LAMININ ISOFORMS AND EPITHELIAL DEVELOPMENT

2003 ◽  
pp. 235-255
Keyword(s):  
Epithelial Development

scholarly journals The Mechanism of Secretion and Metabolism of Gut-Derived 5-Hydroxytryptamine

2021 ◽  
Vol 22 (15) ◽  
pp. 7931
Author(s):  
Ning Liu ◽  
Shiqiang Sun ◽  
Pengjie Wang ◽  
Yanan Sun ◽  
Qingjuan Hu ◽  
...  
Keyword(s):  
Cell Metabolism ◽  
Circulatory System ◽  
Vital Role ◽  
The Body ◽  
Neuroendocrine Cells ◽  
Intestinal Lumen ◽  
Paracrine Signaling ◽  
Inflammatory Conditions ◽  
Epithelial Development ◽  
Ec Cells

Serotonin, also known as 5-hydroxytryptamine (5-HT), is a metabolite of tryptophan and is reported to modulate the development and neurogenesis of the enteric nervous system, gut motility, secretion, inflammation, sensation, and epithelial development. Approximately 95% of 5-HT in the body is synthesized and secreted by enterochromaffin (EC) cells, the most common type of neuroendocrine cells in the gastrointestinal (GI) tract, through sensing signals from the intestinal lumen and the circulatory system. Gut microbiota, nutrients, and hormones are the main factors that play a vital role in regulating 5-HT secretion by EC cells. Apart from being an important neurotransmitter and a paracrine signaling molecule in the gut, gut-derived 5-HT was also shown to exert other biological functions (in autism and depression) far beyond the gut. Moreover, studies conducted on the regulation of 5-HT in the immune system demonstrated that 5-HT exerts anti-inflammatory and proinflammatory effects on the gut by binding to different receptors under intestinal inflammatory conditions. Understanding the regulatory mechanisms through which 5-HT participates in cell metabolism and physiology can provide potential therapeutic strategies for treating intestinal diseases. Herein, we review recent evidence to recapitulate the mechanisms of synthesis, secretion, regulation, and biofunction of 5-HT to improve the nutrition and health of humans.

p63 is essential for regenerative proliferation in limb, craniofacial and epithelial development

Nature ◽  
10.1038/19539 ◽  
1999 ◽  
Vol 398 (6729) ◽  
pp. 714-718 ◽  
Author(s):  
Annie Yang ◽  
Ronen Schweitzer ◽  
Deqin Sun ◽  
Mourad Kaghad ◽  
Nancy Walker ◽  
...  
Keyword(s):  
Epithelial Development

scholarly journals Displacement of basolateral Bazooka/PAR-3 by regulated transport and dispersion during epithelial polarization in Drosophila

2012 ◽  
Vol 23 (22) ◽  
pp. 4465-4471 ◽  
Author(s):  
R. F. Andrew McKinley ◽  
Tony J. C. Harris
Keyword(s):  
Caenorhabditis Elegans ◽  
Transport Mechanism ◽  
Basolateral Membrane ◽  
Adherens Junction ◽  
Pdz Domains ◽  
Zonula Occludens ◽  
Epithelial Development ◽  
Discs Large ◽  
Zonula Occludens 1 ◽  
Acting In Concert

Polarity landmarks guide epithelial development. In the early Drosophila ectoderm, the scaffold protein Bazooka (Drosophila PAR-3) forms apicolateral landmarks to direct adherens junction assembly. However, it is unclear how Bazooka becomes polarized. We report two mechanisms acting in concert to displace Bazooka from the basolateral membrane. As cells form during cellularization, basally localized Bazooka undergoes basal-to-apical transport. Bazooka requires its three postsynaptic density 95, discs large, zonula occludens-1 (PDZ) domains to engage the transport mechanism, but with the PDZ domains deleted, basolateral displacement still occurs by gastrulation. Basolateral PAR-1 activity appears to act redundantly with the transport mechanism. Knockdown of PAR-1 sporadically destabilizes cellularization furrows, but basolateral displacement of Bazooka still occurs by gastrulation. In contrast, basolateral Bazooka displacement is blocked with disruption of both the transport mechanism and phosphorylation by PAR-1. Thus Bazooka is polarized through a combination of transport and PAR-1–induced dispersion from basolateral membranes. Our work complements recent findings in Caenorhabditis elegans and thus suggests the coupling of transport and dispersion is a common protein polarization strategy.

FGF signalling controls the timing of Pax6 activation in the neural tube

Development ◽  
2000 ◽  
Vol 127 (22) ◽  
pp. 4837-4843 ◽  
Author(s):  
N. Bertrand ◽  
F. Medevielle ◽  
F. Pituello
Keyword(s):  
Spinal Cord ◽  
Neural Tube ◽  
Inhibitory Activity ◽  
Neural Plate ◽  
Presomitic Mesoderm ◽  
Pax6 Expression ◽  
Epithelial Development ◽  
Repressive Effect ◽  
Caudal Regression ◽  
Fgf Signalling

We have recently demonstrated that Pax6 activation occurs in phase with somitogenesis in the spinal cord. Here we show that the presomitic mesoderm exerts an inhibitory activity on Pax6 expression. This repressive effect is mediated by the FGF signalling pathway. The presomitic mesoderm displays a decreasing caudorostral gradient of FGF8, and grafting FGF8-soaked beads at the level of the neural tube abolishes Pax6 activation. Conversely, when FGF signalling is disrupted, Pax6 is prematurely activated in the neural plate. We propose that the progression of Pax6 activation in the neural tube is controlled by the caudal regression of the anterior limit of FGF activity. Hence, as part of its posteriorising activity, FGF8 downregulation acts as a switch from early (posterior) to a later (anterior) state of neural epithelial development.

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