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Adhesion of Bacteria to Solid Surfaces
Published in Girma Biresaw, K.L. Mittal, Surfactants in Tribology, 2019
Nabel A. Negm, Dina A. Ismail, Sahar A. Moustafa, Maram T.H. Abou Kana
Phosphorylated WspR catalyzes the synthesis of cyclic diguanylate monophosphate (c-di-GMP) [127], which is implicated in biofilm formation; the suppression of swarming motility in P. aeruginosa [128,129]; and the regulation of several motility or attachment-related systems in bacteria [130]. In P. aeruginosa, c-di-GMP (Figure 7.12) affects the activity of the transcription factor FleQ. FleQ is the master regulator of flagella gene expression (Figure 7.13). FleQ also inhibits the expression of genes required for EPS synthesis. The surface-induced increase and subsequent role of c-di-GMP in P. aeruginosa are among the best-characterized mechanisms of bacterial surface sensing, and provide an example of the influence of physical properties of the interfaces on bacterial biochemistry and physiology [131].
Human-Induced Pluripotent Stem Cells: Derivation
Published in Deepak A. Lamba, Patient-Specific Stem Cells, 2017
Uthra Rajamani, Lindsay Lenaeus, Loren Ornelas, Dhruv Sareen
Nanog: Nanog is known to be a master regulator of stem cell pluripotency (29), which is expressed in the inner cell mass, the primordial germ cell, and the epiblast in early embryos (30). The name of the Nanog gene was chosen by Professor Ian Chambers, taking a cue from Irish mythology legend, “Tír na nÓg,” which signifies immortality conferred by Nanog upon the stem cells. Nanog plays a key role in suppressing Cdx2, which in turn leads to the specification of the fate of the inner cell mass (31). Nanog also works in synchrony with Oct4 and Sox2 in maintaining the pluripotency of stem cells (32,33). Although Dr. Yamanaka and his group proved that the initial derivation of iPSCs was possible without the ectopic expression of Nanog (2,3), Dr. Thomson’s group showed that Nanog is a key component of the reprogramming factor cocktail. It is, nonetheless, an important marker for the fully reprogrammed germ line-competent human iPSC state (34–36).
The effects of mineral trioxide aggregate on osteo/odontogenic potential of mesenchymal stem cells: a comprehensive and systematic literature review
Published in Biomaterial Investigations in Dentistry, 2020
Danial Babaki, Sanam Yaghoubi, Maryam M. Matin
In particular, osteo/odontogenic markers such as Osteocalcin (OCN), Osteopontin (OPN), Alkaline phosphatase (ALP), Bone sialoprotein (BSP), and Collagen I (COLI) were upregulated in direct contact with MTA or its eluent. The most crucial point to note is that several studies reported increased expression of Runt-related transcription factor 2 (RUNX2), Osterix (OSX), and DSPP. The transcription factor RUNX2 functions as the master regulator of mineralization-related genes at the early stages of mineralized tissue development directly or through RUNX2-related signaling pathways [74]. Consequently, downstream regulators such as OSX continue to be expressed at later stages and stimulate differentiation into osteo/odontoblast-like cells and expression of bone or tooth-related genes, specially DSPP and OCN, which are involved in the nucleation phase of dentin calcification and late stages of bone development, respectively [75–77].
