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  • A putative sub-10-kDa basement membrane activity required for lung alveolar formation in vitro. 8843800

    Basement membrane promotes the reassembly of isolated type II alveolar cells into alveoli-like structures, a process attributable in part to a novel cell adhesion site in the alpha 1-chain of laminin-1 (M. L. Matter and G. W. Laurie. J. Cell Biol. 124: 1083-1090, 1994). The possibility that basement membrane contains other alveolarization activities was probed by subtraction analysis and use of neutralizing antibodies. Deletion of components 100 kDa, and subsequently 10 kDa, reduced alveolar cross-sectional area by 70% to 22-25 x 10(3) microns2: the approximate size of alveolar-like structures formed on purified laminin-1 alone. The deleted basement membrane material was adhesive for type II alveolar cells but failed to support alveolar formation in the absence of laminin-1. Preincubation of basement membrane with neutralizing anti-epidermal growth factor (EGF), -basic fibroblast growth factor (bFGF), -insulin-like growth factor (IGF)II, or -transforming growth factor (TGF)-beta antibodies had no inhibitory effect. Because both subtracted basement membrane preparations have in common the exclusion of components 10 kDa, these results are interpreted as pointing to a sub-10-kDa alveolarization activity(s) that plays a key accessory role in laminin-1-dependent alveolar formation.
    Tipo de documento:
    Referencia
    Referencia del producto:
    Múltiplo
    Nombre del producto:
    Múltiplo

  • An apolipoprotein E4 fragment affects matrix metalloproteinase 9, tissue inhibitor of metalloproteinase 1 and cytokine levels in brain cell lines. 22445724

    Apolipoprotein (apo) E4 isoform, a major risk factor for Alzheimer disease (AD), is more susceptible to proteolysis than apoE2 and apoE3 isoforms. ApoE4 fragments have been found in AD patients' brain. In the present study, we examined the effect of full-length apoE4 and apoE4 fragments apoE4[Δ(186-299)] and apoE4[Δ(166-299)] on inflammation in human neuroblastoma SK-N-SH and human astrocytoma SW-1783 cells. Western blot and zymography analysis showed that treatment of SK-N-SH cells with apoE4[Δ(186-299)], but not full-length apoE4 or the shorter apoE4[Δ(166-299)] fragment, leads to increased extracellular levels of matrix metalloproteinase 9 (MMP9) and tissue inhibitor of metalloproteinase 1 (TIMP1). Real-time PCR showed that interleukin (IL)-1β gene expression is also increased in SK-N-SH cells treated with apoE4[Δ(186-299)]. Treatment of SK-N-SH cells with IL-1β leads to increased MMP9 and TIMP1 extracellular levels, suggesting that the induction of IL-1β may be the mechanism by which apoE4[Δ(186-299)] regulates MMP9 and TIMP1 levels in these cells. In contrast to SK-N-SH cells, treatment of SW-1783 cells with apoE4[Δ(186-299)], and to a lesser extent with apoE4, leads to increased TIMP1 extracellular levels without affecting MMP9 levels. Additionally, apoE4[Δ(186-299)] leads to decreased IL-10 gene expression in SK-N-SH cells, whereas both apoE4 and apoE4[Δ(186-299)] lead to decreased TNFα gene expression without affecting IL-1β and IL-10 gene expression in SW-1783 cells. Overall, our findings indicate that a specific apoE4 fragment (apoE4[Δ(186-299)]), with molecular mass similar that of apoE4 fragments detected in AD patients' brain, can influence the level of inflammatory molecules in brain cell lines. It is possible that these phenomena contribute to AD pathogenesis.
    Tipo de documento:
    Referencia
    Referencia del producto:
    AB19016
    Nombre del producto:
    Anti-MMP-9 Antibody, Catalytic domain
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