Mechanical forces drive neuroblast morphogenesis and are required for epidermal closure.

Tissue morphogenesis requires myosin-dependent events such as cell shape changes and migration to be coordinated between cells within a tissue, and/or with cells from other tissues. However, few studies have investigated the simultaneous morphogenesis of multiple tissues in vivo. We found that during Caenorhabditis elegans ventral enclosure, when epidermal cells collectively migrate to cover the ventral surface of the embryo, the underlying neuroblasts (neuronal precursor cells) also undergo morphogenesis. We found that myosin accumulates as foci along the junction-free edges of the ventral epidermal cells to form a ring, whose closure is myosin-dependent. We also observed the accumulation of myosin foci and the adhesion junction proteins E-cadherin and α-catenin in the underlying neuroblasts. Myosin may help to reorganize a subset of neuroblasts into a rosette-like pattern, and decrease their surface area as the overlying epidermal cells constrict. Since myosin is required in the neuroblasts for ventral enclosure, we propose that mechanical forces in the neuroblasts influence constriction of the overlying epidermal cells. In support of this model, disrupting neuroblast cell division or altering their fate influences myosin localization in the overlying epidermal cells. The coordination of myosin-dependent events and forces between cells in different tissues could be a common theme for coordinating morphogenetic events during metazoan development.

Meibomian gland cells display a differentiation-dependent composition of desmosomes.

Meibomian glands are a modified type of sebaceous glands within the eye lid, which produce an oily secretion important for the stabilization and the prevention of evaporation of the tear film. The holocrine secretory mode of Meibomian glands is characterized by the centripetal movement, the maturation and finally degeneration of the acinar epithelial cells. The process of maturation and degeneration is paralleled by altered expression pattern of certain proteins and the intracellular accumulation of Meibomian gland lipids. In this study, we investigated the correlation between the differentiation status of Meibomian acinus cells and the presence of adhesive junctions. By ultrastructural analyses, we showed for the first time that the frequency of desmosomes increased with the degree of differentiation. Importantly, we detected a differentiation-dependent distribution pattern of desmosomes within the Meibomian gland cells of the acinus, whereas molecules of other cell junctions, e.g., adherens junctions, are equally distributed. Together, these findings provide new insights into the processes of Meibomian gland secretion and may be important for the interpretation of Meibomian gland dysfunction causing diseases like the dry eye syndrome.

Molecular mechanism of VE-cadherin in regulating endothelial cell behaviour during angiogenesis.

Vascular endothelial (VE)-cadherin, an endothelium-specific adhesion protein, is found in the junctions between endothelial cells (ECs). It's crucial to maintain the homogeneity of ECs. Keeping and controlling the contact between ECs is essential. In addition to its adhesive function, VE-cadherin plays important roles in vascular development, permeability, and tumour angiogenesis. Signal transfer, cytoskeletal reconstruction, and contractile integrating, which are crucial for constructing and maintaining monolayer integrity as well as for repair and regeneration, are the foundation of endothelial cell (EC) junctional dynamics. The molecular basis of adhesion junctions (AJs), which are closely related and work with actin filaments, is provided by the VE-cadherin-catenin complex. They can activate intracellular signals that drive ECs to react or communicate structural changes to junctions. An increasing number of molecules, including the vascular endothelial growth factor receptor 2 (VEGFR2) and vascular endothelial protein tyrosine phosphatase (VE-PTP), have been connected to VE-cadherin in addition to the conventional VE-cadherin-catenin complex. This review demonstrates significant progress in our understanding of the molecular mechanisms that affect VE-cadherin's function in the regulation of EC behaviour during angiogenesis. The knowledge of the molecular processes that control VE-cadherin's role in the regulation of EC behaviour during angiogenesis has recently advanced, as shown in this review.

Research progress in mechanism of Astragali Radix and its active components on endothelial cells and their junction / 中草药

To summarize the research progress in vascular endothelial cells junction as well as mechanism of effective components in Yiqi Chinese medicine Astragali Radix in vascular endothelial cells junction based on referring literature in recent year. Astragalus polysaccharides and Astragalus saponins can protect the integrity of endothelial cells junction by increasing tight junction protein and decreasing endothelial cell adhesion molecule. Its protection takes effect by inhibiting endothelin secretion, increasing NO release, inhibiting apoptosis, and promoting endothelial cells proliferation and migration in angiogenesis in addition, while Astragalus flavonoids inhibits apoptosis to protect the junction of endothelial cells. The multiple-targeted protective effect of Astragali Radix in vascular endothelial cells involved in p38 MAPK/NF-κB, Rho/ROCK, PI3K/Akt, and VEGF/Ang-1 signaling pathways. The current study focused on tight junctions as well as adhesion molecule inhibition of monocyte adhesion to endothelial cells. But its protection of gap junctions has rarely been studied.