancer, Conventional Therapies, and Bionano-Based Advanced Anticancer Strategies
Published in D. Sakthi Kumar, Aswathy Ravindran Girija, Bionanotechnology in Cancer, 2023
Most solid cancers have blood vessels that produce an extensive number of vascular permeability factors. Therefore, most solid tumors show enhanced vascular permeability that will enable a sufficient supply of oxygen and nutrients to the tumor for rapid growth. Angiogenesis results in high vascular density in these types of tumors, which exhibit extravasation and retention of drugs. This enhanced permeability retention (EPR) serves as a basis for anticancer therapy development. This is because the nature of blood vessels in tumors facilitates the transport of drugs into tumor tissues, unlike in normal tissue, in which this EPR effect driven the delivery of macromolecules does not occur. The EPR effect is dependent on the molecular weight of molecules; particles that are larger than 40 kDa seem to have a prolonged circulation time in the body, thus gradually permeating tumors in a selective manner. In addition, the accumulated macromolecules remain in the tumors for a relatively extended time. The EPR effect is also shown to be mediated by several vascular factors, hence modulating these factors seems critical in augmenting the EPR effect and, therefore, the anticancer drug effects [76].
Polymeric Nanoparticles for Targeted Delivery of Bioactive Agents and Drugs
Published in Severian Dumitriu, Valentin Popa, Polymeric Biomaterials, 2020
Cesare Errico, Alberto Dessy, Anna Maria Piras, Federica Chiellini
In a site of inflammation, one of the cardinal features of the inflammatory reaction is the increase in vascular permeability to solutes and macromolecules (Rossler et al. 1995). This phenomenon determines the extravasation of the nanoparticles at the diseased site (Coester et al. 2000). As an example, during multiple scleroses (MS), the permeability of the blood brain barrier (BBB) is increased and the passage of nanoparticulate systems could be facilitated. PACA nanoparticles have been investigated in experimental allergic encephalomyelitis (EAE), which serves as an animal model for MS, in order to determine their capacity to reach the central nervous system (CNS). Their concentration has been found to increase in the CNS, particularly in the white substance. Long-term circulating PACA nanoparticles with PEG moieties were found in the CNS in greater amounts than non-PEGylated PACA nanoparticles (Gupta et al. 2004).
Stimuli-Regulated Cancer Theranostics Based on Magnetic Nanoparticles
Published in Nguyễn T. K. Thanh, Clinical Applications of Magnetic Nanoparticles, 2018
Yanmin Ju, Shiyan Tong, Yanglong Hou
In fact, tumours have unique physiopathologic characteristics, which are not observed in normal tissues. Compared with blood vessels of normal tissue, tumour blood vessels have more porous structures, with pores varying from 100 to 780 nm in diameter.2 Therefore, tumours exhibit enhanced vascular permeability, ensuring a sufficient supply of nutrients and oxygen for rapid growth. Meanwhile, nanoparticles (NPs) less than 200 nm can gradually accumulate at tumour sites after intravenous administration by enhanced permeability and retention (EPR) effect.3
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.
Inhibitory effects of cudratricusxanthone O on particulate matter-induced pulmonary injury
Published in International Journal of Environmental Health Research, 2021
Wonhwa Lee, Sae-Kwang Ku, Tae In Kim, Eun-Nam Kim, Eui Kyun Park, Gil-Saeng Jeong, Jong-Sup Bae
Lung is the primary target of PM2.5 exposure. After being inhaled into the respiratory tract and redistributed through the blood circulation, PM2.5 can be transferred to pulmonary tissues. These toxic particles adversely affect lung structure and function, and even cause serious lung diseases. Previous reports showed that inflammation and oxidative stress are often induced as a response to this phenomenon (Mazzoli-Rocha et al. 2010; van Berlo et al. 2010; Lee and Bae 2019b). Furthermore, vascular hyperpermeability and endothelial integrity disruption are hallmarks of vascular inflammatory diseases including severe inflammatory response syndrome, sepsis, pulmonary diseases, and atherosclerosis (Komarova et al. 2007; Curry and Adamson 2013). Therefore, the prevention of endothelial barrier disruption would have therapeutic potential. Airborne particulates with transition metals and polycyclic aromatic hydrocarbons in high concentrations stimulate the excessive generation of ROS in multiple lung tissues. In particular, the vascular endothelium, which is vulnerableto PM-induced oxidative stress plays a critical role in the pathophysiology of several vascular disorders (de Kok et al. 2005; Sun et al. 2008; Wu et al. 2014). The vascular endothelium is a dynamic barrier that selectively restricts the transportation of plasma and cells from the blood to the adjacent tissues. Typically, changes in barrier function occur upon inflammatory responses, in which inflammatory mediators lead to a transient increase in vascular permeability (Komarova et al. 2007; Mehta et al. 2014). Inflammatory mediators irreversibly disrupt vascular integrity, which results in the extreme loss of fluids from the circulation during inflammatory diseases (Komarova et al. 2007; Mehta et al. 2014). Therefore, the prevention of vascular disruptive responses might improve the survival of patients from inflammatory diseases. This study demonstrated that CTXO inhibited PM2.5-induced endothelial barrier disruption and attenuated PM2.5-induced lung vascular leakage via the p38 MAPK pathway. These results indicate the potential barrier-protective functions of CTXO in preserving endothelial integrity against PM challenge.