Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 2 de 2
Filter
Add filters








Language
Year range
1.
Journal of Experimental Hematology ; (6): 533-536, 2007.
Article in Chinese | WPRIM | ID: wpr-276878

ABSTRACT

The aim of this study was to detect the expression and cell cycle specificity of Fas, TNFRI and TNFRII in human peripheral blood lymphocytes (PBL), and to study the potential role of Fas, TNFRIand TNFRII in cell cycle specific apoptosis. The improved double-parameter flow cytometry was used to detect the expressions of Fas, TNFRI and TNFRII and cell cycle specificity in PBL which were incubated for 24 hours in the presence or absence of phytohaematoagglutinin (PHA) respectively. Apoptosis induced by IgM type anti-Fas and TNF-alpha was detected by API method. The results showed that compared with PBL treated in the absence of PHA in G(0) phase, the ratio of Fas, TNFRI and TNFRII expressions in PHA-stimulated PBL entering cell cycle increased (35.55 +/- 6.63)%, (30.63 +/- 2.66)%, (26.62 +/- 5.14)% respectively (P < 0.01), and mainly appeared at G(1)-phase; no apoptosis was induced by anti-Fas and TNF-alpha in G(0)-phase PBL cultured in the absence of PHA. On the contrary, the apoptosis was induced by anti-Fas and TNF-alpha in PBL which entered cell cycle after stimulation with PHA and mainly initiated at G(1)-Phase. It is concluded that there is evident dose-effect relationship between apoptotic receptor and receptor-mediated apoptosis. Moreover, the cell cycle specificity of receptor-mediated apoptosis is correlated with the cell cycle specific expressions of apoptotic receptor. The induction of apoptosis by apoptotic factors (anti-Fas and TNF-alpha) depends on whether cell entering cell cycle or not.


Subject(s)
Humans , Apoptosis , Cell Cycle , Lymphocytes , Cell Biology , Receptors, Tumor Necrosis Factor, Type I , Metabolism , Receptors, Tumor Necrosis Factor, Type II , Metabolism , fas Receptor , Metabolism
2.
Acta Academiae Medicinae Sinicae ; (6): 401-405, 2003.
Article in Chinese | WPRIM | ID: wpr-327072

ABSTRACT

<p><b>OBJECTIVE</b>To investigate apoptosis induced by sodium butyrate in cervix cancer cell line HeLa and primary human embryo lung fibroblasts and its mechanism.</p><p><b>METHODS</b>Cell apoptosis was assessed by morphology, cell viability, DNA fragmentation, the percentage of sub-G1 cells and phosphatidylserine (PS) externalization. The effects of sodium butyrate on transcription of Bax and Bcl-2 was analyzed by RT-PCR.</p><p><b>RESULTS</b>Sodium butyrate inhibited proliferation in a time and dose-dependant manner. The inhibition of proliferation in HeLa cells was more significant than that in primary human embryo lung fibroblasts. DNA fragmentation, sub-G1 peak and AnnexinV/PI by flow cytometry showed very high apoptosis rates in HeLa cells 72 hours after treated with sodium butyrate, while pretty low in primary human embryo lung fibroblasts. RT-PCR showed sodium butyrate had little effects on transcription of Bax and Bcl-2 in HeLa cells.</p><p><b>CONCLUSION</b>Sodium butyrate can induce apoptosis in HeLa cells without changing the expression of Bax and Bcl-2. Sodium butyrate comparatively has little effects on fibroblasts.</p>


Subject(s)
Female , Humans , Antineoplastic Agents , Pharmacology , Apoptosis , Butyrates , Pharmacology , Cell Division , DNA Fragmentation , Flow Cytometry , HeLa Cells , Proto-Oncogene Proteins , Genetics , Proto-Oncogene Proteins c-bcl-2 , Genetics , Reverse Transcriptase Polymerase Chain Reaction , bcl-2-Associated X Protein
SELECTION OF CITATIONS
SEARCH DETAIL