![]() ![]() As the lumen develops, the dimensions of the spherical caps vary, but the cell contact remains fixed with a total size L. ![]() The remaining paracellular adhesive cleft has a thickness e. The lumen elongates parallel to the cell–cell contact over a distance r l and its apex height is h. 2) with a radius of curvature R and a contact angle θ at the lumen edge. We consider the lumen as two symmetrical contractile spherical caps ( Fig. For intercellular lumens, however, the morphogenetic consequences of the leak modulation by the paracellular cleft property have hardly been investigated, either experimentally or theoretically. In the case of multicellular lumen, a few models and experimental studies have considered the role of leaks during the growth of the lumen. Its nature is likely paracellular (through the nanometer cleft between cells). A steady secretion in a closed lumen implies the concomitant existence of leakage. 1 D) depending on the periluminal tension and secretory activity. The growth of the lumen can either be monotonous ( Fig. 1 B and C also shows that the steady shape of the lumen depends on the secretory activity, which is boosted by the addition of Ursodeoxycholic acid (UDCA). However, this process is rather generic for many kinds of lumen such as Ciona Notochord lumen ( 1, 13, 14) or kidney lumens ( 15). In the case of the intercellular domain, the tension arises from the cortical actin layer surrounding the cavity ( 8). In the case of multicellular lumens, tension results from the contraction of the cells surrounding the lumen. The expansion is mechanically restrained by periluminal tension. This osmotic pressure hypothesis was experimentally proposed in the 1960s ( 2– 4). This results in the passive transport of water into the lumen (most often mediated by aquaporins), which constitutes a major driving component for lumen expansion. In the case of closed lumens (such as acini, blastocytes, and canaliculi), ion secretion into the forming cavity creates an osmotic pressure. The creation of the lumens originates from several classes of morphogenetic events ( 1). Ions and other bioactive molecules are secreted into the cavities and, if the lumen is open, flow with the physiological medium. They originate from cavities or tubes surrounded by one (seamless lumen) or multiple cells ( 1). We here discuss progress in understanding common design principles underpinning de novo lumen formation and expansion.Epithelial lumens are ubiquitous in organs. Recent studies using in vivo and in vitro models of lumen formation have shed new light on the molecular networks regulating this fundamental process. Although tubular networks are present in seemingly different organ systems, such as the kidney, lung, and blood vessels, common underlying principles govern their formation. The defining feature of such tissues is the presence of a central, interconnected luminal network. For instance, coordinated apical-basal polarization of epithelial and endothelial cells allows transport of nutrients and metabolites across cell barriers and tissue microenvironments. Spatiotemporal coordination of polarization between groups of cells allowed the evolution of metazoa. The asymmetric polarization of cells allows specialized functions to be performed at discrete subcellular locales. ![]()
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