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Approaches to Studying Polycystic Kidney Disease in Zebrafish
Published in Jinghua Hu, Yong Yu, Polycystic Kidney Disease, 2019
Defects in the cell polarity and cell migration are closely associated with PKD in both zebrafish and mammals. Cell polarity refers to both apical-basal polarity and planar cell polarity. Similar to other epithelial cells, renal epithelial cells have established apical-basolateral polarity with the apical side facing the lumen and basolateral connecting to the neighboring cells or cellular matrix. In both mice and zebrafish, defects in apical-basolateral polarity have been discovered in several PKD models, for example, ADPKD, JBTS (Figure 12.2c).14,32,33 Meanwhile, disruption of proteins required for apical-basolateral polarity (e.g., Dlg5, Scribble, Crumbs) in both mice and zebrafish also leads to PKD.34–36
Differentiation of Colon Cells in Culture
Published in Leonard H. Augenlicht, Cell and Molecular Biology of Colon Cancer, 2019
All those cell lines which express an integrated program of differentiation have some common characteristics. First, these lines form at confluency a monolayer of highly polarized cells. Second, the kinetic analysis of the development of the cell polarity and of the functional differentiation shows that the polarization is fully established and maintained only upon the formation of a continuous monolayer of cells. The coincidental timing of these events suggests that extensive cell-cell contact is an important factor in the development of cell polarity. Interestingly, this hypothesis is in line with the recent finding that cell-cell contacts in the epithelial MDCK cells initiate the formation of a stable, insoluble matrix of the membrane skeleton protein fodrin with preexisting proteins at the cell periphery.63 This matrix might result in the maintenance of membrane domains.
Junctional adhesion molecule (JAM) family
Published in C. Yan Cheng, Spermatogenesis, 2018
JAM plays a role in the recruitment of cell polarity complex for the establishment of polarity.16,57 Loss of JAM-C hinders the recruitment of Par6/Cdc42/PKCλ complex to the anterior region of spermatid head for the polarization of round spermatids, resulting in male infertility.37 Testis from JAM-C knockout mouse is significantly reduced in size and has no elongated spermatids in the seminiferous tubules.37 It is known that JAM-B is the heterophilic interacting partner of JAM-C at the apical ES of the seminiferous epithelium. However, JAM-B-deficient mice show normal reproductive function without any detectable sperm abnormality.62 Still, we could not rule out the functional role of JAM-B in spermatogenesis since the fertility tests were observed using mice at age 8 weeks old62; it remains unknown if abnormalities of spermatogenesis might appear in aging JAM-B-null mice as was reported in occludin knockout.63 It is also possible that other JAMs may complement one another in some ways due to functional redundancy.
COP1 facilitates the proliferation, invasion, and migration of glioma cells by ubiquitination of DLG3 protein
Published in Neurological Research, 2023
Tumor growth involves the reorganization of cell polarity and the abnormal alteration in the expression of scaffolding proteins related to polarity complexes [10]. Discs large homolog 3 (DLG3) scaffolding protein, a member of the membrane-associated guanylate kinase family, is abundantly expressed in the brain and participates in the modulation of synaptic functions [11]. Downregulation of DLG3 contributes to the initiation and progression of human malignancies, such as oral squamous cell carcinoma [12], colon cancer [13], and pancreatic cancer [14]. DLG3 expression is aberrantly reduced in glioblastoma, and DLG3 overexpression triggers glioblastoma cell apoptosis but depresses proliferation and migration [15]. The functions of DLG3 regulating apical-basal polarity and tight junction consolidation require the involvement of E3 ubiquitin ligases [16]. However, whether E3 ubiquitin ligase COP1 participates in glioma progression by manipulating the ubiquitination of DLG3 remains unknown. Herein, this study set out to determine the molecular mechanism of COP1-mediated ubiquitination in glioma cell proliferation, invasion, and migration, hoping to confer a novel theoretical basis for COP1 as a molecular target in the treatment of glioma.
Roles of the ACE/Ang II/AT1R pathway, cytokine release, and alteration of tight junctions in COVID-19 pathogenesis
Published in Tissue Barriers, 2023
Claudins are transmembrane proteins that play a critical role in the TJs between epithelial and endothelial cells. That is, they regulate paracellular permeability and maintain cell polarity in cell sheets.79,80 To date, 27 members of the claudins family were discovered. Claudins are ubiquitously present in the body, and their roles differ according to the organ they localize in. Certain claudins work as “sealing” claudins, with no permeability to ions or water, such as claudins 1, 3, 5, 6, 9, 11, and 18.81 Of note, all the mentioned sealing claudins are present in the airways, working as a fence that prevents liquid movement to the airway in physiological conditions.81 However, other claudins allow liquid and ions movements through TJs, representing “pore-forming” claudins. These include claudin 2,10, 15, 16, and other ones.81 Of note, all mentioned pore-forming claudins are present in kidneys’ nephorns.81 It is noteworthy that claudin-2, and recently claudin-15, were found to be permeable to water.82 Other claudins were found to do both things. That is, being permeable in certain conditions -or tissues- and working as fences in other ones. For example, claudin-19 is impermeable in peripheral neurons, but when became in contact with claudin-16 in the thick ascending limb of kidneys’ nephrons, it forms a permeable pore for ions.81 Other similar claudins include claudins 4, 7, 8, and 12.81
EHD2 Overexpression Suppresses the Proliferation, Migration, and Invasion in Human Colon Cancer
Published in Cancer Investigation, 2021
Chengqi Guan, Cuihua Lu, Mingbing Xiao, Weichang Chen
Metastasis is the transmission of malignant tumor cells to a distant site from the original site of the tumor. It remains to be the most common cause of lethal outcomes in various malignant tumors. It is a great challenge to obtain an understanding of the molecular mechanisms that lead to metastasis in therapeutic strategies (8). An increasing amount of research suggests that the invasive feature of cancers is usually achieved by membrane trafficking (9). Specifically, membrane trafficking can modulate nutrient uptake and extracellular molecular signals by regulating the receptor and transporter locations on the plasma membrane. It also stabilizes the cell polarity, shape, and structure, together with organ function and architecture (10). Thus, membrane trafficking is crucial for cell proliferation, differentiation and apoptosis, especially tumorigenesis and development (11).