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Drug Targeting: Principles and Applications
Published in Raj K. Keservani, Anil K. Sharma, Rajesh K. Kesharwani, Drug Delivery Approaches and Nanosystems, 2017
Ruslan G. Tuguntaev, Ahmed Shaker Eltahan, Satyajeet S. Salvi, Xing-Jie Liang
VEGF is a key proangiogenic factor, and its activation and binding to receptor (VEGFR), is specifically expressed in endothelial cells, and this causes proliferation and migration of endothelial cells. After endothelial cells migrate to surrounding tissues, they begin to divide and form hollow tubes that soon organize a network of blood vessels (Nishida et al., 2006). Non-hypoxia mediated mechanisms, such as up-regulation of VEGF by oncogene activation, are also involved in angiogenesis process. Moreover, VEGF induce antiapoptotic molecules in order to protect the tumor vasculature from apoptosis, and thus cause degradation of the extracellular matrix through promotion of certain enzymes to facilitate tumor angiogenesis (Carmeliet, 2005). In addition, vascular cell adhesion molecule-1 (VCAM-1), an immunoglobulin-like transmembrane glycoprotein that is expressed on the surface of endothelial cancer cells, mediates cell-cell adhesion, and thereby, promotes angiogenesis (Dienst et al., 2005).
Multimodality probes for cardiovascular imaging
Published in Yi-Hwa Liu, Albert J. Sinusas, Hybrid Imaging in Cardiovascular Medicine, 2017
James T. Thackeray, Frank M. Bengel
Kelly et al. identified a specific moiety within adhesion molecule vascular cell adhesion molecule (VCAM)-1 mediated cell internalizing peptides that bound VCAM-1 and blocked leukocyte endothelial interactions (Kelly et al. 2005). They incorporated this moiety into an iron oxide-fluorescence-labeled nanoparticle to target inflammation, induced in mice by tumor necrosis factor (TNF)-α injection to the ear. Nanoparticles were imaged by confocal microscopy, revealing accumulation in the inflamed ear vessels at 4 h and 24 h after administration, while accumulation was absent in the contralateral ear. MR imaging in ApoE−/− mice showed enhancement of the aortic arch and root, consistent with inflammation of atherosclerotic plaque and accumulation of nanoparticles. Flow cytometry demonstrated nanoparticle binding to endothelial cells, with limited accumulation in macrophages, suggesting an alternative target for atherosclerotic imaging (Kelly et al. 2005). Subsequently, Nahrendorf et al. demonstrated 20× greater enhancement on T2-weighted MR than previously reported, confirming uptake into endothelial cells of ApoE−/− mice by immunohistochemistry (Nahrendorf et al. 2006). Treatment with atorvostatin reduced the accumulation of nanoparticles in the aortic root, with ~50% reduction of MR contrast enhancement and fluorescence, which occurred in parallel with markedly lower VCAM-1 expression at the aortic root. Binding of VCAM-1 is suggested to provide an early indicator of plaque inflammation and may be a functional early biomarker of plaque vulnerability (Nahrendorf et al. 2006).
Magnetic Nanoparticles for Cancer Diagnosis
Published in D. Sakthi Kumar, Aswathy Ravindran Girija, Bionanotechnology in Cancer, 2023
R. G. Aswathy, D. Sakthi Kumar
Although the application of antibody for tumor targeting is considered to be appropriate, the antibody NPs conjugate suffers from several disadvantages, such as large hydrodynamic size and poor diffusion and uptake by RES. Therefore, small targeting moieties are gaining more attention. Arginine-glycine-aspartic acid (RGD) [70–73] peptides are often coupled with IO NPs for the detection of various cancers, including breast cancer, squamous cell carcinomas, and malignant melanomas. Owing to the multivalent binding property, binding efficacy of IO particles to the RGD peptide can be improved. Thus, more numbers of RGD peptides have been attached to the IO particles, due to their very small size and multivalent binding property [74]. Another functional peptide employed was Chlorotoxin (36 amino acid peptide), concurrently used for both molecular imaging by MRI and tumor therapeutics [75]. Adhesion molecule vascular cell adhesion protein 1 (VCAM-1) was recognized as a target for macrophage and endothelial cells that may lead to atherosclerosis. VCAM-1 targeted peptide was conjugated with MNPs and MRI contrast enhancement of early lesions in juvenile mice and resected human carotid artery plaques was observed [76]. Studies of in vitro cellular targeting experiments suggest that Fe3O4-folic acid (FA) nanoconjugate binds specifically to tumor cells [66]. Tumor detection studies with SPIO-PEG-FA as MRI contrast agent demonstrated signal intensity difference in positive in human nasopharyngeal epidermal carcinoma cells (KB cells) tumors (around 20–25%), which was considerably less than the negative HT-1080 cell tumor from pre-contrast to post-contrast image of the tumor in in vivo MR imaging.
