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Cancer cell invadopodia
Published in Raquel Seruca, Jasjit S. Suri, João M. Sanches, Fluorescence Imaging and Biological Quantification, 2017
Angela Margarida Costa, Maria José Oliveira
Even in in vitro studies, the already developed methodologies may improve our knowledge about the invasion. The work of Berginski et al. [37], when applied to high-throughput imaging technologies can contribute to simplified analysis of screening of inhibitors of invadopodia formation in cancer cells, and to quantify cell heterogeneity in the cells. Another tool that can help in the study on invadopodia–ECM relationship is the adaptation of the computational modeling tool developed by Kim et al. to study filopodia, in which it is possible to predict the behavior of filopodia that penetrate in a particular 3D ECM fiber network [60]. In addition, the work in podosomes of Proag and colleagues can be adapted to the study of invadopodia [61]. In this work, it was shown a technique that allows the simultaneous tracking of multiple podosomes, which is very useful to understand the dynamic of these protrusions organization, their mechanical characteristics, and to study its collective behavior overtime.
The Mechanobiology of Aqueous Humor Transport across Schlemm's Canal Endothelium
Published in Jiro Nagatomi, Eno Essien Ebong, Mechanobiology Handbook, 2018
As was reported in several studies [113–116], adherent leukocytes extend numerous cytoplasmic processes into the underlying endothelium, and these protrusive processes always precede, and are functionally required for, transcellular diapedesis. Carmen and colleagues [116] identified these processes as podosomes; cylindrical protrusive organelles ~0.5 μm in length and diameter that are enriched in F-actin and focal adhesion proteins. They observed that these structures were highly dynamic, with dozens forming and disappearing within minutes, as if the leukocyte was palpating the endothelium to identify a suitable location for diapedesis. This palpation occurred stochastically over the endothelium, but transcellular openings only formed in regions where podosomes could extend deeply, at which point they lengthened into invasive podosomes (>1 μm) that often spanned the full cell thickness, placing the apical and basal membranes in close proximity (Figure 21.9) [116]. At the site of invasive podosomes, the endothelial cell was enriched in vesicles and VVOs that were fused to the endothelial plasma membrane and there was a local increase in fusogenic proteins VAMP2 and 3 [116] involved in regulating membrane fusion events. Inhibition of fusogenic activity by NEM or by intracellular calcium chelation markedly reduced transcellular diapedesis, suggesting that vesicle fusion is necessary to form transcellular openings [116]. The process also required leukocyte protrusion because WASP-deficient leukocytes that are unable to form podosomes exhibited more than an 80% reduction in transcellular diapedesis [116].
Biomaterials and Immune Response in Periodontics
Published in Nihal Engin Vrana, Biomaterials and Immune Response, 2018
Sivaraman Prakasam, Praveen Gajendrareddy, Christopher Louie, Clarence Lee, Luiz E. Bertassoni
Upon adhesion to the biomaterial, the macrophage cytoskeleton changes allow for macrophages to spread over the material surface. This adhesion is facilitated by podosomes that form during the early stages of the adhesion process.31–33 The adhered macrophages subsequently fuse to form foreign body giant cells.34 Reflective of their origin, these foreign body giant cells display antigenic properties similar to monocytes and macrophages.35
Benzo[a]pyrene osteotoxicity and the regulatory roles of genetic and epigenetic factors: A review
Published in Critical Reviews in Environmental Science and Technology, 2022
Jiezhang Mo, Doris Wai-Ting Au, Jiahua Guo, Christoph Winkler, Richard Yuen-Chong Kong, Frauke Seemann
The fusion of OCPs to MOCs involves recognizing and binding the integrins expressed in OCPs to the amino acid motif Arg-Gly-Asp (RGD) presented in various proteins (such as osteopontin and bone sialoprotein) at the surface of the bone matrix (Boyle et al., 2003). The binding of αvβ3 integrin then activates cytoskeletal reorganization within the OCPs, inducing podosome formation. Integrin signaling and subsequent podosome formation depend on several adhesion kinases including the tyrosine kinases c-Src, proline-rich tyrosine kinase 2 (PYK2), and spleen tyrosine kinase (SYK) (Crockett et al., 2011; Hadjidakis & Androulakis, 2006). Polarized MOCs contain numerous transport vesicles loaded with lysosomal enzymes, such as TRAcP and CTSK. When MOCs begin bone resorption, the cell develops special membrane domains, such as a sealing zone, a ruffled border and a functional secretory domain (Boyle et al., 2003). MOCs resorb bone through the acidification and proteolysis of the bone matrix and hydroxyapatite crystals in the sealing zone. The hydroxyapatite crystals are first mobilized by the enzymatic digestion of the collagen connection. Alternatively, smooth bone resorption without formation of sealing zone by single-nuclear OCs can play a significant role in some teleost such as medaka (Witten & Huysseune, 2009). The residual collagen fibers are then digested by both cathepsins, such as CTSK and collagenases (MMP-9 and MMP-2, for example) (Hadjidakis & Androulakis, 2006). Bone resorption produces a high level of degraded collagen fragments, calcium and phosphate in the resorption lacuna. These fragments and minerals are endocytosed by MOCs, transported through the cell and released at the functional secretory domain. OC activity is regulated by both cytokines and hormones. Notably, receptors for calcitonin, androgens, thyroid hormone, insulin, PTH, IGF-1, IL-1, CSF-1, and PDGF were also identified in OCs (Boyle et al., 2003; Crockett et al., 2011).