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9篇 您的检索式:作者名="Kontargiris"
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1Ectopic expression of clusterin/apolipoprotein J or Bcl-2 decreases the sensitivity of HaCaT cells to toxic effects of ropivacaine显示文摘Local anesthetics inhibit cell proliferation and induce apoptosis in various cell types. Ropivacaine, a unique, novel tertiary amine-type anesthetic, was shown to inhibit the proliferation of several cell types including keratinocytes. We found that Ropivacaine could inhibit the proliferation and induce apoptosis in an immortalized human keratinocyte line, HaCaT, in a dose- and time-dependent manner and with the deprivation of serum. The dose-dependent induction of apoptosis by ropivacaine was demonstrated by DNA fragmentation analysis and the proteolytic cleavage of a caspase-3 substrate — poly (ADP-ribose) polymerase (PARP). In addition, ropivacaine downregulated the expression of clusterin/ apoliporotein J, a protein with anti-apoptotic properties, in a dose-dependent manner, which well correlated with the induction of apoptosis of HaCaT cells. To investigate the role of clusterin/apoliporotein J in ropivacaine-induced apoptosis, HaCaT cells overexpressing clusterin/apoliporotein J were generated and compared to cells expressing the well estab- lished anti-apoptotic Bcl-2 protein. Ectopic overexpression of the secreted form of clusterin/apoliporotein J or Bcl-2 decreased the sensitivity of HaCaT cells to toxic effects of ropivacaine as demonstrated by DNA fragmentation, the proteolytic cleavage of PARP and by a reduction in procaspase-3 expression. Furthermore, the downregulation of endogenous clusterin/apolipoprotein J levels by ropivacaine suggested that this might be one mechanism by which ropivacaine induced cell death in HaCaT cells. In conclusion, the ability of ropivacaine to induce antiproliferative responses and to suppress the expression of the anti-apoptotic protein clusterin/apolipoprotein J, combined with previ- ously reported anti-inflammatory activity and analgesic property of the drug, suggests that ropivacaine may have poten- tial utility in the local treatment of tumors.Evangelos KONTARGIRIS Evangelos KOLETTAS Athina VADALOUCA Ioannis P. TROUGAKOS Efstathios S. GONOS Vasiliki KALFAKAKOU 2004Cell Research2004,14,5:2
2Bcl-2 blocks 2-methoxyestradiol induced leukemia cell apoptosis by a p27Kip1-dependent G1/S cell cycle arrest in conjunction with NF-~B activation显示文摘Batsi C Markopoulou S Kontargiris E 2009Biochem Pharmacol2009,78,1:1
3Bcl-2 blocks 2-me- thoxyestradiol induced leukemia cell apoptosis by a p27( Kipl )-de- pendent Gl/S cell cycle arrest in conjunction with NF-kappaB activa- tion 显示文摘Batsi C Markopoulou S Kontargiris E 2009Biochem Pharmacol2009,78,1:1
4Bcl-2 blocks 2-methoxyestradiol induced leukemia cell apoptosis by a p27 (Kip1)-dependent G1/S cell cycle arrest in conjunction with NF-kappaB activation显示文摘Batsi C Markopoulou S Kontargiris E Charalambous C Thomas C Christoforidis S 0,,:1
5Bcl-2 blocks 2-metheoestradiol induced leukemia cell apoptosis by a p27 (Kip1)-dependent G1/S cell cycle arrest in conjunction with NF-kappaB activation显示文摘BATSI C MARKOPOULOU S KONTARGIRIS E 2009Biochem Pharmacol2009,78,:1
6Zinc Inhibits Apoptosis and Maintains NEP Downregulation, Induced by Ropivacaine, in HaCaT Cells 显示文摘Kontargiris E Vadalouka A Ragos V 2012Biol Trace Elem Res2012,150,13:1
7Bcl-2 blocks 2-methoxyestradiol induced leukemia cell apoptosis by a p27Kip1-dependent G1/S cell cycle arrest in conjunction with NF-κB activation显示文摘Batsi C Markopoulou S Kontargiris E 2009Biochem Pharmacol2009,78,1:1
8Bcl-2 blocks 2-methoxyestradiol induced leukemia cell apoptosis by a p27(Kip1)-dependent G1/S cell cycle arrest in conjunction with NF-kB activation显示文摘Batsi C Markopoulou S Kontargiris E 2009Biochem Pharmacol2009,78,1:1
9Bcl- 2 blocks 2-methoxyestradiol induced leukemia cell apoptosis by a p27(Kip1)-dependent G1/S cell cycle arrest in conjunction with NF-kappa B activation 显示文摘BATSI C MARKOPOULOU S KONTARGIRIS E 2009Biochem Pharmacol2009,78,1:1
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