Significance: The endosomal sorting complex required for transport (ESCRT) proteins remodel and sever membranes in a wide range of biology, including HIV budding. Electron microscopy has shown that ESCRT-III is often found in contact with concave (negatively curved) membrane surfaces. It has not been possible until now to determine whether the ESCRTs have an inherent preference for binding to concave membrane because it is difficult to make nanoscale concave membranes. Here we have made such membranes on the dimensions of an HIV budding site. We show that ESCRT-III assembly begins (nucleates) much faster on concave membranes, which explains why this complex is recruited in a rapid burst late in HIV budding.

We report a porous polymer microneedle array with continuous micropores that has high mechanical strength and water absorption speed.

Angiogenesis plays a critical role in many diseases, including macular degeneration. At present, the pathological mechanisms remain unclear while appropriate models dissecting regulation of angiogenic processes are lacking. We propose an in vitro angiogenesis process and test it by examining the co-culture of human retinal pigmental epithelial cells (ARPE-19) and human umbilical vein endothelial cells (HUVEC) inside a microfluidic device. From characterisation of the APRE-19 monoculture, the tight junction protein (ZO-1) was found on the cells cultured in the microfluidic device but changes in the medium conditions did not affect the integrity of monolayers found in the permeability tests. Vascular endothelial growth factor (VEGF) secretion was elevated under low glucose and hypoxia conditions compared to the control. After confirming the angiogenic ability of HUVEC, the cell-cell interactions were analyzed under lowered glucose medium and chemical hypoxia by exposing ARPE-19 cells to cobalt (II) chloride (CoCl₂). Heterotypic interactions between ARPE-19 and HUVEC were observed, but proliferation of HUVEC was hindered once the monolayer of ARPE-19 started breaking down. The above characterisations showed that alterations in glucose concentration and/or oxygen level as induced by chemical hypoxia causes elevations in VEGF produced in ARPE-19 which in turn affected directional growth of HUVEC.