Product-State Distributions of Three-Body Recombination in Zero-Collision-Energy 4He2-Alkaline-Earth-Metal Systems.

The distributions of product states after three-body recombination (TBR) of zero-collision-energy 4He2X systems, with X being 9Be, 24Mg, 40Ca, 88Sr, or 138Ba, are investigated in the hyperspherical representation by quantum mechanically solving the Schrödinger equation. It is found that the weakly bound (dimer) product states are preferentially populated for all of these cases, which could be understood from the joint effects of the lowest incident channel and the relatively long-range behavior of the corresponding nonadiabatic couplings among these lowest incident and shallow recombination channels. For the strongly bound products, since the flow is accessible in the small hyperradial region, their distributions are closely related to the behavior of the nonadiabatic couplings among the corresponding deep recombination channels. Particularly, our results indicate that the products are not always formed exclusively in the most weakly bound state when the scattering lengths among the reactants are relatively large and that there may exist a large fluctuation of the strongly bound products versus their binding energies in the universal region. In addition, the total TBR rates of these nonuniversal systems are also accounted for by the joint effects of the main adiabatic potentials and nonadiabatic couplings.

Cold atom-atom-anion three-body recombination of 4He4HexLi- (x = 6 or 7) systems.

Atom-atom-anion three-body recombination (TBR) in mixed 4He and xLi- (x = 6 or 7) is investigated in the adiabatic hyperspherical representation by quantum mechanically solving the Schrödinger equation. The distributions of product states following these TBR processes are found to be relatively different for the two systems when the collision energy is less than roughly 0.6 mK × kB or 0.3 mK × kB for 4He4He6Li- and 4He4He7Li- systems, respectively, with kB being the Boltzmann constant. For 4He4He6Li- systems, the rate of recombination into (v=0) l = 04He6Li- molecular anions is the largest with v and l denoting the rovibrational quantum numbers, while the TBR rate that leads to the formation of l = 14He6Li- molecular anions is a little smaller than that of neutral 4He2 molecules. For 4He4He7Li- systems, neutral 4He2 molecules tend to be the most products, following the yields of l = 0 and 1 4He7Li- molecular anions. However, in spite of these distinctly different distributions, the products of molecular anions, the sum of l = 0 and 1 4HexLi- products, are relatively larger than that of neutral 4He2 molecules for both the two systems.

MicroRNA-10b promotes the migration of mouse bone marrow-derived mesenchymal stem cells and downregulates the expression of E-cadherin.

The ability of mesenchymal stem cells (MSCs) to migrate is an important determinant of the efficiency of MSC transplant therapy. MicroRNA-10b (miR-10b) has been positively involved in the migration of a number of tumor cells lineages. To date, it remains unknown whether miR-10b affects the migration of MSCs. In the current study, the effect of miR-10b on the migration of mouse bone marrow-derived MSCs (bmMSCs) was investigated. Third-passage bmMSCs were transfected with miR-10b mimic and negative control precursor miRNA using Lipofectamine™ 2000. miR-10b and E-cadherin expression and bmMSC migration were determined. The present results showed that primary bmMSCs exhibit a spindled or triangular morphology and that third­passage bmMSCs present a typical fibroblast-like morphology, exhibiting CD90-positive and CD45-negative expression. Compared with the transfection of negative control miRNA, transfection of miR-10b mimic markedly upregulated miR-10b expression in bmMSCs, increased their migration and downregulated E-cadherin expression. The current observations indicate that the upregulation of miR-10b increases bmMSC migration ability, which may be involved in the downregulation of E-cadherin.

Lectin-like oxidized LDL receptor-1 expresses in mouse bone marrow-derived mesenchymal stem cells and stimulates their proliferation.

The bone marrow-derived mesenchymal stem cells (bmMSCs) have been widely used in cell transplant therapy, and the proliferative ability of bmMSCs is one of the determinants of the therapy efficiency. Lectin-like oxidized low density lipoprotein receptor-1 (LOX-1) as a transmembrane protein is responsible for binding, internalizing and degrading oxidized low density lipoprotein (ox-LDL). It has been identified that LOX-1 is expressed in endothelial cells, vascular smooth muscle cells, cardiomyocytes, fibroblasts and monocytes. In these cells, low concentration of ox-LDL (<40 µg/mL) stimulates their proliferation via LOX-1 activation. However, it is poor understood that whether LOX-1 is expressed in bmMSCs and which role it plays. In this study, we investigated the status of LOX-1 expression in bmMSCs and its function on bmMSC proliferation. Our results showed that primary bmMSCs exhibiting a typical fibroblast-like morphology are positive for CD44 and CD90, but negative for CD34 and CD45. LOX-1 in both mRNA and protein levels is highly expressed in bmMSCs. Meanwhile, bmMSCs exhibit a strong potential to take up ox-LDL. Moreover, LOX-1 expression in bmMSCs is upregulated by ox-LDL with a dose- and time-dependent manner. Presence of ox-LDL also enhances the proliferation of bmMSCs. Knockdown of LOX-1 expression significantly inhibits ox-LDL-induced bmMSC proliferation. These findings indicate that LOX-1 plays a role in bmMSC proliferation.

Co-culture with Sertoli cells promotes proliferation and migration of umbilical cord mesenchymal stem cells.

Human umbilical cord mesenchymal stem cells (hUCMSCs) have been recently used in transplant therapy. The proliferation and migration of MSCs are the determinants of the efficiency of MSC transplant therapy. Sertoli cells are a kind of "nurse" cells that support the development of sperm cells. Recent studies show that Sertoli cells promote proliferation of endothelial cells and neural stem cells in co-culture. We hypothesized that co-culture of UCMSCs with Sertoli cells may also promote proliferation and migration of UCMSCs. To examine this hypothesis, we isolated UCMSCs from human cords and Sertoli cells from mouse testes, and co-cultured them using a Transwell system. We found that UCMSCs exhibited strong proliferation ability and potential to differentiate to other cell lineages such as osteocytes and adipocytes. The presence of Sertoli cells in co-culture significantly enhanced the proliferation and migration potential of UCMSCs (P<0.01). Moreover, these phenotypic changes were accompanied with upregulation of multiple genes involved in cell proliferation and migration including phospho-Akt, Mdm2, phospho-CDC2, Cyclin D1, Cyclin D3 as well as CXCR4, phospho-p44 MAPK and phospho-p38 MAPK. These findings indicate that Sertoli cells boost UCMSC proliferation and migration potential.