Transformation by murine and feline sarcoma viruses specifically blocks binding of epidermal growth factor to cells.

Normal cells in culture have membrane receptors for epidermal growth factor (EGF); EGF stimulates cells to divide by binding to these receptors. Cells transformed by murine and feline sarcoma viruses rapidly lose the ability to bind EGF, whereas cells transformed by the DNA tumour viruses, polyoma and SV40, or infected with non-transforming RNA tumour viruses have normal levels of functional EGF receptors. The results suggest that a product of the sarcoma virus genome specifically changes cell EGF receptors; the sarcoma gene product may, then, be functionally related to EGF.     

Interleukins 4 and 5 control expression of IL-2 receptor on murine B cells through independent induction of its two chains

Resting B cells express few, if any, receptors for interleukin-2 (IL-2), whereas activated B cells can express receptors for and respond to IL-2. IL-2 receptors can exist on the cell surface in three different forms; the complete high-affinity receptor, a heterodimer consisting of a chain of relative molecular mass (Mr) 70-75,000 (70-75K) and a chain of Mr 55K; the 70-75K chain alone, with intermediate affinity for IL-2; or the 55K chain alone, with low affinity for IL-2. We have previously reported that IL-5-stimulated B cells are induced to express the 55K chain. We report here evidence for the differential regulation of the expression of the two chains, namely that IL-4 and IL-5 can independently induce expression of the 70-75K and 55K chains respectively on murine B cells. As expected, cells stimulated to express the 55K chain alone are unresponsive to IL-2, whereas cells stimulated to express either the 70-75K chain or the 70-75/55K heterodimer respond to IL-2, at a high and low ligand concentration respectively, with a marked increase in proliferation. This orchestration of receptor expression and factor responsiveness may represent a novel activation pathway for B cells, where the two chains of a compound receptor are shown to be independently regulated.     

Role of Notch expression in premature senescence of murine bone marrow stromal cells

The aim of the present study was to investigate the role of the Notch signaling pathway in premature senescence of murine bone marrow stromal cells in vitro. The intracellular domain of Notch 1 (ICN) was transfected into cultured murine bone marrow stromal cells by lipofectamine transfection. After three days, the proliferation of transfected cells was measured by MTT assay. Cell cycle distribution was analyzed by flow cytometry. Senescence-associated beta-galactosidase (SA-beta-gal) was measured, and the percentage of positive cells was evaluated by assessing 1000 cells in random fields of view. The expressions of p53 and p21Cip1/Waf1 were analyzed by both RT-PCR and Western blot analysis. The results showed that activation of Notch signaling inhibited proliferation of murine bone marrow stromal cells with induction of G1 arrest, increased the percentage of SA-beta-gal positive cells, and upregulated p53 and p21Cip1/Waf1 mRNA and protein expression levels. Thus, the activated Notch signaling could induce premature senescence of bone marrow stromal cells through the p53-p21Cip1/Waf1 pathway.     

VPA及其同系物对PrPc在小鼠胚胎干细胞表达的影响

PrP^c在小鼠胚胎干细胞诱导分化形成的胚胎小体（EBs)中有所表达，其表达水平与丙戊酸（VPA）及其衍生物（VPA-A，VPA-B，VPA-C）的DCF值、ROS产量以及VPA-E的浓度成正比，VPA及其衍生物可以使PrP^c的表达上调，抗氧化剂维生素E（V-E）和VPA共同使用，可使VPA诱发的PrP^c表达减少，VPA及其衍生物处理的（EBs)的PrP^c表达水平与它们的胚胎毒性相一致，胚胎毒性越大，PrP^c表达越多，以上结果表明，PrP^c的表达与细胞的氧化还原状态相关，PrP^c很可能参与细胞的抗氧化防御过程。     

Regulation of T-cell receptor gamma-chain RNA expression in murine Thy-1+ dendritic epidermal cells

The epidermis of normal mice contains two distinct populations of dendritic cells derived from the bone marrow, Ia+ Langerhans cells and Ia- cells that express the Thy-1 alloantigen. The Thy-1-bearing dendritic epidermal cells (Thy-1+ dEC) have a surface phenotype similar to that of very early T-lineage cells, produce IL-2-like growth factors and exhibit cytotoxicity which is not restricted by the major histocompatibility complex (MHC). The relationship of Thy-1+ dEC to the T-cell lineage is unclear. Most T lymphocytes bear a receptor for antigen composed of an alpha chain and a beta chain associated with a nonpolymorphic complex termed CD3 (T3). A minor population carries a receptor in which CD3 is associated with a gamma/delta complex. We have analysed clones of Thy-1+ dEC for rearrangement and expression of the genes for the alpha-, beta- and gamma-chains of the T-cell receptor (TCR). They do not express alpha or beta but do carry a gamma/delta complex. Activation of the cells with Con A is associated with a rapid decrease in the steady-state level of gamma-chain RNA. Because Thy-1+ dEC resemble early stage T lymphocytes, down-regulation of TCR expression may reflect a necessary event during T cell differentiation.