Preparation and evaluation of stingray skin collagen/oyster osteoinductive composite scaffolds
Published in Journal of Biomaterials Science, Polymer Edition, 2023
Yue Wu, Yingkun Fu, Hongfu Pan, Cong Chang, Ningjian Ao, Hui Xu, Zhengnan Zhang, Ping Hu, Riwang Li, Shuxia Duan, Yan Yan Li
We detected the expressions of osteogenesis-related genes OCN, COL-I and RUNX2 after co-culture of MC3T3-E1 cells with composite scaffolds by RT-PCR. OCN is the most specific gene during osteoblast differentiation. It is late-expressed in cell proliferation and reaches maximum expression during mineralization [65]. It can be seen from Figure 7B(a) that the MC3T3-E1 cells cultured on the scaffolds all expressed the OCN gene normally, and the relationship with the culture time was positively correlated. Furthermore, the expression of OCN genes was associated with OSP doping. Col-OSP6 composite scaffolds exhibited higher levels of OCN gene expression compared to Col scaffolds. The possible reason was that OSP contained one or more signaling molecules capable of activating osteogenic capacity. This is consistent with the findings of Lamghari et al. [34, 66]. COL-I is the most abundant form of collagen protein in the human body and an important component of the extracellular matrix of bone [67]. COL-I gene expression was shown in Figure 7B(b). From the figure, we can see that the expression of COL-I gene increased with the extension of culture time. Moreover, the expression of COL-I gene was also related to the OSP in the composite scaffolds, that is, the Col-OSP6 composite scaffolds containing OSP was more favorable for the expression of COL-I gene. RUNX2 is a master regulator of osteogenic gene expression and osteogenic differentiation. It has been reported in the literature that RUNX2 knockout mice do not exhibit osteogenic differentiation, suggesting that osteogenic differentiation is completely blocked in the absence of RUNX2 [68]. Figure 7B(c) showed the expression of RUNX2 gene in MC3T3-E1 cells cultured on the composite scaffolds. In the early stage of culture, the expression level of RUNX2 gene was low, but with the extension of time, the scaffold material showed higher expression of RUNX2 gene. We believed that the RUNX2 gene expression of the Col-OSP6 composite scaffolds was higher than that of the pure Col scaffolds. Possible reason was that OSP contained one or more signaling molecules that activated osteogenic ability, and these signaling molecules had an activating effect on the gene markers OCN, COL-I and RUNX2 of osteogenic differentiation.
Understanding the complex microenvironment in oral cancer: the contribution of the Faculty of Dentistry, University of Otago over the last 100 years
Published in Journal of the Royal Society of New Zealand, 2020
Alison Mary Rich, Haizal Mohd Hussaini, Benedict Seo, Rosnah Bt Zain
A further line of enquiry has been examining the effects of intrinsic and extrinsic stressful stimuli on the TME, specifically endoplasmic reticulum (ER) stress. ER stress leads to the activation of the unfolded protein response (UPR). This is an evolutionarily conserved set of mechanisms designed to ameliorate ER homeostatic imbalance or to induce cell death through apoptosis when ER stress cannot be mitigated. The UPR is extensively intertwined with other vital processes, including those that influence development and progression of cancer. As such, UPR has been implicated in either driving lesional dormancy or promotion and progression in multiple cancer types in a context-dependent manner, and it has been experimentally exploited as potential anti-cancer targets (Shen et al. 2018; Hsu et al. 2019). However, at this stage, the understanding of the role of ER stress-induced UPR in the pathogenesis and progression of OSCC is still in its infancy, requiring further elucidation. We undertook a series of investigations examining ER stress and the maintenance of OSCC cell viability and apoptosis and the differential regulation of key UPR and ER stress-associated genes in an established in-vitro model using the potent inducer of ER stress, tunicamycin. Seven extensively substantiated cell lines derived from normal, dysplastic and malignant oral keratinocytes were used. They were subjected to tunicamycin-induced ER stress of varying intensity and chronicity. In the cell viability experiments it was demonstrated that OSCC cells maintained cell viability in the presence of ER stress at a significantly greater level, compared to normal oral keratinocytes (Seo 2019). Furthermore, caspase-3/7 activity and DNA fragmentation, hallmarks of cell death, were suppressed in OSCC (Seo 2019) (Figure 7A,B). It was also discovered, for the first time, that UPR-induced apoptosis-related factors, most notably DNA damage inducible transcript (DDIT)-3, were significantly up-regulated in OSCC. Also, the master regulator of lipid metabolism, sterol regulatory binding factor (SREBP)-1, and CAMP responsive element binding protein 3-Like (CREB3L)-3, an ER-resident transcription factor closely related to activating transcription factor (ATF)-6, which plays an important role in linking ER stress with immune–inflammatory responses, were significantly up-regulated in OSCC (Seo 2019). These studies highlighted the importance of, and the influence of ER stress and UPR, on the pathogenesis and pathobiology of OSCC, especially centred around factors that influence apoptosis, TME and lipid metabolism.