Ets homologous factor (EHF) has critical roles in epithelial dysfunction in airway disease

The airway epithelium forms a barrier between the internal and external environments. Epithelial dysfunction is critical in the pathology of many respiratory diseases, including cystic fibrosis. Ets homologous factor (EHF) is a key member of the transcription factor network that regulates gene expression in the airway epithelium in response to endogenous and exogenous stimuli. EHF , which has altered expression in inflammatory states, maps to the 5' end of an intergenic region on Chr11p13 that is implicated as a modifier of cystic fibrosis airway disease. Here we determine the functions of EHF in primary human bronchial epithelial (HBE) cells and relevant airway cell lines. Using EHF ChIP followed by deep sequencing (ChIP-seq) and RNA sequencing after EHF depletion, we show that EHF targets in HBE cells are enriched for genes involved in inflammation and wound repair. Furthermore, changes in gene expression impact cell phenotype because EHF depletion alters epithelial secretion of a neutrophil chemokine and slows wound closure in HBE cells. EHF activates expression of the SAM pointed domain-containing ETS transcription factor, which contributes to goblet cell hyperplasia. Our data reveal a critical role for EHF in regulating epithelial function in lung disease

E-Cadherin is stabilized at the cell periphery in collagen XV expressing cells.

<p>Confocal microscopy with an antibody specific for the extracellular domain of E-Cad (green) and nuclei stained with DAPI (blue). BxVC1 vector clone and Bx15.23 COLXV clone grown on plastic A) or COLI B). E-Cad is most abundant at the cell surface in both clones on plastic. On COLI, E-Cad moves from the cell periphery into the cytoplasm in BxVC1, but this redistribution is inhibited in the presence of COLXV (BX15.23). C) EEA1 (red) is found in the endoplasmic reticulum (ER)/Golgi zone of the cells grown on plastic, while E-Cad is at the cell periphery. D) After relocation of E-Cad on COLI, EEA1 colocalizes with E-Cad (white arrowheads) in BxVC1 cells but not Bx15.23 cells. Images are representative of several clones. E) Flow cytometry after staining cells with an E-Cad antibody shows increased cell-surface expression of E-Cad in cells with COLXV (Bx15.5 and 15.24) in comparison to vector controls (BxVC4 and BxVC1). All experiments performed a minimum of 3 times with consistent results.</p

Evidence for High-Efficiency Exciton Dissociation at Polymer/Single-Walled Carbon Nanotube Interfaces in Planar Nano-heterojunction Photovoltaics

There is significant interest in combining carbon nanotubes with semiconducting polymers for photovoltaic applications because of potential advantages from smaller exciton transport lengths and enhanced charge separation. However, to date, bulk heterojunction (BM) devices have demonstrated relatively poor efficiencies, and little is understood about the polymer/nanotube junction. To investigate this interface, we fabricate a planar nano-heterojunction comprising well-isolated millimeter-long single-walled carbon nanotubes underneath a poly(3-hexylthiophene) (P3HT) layer. The resulting junctions display photovoltaic efficiencies per nanotube ranging from 3% to 3.82%, which exceed those of polymer/nanotube BM by a factor of 50-100. The increase is attributed to the absence of aggregate formation in this planar device geometry. It is shown that the polymer/nanotube interface itself is responsible for exciton dissociation. Typical open-circuit voltages are near 0.5 V with All factors of 0.25-0.3, which are largely invariant with the number of nanotubes per device and P3HT thickness. A maximum efficiency is obtained for a 60 nm-thick P3HT layer, which is predicted by a Monte Carlo simulation that takes into account exciton generation, transport, recombination, and dissociation. This platform is promising for further understanding the potential role of polymer/nanotube interfaces for photovoltaic applicationsclose545