InGaN/GaN multiple-quantum-well light-emitting-diode structures utilizing tunnel contact junctions grown by metalorganic chemical vapor deposition have been demonstrated. The p+/n+ GaN tunnel junctions are located in the upper cladding layers of conventional devices, allowing n-type GaN instead of p-type GaN as a top contact layer. Thus, metal ohmic contacts are done at the same time on the top and the lower contact layers. The reverse-biased tunnel contact junction provides lateral current spreading without semitransparent electrode and spatially uniform luminescence exhibiting an improved radiative efficiency. The tunnel contact junction is shown to be an effective method to make possible hole injection via a lateral electron current, with only a small penalty in voltage drop compared to conventional devices.
V-defect formation of the In x Ga 1Ϫx N/GaN multiple quantum wells ͑MQWs͒ grown on GaN layers with different threading dislocation ͑TD͒ densities was investigated. From cross-sectional transmission electron microscopy, we found that all V defects are not always connected with TDs at their bottom. By increasing the indium composition in the In x Ga 1Ϫx N well layer or decreasing the TD density of the thick GaN layer, many V defects are generated from the stacking mismatch boundaries induced by stacking faults which are formed within the MQW due to the strain relaxation. Also, TD density in the thick GaN layer affects not only the origin of V-defect formation but also the critical indium composition of the In x Ga 1Ϫx N well on the formation of V defects.
Mouse bone marrow-derived Lin − -Sca-1 + endothelial progenitor cell (EPC) has pluripotent abilities such as supporting neovascularization. Vascular endothelial growth factor (VEGF) receptor 1 (VEGFR1) (Flt1) recognizes various VEGF isoforms and is critically implicated in a wide range of physiological and pathological settings, including vasculogenesis. Mouse EPC expresses two isoforms of VEGFR1: mFlt1, which transmits ligand-induced signals; and sFlt1, which acts as a negative regulator by sequestering ligands of VEGF receptors. How the relative levels of mFlt1 and sFlt1 are regulated is not yet clear. We report here that tumor necrosis factor superfamily 15 (TNFSF15) (also known as VEGI or TL1A), an endothelial cell-secreted cytokine, simultaneously promotes mFlt1 degradation and up-regulates sFlt1 expression in EPC, giving rise to disruption of VEGF-or PlGF-induced activation of eNOS and MAPK p38 and effective inhibition of VEGF-driven, EPC-supported vasculogenesis in a murine Matrigel implant model. TNFSF15 treatment of EPC cultures facilitates Akt deactivationdependent, ubiquitin-assisted degradation of mFlt1 and stimulates sFlt1 expression by activating the PKC, Src, and Erk1/2 signaling pathway. Additionally, TNFSF15 promotes alternative splicing of the Flt1 gene in favor of sFlt1 production by down-regulating nuclear protein Jumonji domain-containing protein 6 (Jmjd6), thus alleviating Jmjd6-inhibited sFlt1 expression. These findings indicate that TNFSF15 is a key component of a molecular mechanism that negatively modulates EPC-supported vasculogenesis through regulation of the relative levels of mFlt1 and sFlt1 in EPC.
Telocyte (TC) as a special stromal cell exists in mammary gland and might play an important role in the balance of epithelium-stroma of mammary gland. Considering that different types of breast interstitial cells influence the development and progression of breast cancer, TCs may have its distinct role in this process. We here studied the roles of TCs in the self-assembly of reconstituted breast cancer tissue. We co-cultured primary isolated TCs and other breast stromal cells with breast cancer EMT-6 cells in collagen/Matrigel scaffolds to reconstitute breast cancer tissue in vitro. Using histology methods, we investigated the immunohistochemical characteristics and potential functions of TCs in reconstituted breast cancer tissue. TCs in primary mammary gland stromal cells with long and thin overlapping cytoplasmic processes, expressed c-kit/CD117, CD34 and vimentin in reconstitute breast cancer tissue. The transmission electron microscopy showed that the telocyte-like cells closely communicated with breast cancer cells as well as other stromal cells, and might serve as a bridge that directly linked the adjacent cells through membrane-to-membrane contact. Compared with cancer tissue sheets of EMT-6 alone, PCNA proliferation index analysis and TUNEL assay showed that TCs and other breast stromal cells facilitated the formation of typical nest structure, promoted the proliferation of breast cancer cells, and inhibited their apoptosis. In conclusion, we successfully reconstituted breast cancer tissue in vitro, and it seems to be attractive that TCs had potential functions in self-assembly of EMT-6/stromal cells reconstituted breast cancer tissue.
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