China
Africa
Explore chapters and articles related to this topic
Innate and Adaptive Immune Dysfunction and Necrotizing Enterocolitis
Published in David J. Hackam, Necrotizing Enterocolitis, 2021
Paula Osterhout, Christina S. Kim, Erika C. Claud
The intestinal mucosal barrier is a key aspect of innate immune defense (Figure 40.1). This barrier is maintained by three cell types that contribute to host defense: intestinal epithelial cells, goblet cells, and paneth cells. This critical barrier is responsible for allowing nutrients and beneficial macromolecules to cross while preventing translocation of bacteria and bacterial products (5, 6). The intestinal barrier comprises a mucin layer covering the intestinal epithelial cells, the epithelial cell plasma membrane, and the apical junctional complex between cells (5, 6). The apical junctional complex consists of a network of tight junction proteins and the adherens junction, both anchored by a perijunctional actomyosin ring (7).
Nanocarrier-based systems for wound healing
Published in Drug Development and Industrial Pharmacy, 2019
S. Bernal-Chávez, M. G. Nava-Arzaluz, R. I. Y. Quiroz-Segoviano, A. Ganem-Rondero
Wound healing is an important physiological process that involves a complex, dynamic, and highly intricate interaction between hemostasis, inflammation, proliferation, and tissue remodeling that overlap on time (Figure 1) [3,10–13]. The process requires a well-orchestrated series of responses, resulting in blood clotting, vascular wall repair, protection against infection, cell proliferation, and migration, and the creation of new blood vessels for the provision of nutrients to those cells [14]. These activities are supported by one of the characteristics presented by organisms, the ability to perform self-repair of wounds by the migration of cells to the site of injury, due to an energetically unfavorable situation on lipid bilayers [15]. This involves important cellular processes like cell crawling and ‘purse-string’ contraction of a supracellular actomyosin ring, that have been evaluated experimentally by Brugues et al. [10]. Furthermore, the communication of appropriate cellular and biochemical species, coupled with the mechanical status of the affected tissue has shown to be critical [11].
Ultra-long silver nanowires induced mitotic abnormalities and cytokinetic failure in A549 cells
Published in Nanotoxicology, 2019
Fengbang Wang, Ying Chen, Yuanyuan Wang, Yongguang Yin, Guangbo Qu, Maoyong Song, Hailin Wang
At anaphase and telophase, RhoA protein can activate myosin IIb by increasing the phosphorylation of myosin light chain (p-MLC), and myosin IIb can accumulate and assembly along actin to form actomyosin ring (Fededa and Gerlich 2012). Contraction of the ring promotes the ingression of attached plasma membrane to form cytokinetic furrow and partitions the cytoplasm into two domains. The aggregates of ultra-long AgNWs at the bridge between two daughter cells exactly located through the actomyosin ring. Here, we assume the ultra-long AgNWs probably obstruct the contraction of actomyosin ring and then further inhibit the division of two daughter cells. To continue accomplishment of their mission, cells may increase to produce more Rho A, the downstream p-MLC and myosin IIb for enhanced contractility, however, still failed and finally resulted in multinucleation.
Pathophysiology of IBD associated diarrhea
Published in Tissue Barriers, 2018
Arivarasu N. Anbazhagan, Shubha Priyamvada, Waddah A. Alrefai, Pradeep K. Dudeja
Apart from the targeted deletion of TJ or AJ protein in mice, the gut permeability is also affected by the alterations in cytoskeletal proteins. One such example is regulation of myosin II phosphorylation by MLCK (myosin light chain kinase). The active enzyme phosphorylates myosin II leading to contraction of actomyosin ring thereby upregulating TJ permeability.142 Studies have shown that MLCK is upregulated in IBD and in models of experimental colitis.143 The transgenic model of mice with constitutively active MLCK, show increased gut permeability and susceptibility to experimentally induced colitis regardless of preserved occludin, ZO-1, claudin1 and JAM expression and absence of spontaneous inflammation. Taken together, studies using genetically modified mice with targeted disruption of TJ or AJ proteins highlighted the facts that deficiency of barrier associated proteins i) impairs paracellular permeability ii) perturbs immune homeostasis and intensifies mucosal inflammatory responses and iii) affects epithelial restitution, proliferation and apoptosis and thus can contribute to the pathogenesis of IBD associated diarrhea. These models also elucidated the non-barrier roles of these junctional proteins in the intestine.