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Cardiovascular and Related Complications of Diabetes
Published in Robert Fried, Richard M. Carlton, Type 2 Diabetes, 2018
Robert Fried, Richard M. Carlton
Endothelial dysfunction is an important early occurrence in the pathogenesis of atherosclerosis, contributing to plaque initiation and progression. Reductions in circulating endothelial progenitor cells that participate in regeneration of the endothelium contribute to endothelial pathophysiology.
Surface Chemistry for Cell Capture in Microfluidic Systems
Published in Iniewski Krzysztof, Integrated Microsystems, 2017
ShuQi Wang, Feng Xu, Alexander Chi Fai Ip, Mrudula Somu, Xiaohu Zhao, Altug Akay, Utkan Demirci
Endothelial progenitor cells (EPCs) originate from bone marrow and play an important role in neovascularization of ischemic tissues and in reendothelialization of vascular lesions. In addition, the number of EPCs can serve as a biomarker to predict clinical outcomes in the event of cardiovascular injury. However, the relative scarcity of circulating EPCs restricts its direct use for therapeutic and diagnostic applications. Efforts to isolate EPCs have been focused on density-gradient centrifugation [55] and the use of fluorescent or immunomagnetic beads in flow cytometry [56,57]. These methods are often associated with high-cost and complex isolation procedures. Plouffe et al. [1] have developed a microfluidic device (EPC chip) to capture EPCs. The EPC chip surface was coated with multiple antibodies targeting surface proteins such as CD34+, CD31+, vascular endothelial growth factor receptor-2 (VEGFR-2), CD146+, CD45+, and von Willebrand factor (vWF), which are consistent with the surface protein profile of EPCs. Under the same shear stress, the multiple antibody-coated surface achieved a cell capture efficiency 10 times higher than the single antibody-coated surface (anti-CD45) [1]. Recently, Ng et al. [14] developed impedance-based EPC detection on a microelectrode array for bed-side diagnosis.
Imaging Cell Trafficking with MR Imaging
Published in Martin G. Pomper, Juri G. Gelovani, Benjamin Tsui, Kathleen Gabrielson, Richard Wahl, S. Sam Gambhir, Jeff Bulte, Raymond Gibson, William C. Eckelman, Molecular Imaging in Oncology, 2008
Assaf A. Gilad, Piotr Walczak, Jeff W. M. Bulte, Michael T. McMahon
Although the human body appears to be static, with defined and anatomically distinct organ systems, there are continuous dynamic processes of cell replacement, repair, and immune-mediated cell infiltrations. All these processes involve cell trafficking. Trafficking cells are cells navigating the body in response to different stimuli; some are chemoattractive and others are chemorepulsive. Perhaps the most pronounced example of cell trafficking is within the hematopoietic system, where cells traffic throughout the entire body. Leukocytes enter the circulation from the bone marrow, spleen, lymph nodes, or the thymus and travel to sites of inflammation and immune stimulation in a highly regulated fashion (1). Recently, it has been shown that circulating endothelial progenitor cells (EPCs) can be recruited from the blood and participate in angioneogenesis of infarcted heart (2). Even in an organ considered incapable of any regenerative activity, such as the postnatal brain, neurogenic regions (the hippocampus and the subventricular zone) remain active throughout life and generate a significant number of new neurons that participate in cell trafficking. Notably, in rodents, subventricular zone neurons migrate extensively, navigating along the rostral migratory stream to reach their final destination, the olfactory bulb (3). Thus, even after full postnatal development, cell trafficking is a key biological phenomenon. In this chapter, we will illustrate how magnetic resonance (MR) imaging may be applied to obtain a deeper insight into the processes that govern cell migration, in particular as it relates to cancer.
Longitudinal profile of circulating endothelial cells in post-acute coronary syndrome patients
Published in Biomarkers, 2023
Marie de Bakker, Jaco Kraan, K. Martijn Akkerhuis, Rohit Oemrawsingh, Folkert W. Asselbergs, Imo Hoefer, Isabella Kardys, Eric Boersma
Endothelial cells expressing VCAM-1 (CD106) have been identified as activated endothelial cells, an indicator for atherosclerosis (Radecke et al.2015). A recent study on VCAM-1 expressing endothelial cells reported that VCAM-1 expression was absent on cells in the peripheral circulation among patients with MI, but an increased density was found on coronary artery endothelial cells (from plaque site) (Radecke et al.2015). In contrast, VCAM-1 expressing CECs were detected in the current study, but no differences were observed between cases and controls. Even so, the vascular integrity of an individual is not only reflected by markers of vascular injury or dysfunction, but by the balance between endothelial injury and endothelial regeneration. Circulating cells co-expressing VEGFR-2 (CD309) and CD133 have been identified as endothelial progenitor cells, hallmarking regeneration (Samman Tahhan et al.2018). Previous studies demonstrated that levels of circulating progenitor cells are significantly higher in acute MI patients than those with stable coronary artery disease. Among patients with ACS, a lower number of CD133+, but not CD309+, circulating progenitor cells was associated with a higher mortality (Samman Tahhan et al.2018). In the current study, increased progenitor cell concentrations were detected after index ACS, but no differences were found between cases and controls during follow-up.
Quantile-specific heritability of serum growth factor concentrations
Published in Growth Factors, 2021
Survival in patients with refractory metastatic colorectal cancer is prolonged by the oral multikinase inhibitor regorafenib (Li et al. 2015). Regorafenib increases VEGF-A concentrations during 21 days of treatment which then return to baseline levels following 7-days of treatment rest. The C–C motif chemokine ligand 5/receptor 5 (CCL5/CCR5) pathway affects VEGF-A production via endothelial progenitor cell migration. Suenaga et al. (2018) reported significant differences in VEGF-A concentrations between CCL5 rs2280789 (P = 0.02, Figure 3(B) and CCL5 rs3817655 genotypes (P = 0.01, not displayed) after 21 days of therapy but not before treatment, in accordance with the higher mean VEGF concentrations after treatment than before (499 pg/ml versus 350 pg/ml). The SNPs are in linkage disequilibrium (D’=0.9791, R2=0.6479, https://ldlink.nci.nih.gov/).
Vascular Regeneration for Ischemic Retinopathies: Hope from Cell Therapies
Published in Current Eye Research, 2020
Pietro Maria Bertelli, Edoardo Pedrini, Jasenka Guduric-Fuchs, Elisa Peixoto, Varun Pathak, Alan W. Stitt, Reinhold J. Medina
The definition of endothelial progenitor cells (EPCs) has generated significant debate. The original definition of EPCs as cells circulating in blood that promoted new blood vessel formation was too broad and it encompasses a multitude of very different cell types. Therefore, a recent consensus on nomenclature suggested to avoid using the term EPCs and encouraged to immunophenotypically define the cells of interest.44 EPCs have been isolated from cord blood45, peripheral blood46, bone marrow47, placenta48, lungs49 and adipose tissue.50 The so-called “putative” EPCs were derived from the mononuclear cell fraction of blood51 and from sorted CD34+ cells cultured on fibronectin.52 These ‘EPCs’ were found to express CD31 and vascular endothelial growth factor receptor 2 (VEGFR2).52 However, this was also reported to be caused by direct protein transfer from platelets.53 This ‘first-generation’ of EPCs was useful in establishing the foundation for vascular stem cell therapies. However, with current technological advances, the field needs to move into ‘next-generation’ cell therapies were detailed cell definition at the molecular level is critical to ensure reproducibility.