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Magnetic Nanoparticles: Challenges and Opportunities in Drug Delivery
Published in Jeffrey N. Anker, O. Thompson Mefford, Biomedical Applications of Magnetic Particles, 2020
Allan E. David, Mahaveer S. Bhojani, Adam J. Cole
Not only is the blood vessel formation abnormal in tumors, but the composition of the basement membrane of tumor vessels is also distinct from their normal counterpart. The basement membrane is formed primarily of collagen and other glycoproteins, and serves to envelop the endothelial cells, pericytes, and smooth muscle cells. This, together with the interstitial matrix, forms the extracellular matrix (ECM), which provides mechanical support to the cells. Compared to normal tissue, the ECM in tumors has an aberrantly higher density and stiffness (Jain 1987). It has also been demonstrated that tumors have a relatively higher interstitial fluid pressure (IFP). The dense ECM and high IFP in tumors can both serve as barriers that inhibit the free diffusion of MNPs into the tumor mass, thus limiting the penetration of most therapeutic molecules, and nanoparticles, to the periphery of the tumor volume close to the vasculature. In general, MNPs of smaller hydrodynamic diameter can be expected to penetrate the extracellular space more rapidly than similar larger particles. Surface properties and the strength of interaction between MNPs and cells and extracellular matrix are also important determinants of tumor penetration. MNPs that bind strongly to cells, or the matrix, tend to get “stuck” on the perimeter of the tumor, while those with a weaker interaction could penetrate deeper, but may also offer limited residence time for drug release within the tumor.
Active Targeting of Microcapsules and Microspheres to Specific Regions
Published in Max Donbrow, Microcapsules and Nanoparticles in Medicine and Pharmacy, 2020
Julia J. Wright, Lisbeth Ilium
We have further utilized the poloxamine coating of polystyrene particles. As mentioned earlier the vascular system is to the most part, lined by epithelium without fenestrations. It has been suggested by various authors60,61 that during the process of inflammation, the basement membrane in the area becomes leaky. Mizushima et al.62 found that dexamethasone encapsulated in emulsions was found in increased concentrations in inflamed tissue. Indeed further work by DeSchrijver et al.,63 using 30 nm sized 99mTc labeled colloids in animals with chemically induced edematous/inflamed lesions and patients with rheumatic disorders, showed that inflammatory lesions accumulated the colloid to a greater extent than did edematous tissue. The authors concluded that the nanocolloid compared well with the radiotracers currently used to visualize sites of inflammation (67Ga-citrate and mIn-chloride). Both Mizushima et al.62 and DeSchrijver et al.63 had substantial MPS uptake of the administered colloids. In both reports the dose of colloid actually reaching the site of inflammation was low, less than 0.4% of the dose given.
Physical properties of the body fluids and the cell membrane
Published in Ronald L. Fournier, Basic Transport Phenomena in Biomedical Engineering, 2017
The retention of proteins by the walls of the capillary during filtration of the plasma is readily explained by comparing the molecular sizes of typical plasma protein molecules to the size of the pores within the capillary wall. Figure 3.1 illustrates the relative size of various solutes as a function of their molecular weight. The wall of a capillary, illustrated in Figure 3.2, consists of a single layer of endothelial cells that are surrounded on their outside by a basement membrane. The basement membrane is a mat-like cellular support structure, or extracellular matrix, that consists primarily of a protein called type IV collagen, and is joined to the cells by the glycoprotein called laminin. The basement membrane is about 50–100 nm thick. The total thickness of the capillary wall is about 0.5 μm.
Gelatin coating promotes in situ endothelialization of electrospun polycaprolactone vascular grafts
Published in Journal of Biomaterials Science, Polymer Edition, 2021
Yuehao Xing, Yongquan Gu, Lianrui Guo, Jianming Guo, Zeqin Xu, Yonghao Xiao, Zhiping Fang, Cong Wang, Zeng-Guo Feng, Zhonggao Wang
The vascular wall is composed of intima, media, and adventitia. Intima is the vascular wall's innermost layer, consisting of a single layer of endothelial cells (ECs) and basement membrane. The endothelium can regulate coagulation, inflammation, and thrombosis [9]. Also, a healthy endothelium can inhibit intimal hyperplasia by reducing SMCs proliferation and migration [10]. ECs are anchored to the basement membrane. The major components of the vascular basement membrane are collagen, laminin, and proteoglycan. The basement membrane participates in the regulation of endothelium permeability, shear stress transduction, and angiogenesis, which are essential to vascular biology function [11].
Exploration of type II and III collagen binding interactions with short peptide-phenyl pyrazole conjugates via docking, molecular dynamics and laboratory experiments
Published in Soft Materials, 2023
Lucy R. Hart, Charlotta G. Lebedenko, Beatriz G. Goncalves, Mia I. Rico, Dominic J. Lambo, Diego S. Perez, Ipsita A. Banerjee
Of particular interest in tissue growth is the role of collagen, as it is the most abundant protein in the human body and plays a critical role.[6] Depending upon the type of tissue, the nature of collagen varies. Thus far, it has been reported that 28 different types of collagen exist and the distribution of various types of collagen depends upon the tissue type and location in the body.[7] While Type I collagen accounts for over 90% of collagen in the body, and has been studied in depth, comparatively lesser studies have focused on other types of collagen, and particularly their interactions with scaffolds. Interestingly, it has been reported that Type IV collagen is the primary constituent of basement membrane, particularly in skin tissue.[8] While all collagens share the triple-helix motif, Type IV collagen lacks a glycine in every third amino acid residue which leads to its relatively kinked structure. Type III collagen, on the other hand, makes up a significant part of connective tissue including in skin, lung, and the vascular endothelial systems. An interesting aspect of Type III collagen is the occurrence of cystine knots at the C-terminal, which is necessary for its stabilization.[9] In the articular cartilage of joints, type III collagen is present in different amounts as a part of the collagen fibrillar complex, cross-linked with collagen Type II.[10] Furthermore, Type III collagen is mostly formed in mature articular cartilage, and plays a critical role in wound healing and chondrocyte behavioral changes upon tissue damage by aiding in binding interactions with the collagen network. Additionally, Type III collagen aids in the fibrillogenesis of Type I collagen and in cardiovascular development,[11] and its mutation or abnormality leads to Type IV Ehlers–Danlos syndrome.[12] Type II collagen is a major constituent of cartilage, intervertebral discs, and the vitreous humor of the eye. It is essential for the proper development of bone and teeth.[13] It has been reported that Type II collagen has three identical α1-polypeptide chains, with significant triple-helical regions and relatively short, non-helical regions that do not contain the typical Gly-Pro-Hyp repeats that are generally found in the triple-helices of collagen.[14] Furthermore, proteoglycans bind to Type II collagen fibrils and stabilize its structure.[15] More importantly, Type II collagen is the main constituent of articular cartilage in mammals[16] and reduces articular chondrocyte hypertrophy and osteoarthritis.[17]