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1.
Jaspamide (jasplakinolide) is a natural peptide isolated from marine sponges of Jaspis species and has fungicidal and growth-inhibiting activities. We characterized the jasplakinolide-induced loss of viability
by programmed cell death in the HL-60 human promyelocytic leukemia cell line and found that this process was accompanied by
neutral endopeptidase (NEP)/CD10 expression on the surface of the apoptotic cells. HL-60 cells do not normally express detectable
amounts of NEP/CD10 on their surface or intracytoplasmically, but upon jaspamide treatment, CD10 was synthesized de novo,
its expression being inhibited by cycloheximide pretreatment. Once synthesized, NEP/CD10 interfered with the jasplakinolide
signal delivered to HL-60 cells. Inhibition of NEP/CD10 by the NEP inhibitor phosphoramidon or by an anti-CD10 monoclonal
antibody significantly increased apoptosis induction. The appearance of CD10 on the cell surface was blocked by preincubation
of the cells with the monocytic/macrophage-differentiating agents vitamin D3 and phorbol 12-myristate 13-acetate, but not
by the granulocytic differentiating agents retinoic acid or dimethyl sulfoxide. Moreover, in the promonocytic U937 and mature
monocytic THP-1 cell lines, jaspamide induced apoptosis but not CD10 expression. In HL-60 cells, CD10 expression was partially
but not totally blocked by the broad-spectrum caspase inhibitor benzyloxacarbonyl-Val-Ala-Asp-fluoromethylketone, indicating
a connection between apoptosis induction and CD10 synthesis. Our findings suggest that the CD10 expression is related to the
programmed cell death induction by jaspamide, and also with the process of granulocytic differentiation in HL-60 cells.
Received 22 April 2002; received after revision 8 June 2002; accepted 10 June 2002 相似文献
2.
MDA-MB-468 is a human mammary adenocarcinoma cell line that overexpresses the epidermal growth factor (EGF) receptor and
undergoes programmed cell death (apoptosis) in response to EGF treatment. Programmed cell death was shown to be greatly enhanced
when cells were growth-arrested prior to EGF treatment. Apoptosis was characterized by an initial rounding up and detachment
of the cells from their substrate starting about 12 h after EGF treatment, followed by chromatin condensation, nuclear fragmentation
and oligonucleosomal fragmentation of the DNA at about 24 to 48 h. Cell death was dependent on de novo protein synthesis.
We found a rapid induction of c-fos, c-jun and junB at the mRNA level after about 30 min of EGF treatment and a more delayed upregulation of fosB and fra-1. The junD gene was expressed in the absence of EGF, and it was moderately induced within 30 min of growth factor addition. The increase
of the different fos and jun mRNAs were paralleled by an increase of activator protein-1 (AP-1) DNA binding activity. A characterization of the AP-1 complex
revealed similar levels of several Fos and Jun proteins. Based on the kinetics of AP-1 accumulation and cell death, it seems
likely that AP-1 contributes to the apoptotic cell death of EGF receptor-overexpressing MDA-MB-468 cells.
Received 21 July 1997; received after revision 6 November 1997; accepted 6 November 1997 相似文献
3.
TNF-related apoptosis-inducing ligand (TRAIL) induces apoptosis in TRAIL-sensitive human malignant glioma cells. We show for
the first time that TRAIL stimulates cell growth in TRAIL-resistant glioma cells. TRAIL-induced cell growth in resistant cells
occurred through increased cell cycle progression as determined by flow cytometry and Western blot analysis of retinoblastoma
protein phosphorylation. Western blot analysis of TRAIL-treated resistant cells revealed phosphorylation of ERK1/2 proteins
and in vitro kinase analysis confirmed the activation of the ERK1/2 kinases. Inhibition of MEK1 eliminated both TRAIL-induced ERK1/2 activation
and cell proliferation. In addition, siRNA inhibition of c-FLIP expression eliminates TRAIL-induced ERK1/2 activation and
proliferation. Furthermore, overexpression of c-FLIPL potentiates TRAIL-induced ERK1/2 activation and proliferation of resistant glioma cells. Our results have shown for the first
time that TRAIL-induced ERK1/2 activation and proliferation of TRAIL-resistant human glioma cells is dependent upon the expression
of the long form of the caspase-8 inhibitor c-FLIPL.
Received 2 November 2007; received after revision 14 December 2007; accepted 21 December 2007 相似文献
4.
5.
The processing and presentation of endogenous and exogenous antigen by Schwann cells in vitro 总被引:1,自引:0,他引:1
Lilje O 《Cellular and molecular life sciences : CMLS》2002,59(12):2191-2198
The expression of major histocomatibility complex class II in vitro and in vivo by Schwann cells indicates a potential facultative
role of Schwann cells in the presentation of antigen to neuritogenic T cells during inflammatory demyelinating neuropathies.
Using a T cell proliferation assay, this study demonstrated that processing and presentation of endogenous and exogenous antigen
by Schwann cells influences T cell proliferation. Statistical analysis of proliferation and its relation to processing and
presentation of antigen by Schwann cells had not been previously addressed. Different combinations of factors including treatment
of cultures (untreated, irradiated or fixed), concentration of exogenous antigen (0 or 40 μmg/ml), the presence of interferon-γ
and the timing of exogenous antigen addition influence the proliferation P2-specific, non-mammalian protein ovalbumin-specific T cell lines and naive T cells.
Received 25 July 2002; received after revision 9 September 2002; accepted 7 October 2002 相似文献