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Induction of Controlled Differentiation of Callus in Mosses
Published in R. N. Chopra, Satish C. Bhatla, Bryophyte Development: Physiology and Biochemistry, 2019
Both in Physcomitrium coorgense and in P. pyriforme5,19 induction of callus was possible on a medium containing sucrose (2%). The apogamous sporophytes and callus arose on the linearly growing protonema by first differentiating a special small intercalary cell among the ordinary long cylindrical cells (Figure 2A,C). This specialized cell divided anticlinally and organized a sporophyte with an apical cell having two cutting faces or sometimes divided irregularly to form a callus. A sporophyte or a callus could also arise from a seemingly unmodified cell from which a gametophyte would normally arise (Figure 2B,D). When the callus derived from the secondary protonema of P. pyriforme was subcultured on a kinetinsupplemented liquid medium it formed apogamous sporophytic buds with virtual exclusion of gametophytes. Therefore, it was suggested that, rather than having a morphoregulatory role, kinetin may be responsible merely for enhancing cell proliferation, and the determination of an apical cell with two cutting faces or one with three cutting faces is under the control of other factors, both external and internal.27 It was proposed that accumulation of a sporophytic factor in the gametophytic callus cells is diluted during the process of differentiation. Abscisic acid (ABA) did not suppress the differentiation of the quiescent callus cells. Conceivably, ABA regulates cell growth in mosses before the factors for apical cell determination accumulate in them.28
Nutritional Management of Upper Gastrointestinal Disorders
Published in Mary J. Marian, Gerard E. Mullin, Integrating Nutrition Into Practice, 2017
Francis Okeke, Bani Chander Roland
The evidence of familial clustering supports a genetic basis for EoE, and this is further supported with the identification of a possible susceptibility locus on chromosome 5q22 [32]. A positive family history of EoE has also been observed in some patients. Some genetic defects have additionally been identified that may predispose to EoE, including a defect in filaggrin, a barrier-protective molecule, typically found in the skin [33] and in thymic stromal lymphopoietin, a cytokine involved in Th 2 cell determination [32].
Renal ciliopathies: promising drug targets and prospects for clinical trials
Published in Expert Opinion on Therapeutic Targets, 2023
Laura Devlin, Praveen Dhondurao Sudhindar, John A. Sayer
The primary cilium acts a vital transducer in numerous signaling pathways. Patched 1 (PTCH1), the Sonic hedgehog (Shh) receptor, localizes to the ciliary membrane and prevents entry of Smoothened (SMO) [16]. Upon Shh binding to PTCH1, PTCH1 is trafficked out of the cilium allowing SMO to accumulate in the primary cilium, which activates Gli transcription factors. Shh signaling pathway is vital in processes such as cell determination and patterning, and is involved in proper kidney development and functioning, with defective signaling implicated in various renal ciliopathies [16–19]. Components of the canonical Wnt signaling pathway, which is involved in cell proliferation, differentiation and survival, are located at the primary cilium [20]. Components of the non-canonical Wnt planar cell polarity pathway (PCP), regulating cell morphology, migration, and orientated cell division, are also present at the primary cilium [20]. PCP signaling is required for proper nephron tubular formation and maintenance, defects of which can lead to cystogenesis within the kidney tubules [18,21,22]. There are other ciliary signaling pathways which are vital in cell cycle regulation and proliferation, that have been implicated in proper renal tubular formation and kidney function. These includes cyclic AMP (cAMP) signaling, mammalian target of rapamycin (mTOR) signaling, epidermal growth factor (EGF) signaling, AMP-activated protein kinase (AMPK) signaling and insulin-like growth factor (IGF) signaling, although this list is not exhaustive [23,24].
Epigenome- and Transcriptome-wide Changes in Muscle Stem Cells from Low Birth Weight Men
Published in Endocrine Research, 2020
Christa Broholm, Rasmus Ribel-Madsen, Line Hjort, Anders Henrik Olsson, Juliane Maria Dorothee Ahlers, Ninna Schiøler Hansen, Maren Schrölkamp, Linn Gillberg, Alexander Perfilyev, Petr Volkov, Charlotte Ling, Sine W. Jørgensen, Brynjulf Mortensen, Janne Hingst, Jørgen Wojtaszewski, Camilla Scheele, Charlotte Brøns, Bente Klarlund Pedersen, Allan Vaag
Muscle satellite cells are formed during fetal life and reside quiescent in adult tissues.17,18 In response to growth signals, they are activated, differentiate and fuse to form mature muscle fibers. Hereby they participate in the regeneration of adult tissues. Muscle cell determination and differentiation are tightly controlled by epigenetic mechanisms involving DNA methylations and histone acetylations.19 Interestingly, intrauterine undernourished mice have a decreased number of muscle satellite cells which correlates with reduced muscle mass.20 We recently investigated the function of muscle satellite cells isolated from human study participants with LBW and found that they had an impaired differentiation capacity. Furthermore, when differentiated into myotubes, the cell cultures established from LBW participants had lower glucose uptake and lower mRNA expression levels of the genes for GLUT1 and GLUT.415 The aim of the current study was to identify and characterize the genome-wide DNA methylation and transcriptional changes of myoblasts and myotubes underlying the previous findings of impaired myotube functionality in the study participants with LBW.
Low endometrial beta-catenin and cadherins expression patterns are predictive for primary infertility and recurrent pregnancy loss
Published in Gynecological Endocrinology, 2019
Filippo Bellati, Flavia Costanzi, Maria Paola De Marco, Claudia Cippitelli, Antonella Stoppacciaro, Carlo De Angelis, Ilary Ruscito, Rocco Rago, Donatella Caserta
Molecular mechanisms behind human embryo implantation have not been completely elucidated. It is generally accepted that embryo implantation depends on the quality of the blastocyst and endometrium and on the synchronization of their development. Interactions between the outer blastocyst trophectoderm layer and the luminal epithelium require soluble as well as surface-linked molecules [9,10]. Uterine luminal epithelial cells, indeed, are linked by symmetric ‘adherence junctions’. Preclinical studies in mouse models have shown that expression of adherence and tight-junctions molecules in the primary decidual zone act as a permeability barrier to regulate access of immunologically competent maternal cells and/or molecules to the embryo, thus providing guidance of trophoblast cells into the endometrium [11,12]. Cadherins constitute a family of Calcium-dependent cell–cell adhesion molecules, which are highly concentrated at the adherence junctions [13]. Beta-catenin (β-catenin) molecule binds tightly to the cytoplasmic domain of cadherins and plays an essential role in the structural organization and function of cadherins by linking cadherins through α-catenin to the actin cytoskeleton [14]. β-catenin, indeed, acts in two independent ways: as a transcriptional co-factor of the canonical Wnt/b-catenin signaling pathway and as a mediator of cell–cell interactions [15,16]. Wnt/b-catenin signaling is crucial for cell determination during embryonic development and in adult stem cells [15,17]. Linked by β-catenin to cell cytoskeleton, E-cadherin and K-cadherin modulate various signaling pathways, including Wnt/β-catenin signaling [18].