Serum miRNA-146a and vitamin D values in chronic renal ailment with and without comorbid cardiovascular disease
Published in Egyptian Journal of Basic and Applied Sciences, 2023
Fatma K. A. Hamid, Alshaymaa M. Alhabibi, Mona A. Mohamed, Hanaa Hussein El-Sayed, Nehad Rafaat Ibrahim, Ghadir Mohamed Hassan Elsawy, Entsar M. Ahmad
VCAM-1 is an adhesion molecule that is expressed on the vascular endothelium following neutrophil stimulation. Neutrophils can move and translocate across the intercellular link due to modifications in the cellular endothelium cytoskeleton and increased vascular permeability [28]. The interaction between neutrophils and VCAM-1 is believed to further compromise the integrity of the endothelium by triggering transcellular permeability pathways, and by activating inflammatory cells to secrete proteinases that change the endothelial glycocalyx causing nephropathies that are associated with inflammation.
Synthesis of Harvard Environmental Protection Agency (EPA) Center studies on traffic-related particulate pollution and cardiovascular outcomes in the Greater Boston Area
Published in Journal of the Air & Waste Management Association, 2019
Iny Jhun, Jina Kim, Bennet Cho, Diane R. Gold, Joel Schwartz, Brent A. Coull, Antonella Zanobetti, Mary B. Rice, Murray A. Mittleman, Eric Garshick, Pantel Vokonas, Marie-Abele Bind, Elissa H. Wilker, Francesca Dominici, Helen Suh, Petros Koutrakis
ICAM-1 and VCAM-1 are proteins found on cell surfaces that mediate the recruitment of white blood cells during an inflammatory response. The soluble form of ICAM-1 and VCAM-1 in the plasma are measured in studies. While ICAM-1 and VCAM-1 are both involved in recruiting white blood cells to sites of inflammation, increased plasma ICAM-1 levels may indicate a general inflammatory state and upregulation in non-endothelial cells, whereas VCAM-1 may have a more restricted distribution within the vascular system (Pradhan, Rifai, and Ridker 2002).
Effect of inflammation on endothelial cells induced by poly-L-lactic acid degradation in vitro and in vivo
Published in Journal of Biomaterials Science, Polymer Edition, 2018
Dongping Chen, Zhaobing Su, Linsheng Weng, Longbin Cao, Can Chen, Sufen Zeng, Suzhen Zhang, Tim Wu, Qiang Hu, Jianmin Xiao
This study expanded the investigation of cell growth and inflammation caused by polymers used in biomedical science. PLLA is generally considered to be non-toxic and non-inflammatory [14, 15], because the degraded product of lactic acid can transform H2O and CO2 into tricarboxylic acid cycle. However, adverse effects may appear when degradation speed and product concentration of polymer accidentally reach high levels. PLLA is formed by lactic acid as hydroxyl (OH−), and broken down to low molecular weight polylactic acid or lactic acid, and the hydrogen ion (H+) gains acceleration and positive feedback during the degradation process. So it will be harmful when degraded products are concentrated due to close structure of PLLA stent. Due to its mechanical ability, high molecular weight PLLA, if chosen for stent, will completely degrade in 2–3 years or longer. We chose low molecular weight and pre-degraded PLLA to mimic the effects of degraded PLLA in vitro. A previous report showed that growth inhibition appeared when pH in extract of degraded product was about 4.5 and added into the same volume of culture medium [16], which was in agreement with the findings of the present study. Notably, the growth inhibition showed volume percentage-dependence, suggesting that excessive degradation products led to cell growth inhibition and inflammation. Therefore, the consequences of the accumulation of degradation products cannot be ignored. Furthermore, increasing expression of NF-κB, VEGF and VCAM-1 with volume percentage-dependence of PLLA extract was observed. NF-κB controls transcription of DNA, cytokine production and cell survival, and plays a key role in regulating inflammation [17], while VEGF is the specific mitogen for endothelial cells [18], and promotes vasculogenesis [19]. VCAM-1 functions as a cell adhesion molecule. Increase in VEGF or VCAM-1 is not only related to vasculogenesis or cell adherence but also to inflammation and thrombosis because of platelet adhesion [20].