• Title, Summary, Keyword: apoptosis

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Expression of Tumor Necrosis Factor (TNF)-z${\alpha}$ from Cells Undergoing Death by FADD

  • Kim, Koanhoi
    • Journal of Life Science
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    • v.12 no.2
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    • pp.57-60
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    • 2002
  • Apoptosis of vascular smooth muscle cell is observed in the vascular diseases such as atherosclerosis and restenosis. The death of vascular smooth muscle cells can be induced by cytokines and activation of Fas-pathways. It is widely accepted that apoptosis occurs without inflammation. There are, however, reports that apoptosis is not silent. Vascular smooth muscle cells dying by Fas-pathway secreted inflammatory cytokines including monocyte chemoattractant protein-1. This study have investigated whether apoptosis is associated with potent inflammatory cytokine tumor tumor necrosis factor (TNF)-${\alpha}$. The cells which undergo apoptosis by expressing FADD in the absence of tetracycline expressed and secreted TNF-${\alpha}$. When the level of TNF-${\alpha}$ transcript was investigated, dying smooth muscle cells exhibited transcriptional activation of TNF-${\alpha}$. The data indicate that dying vascular smooth muscle cells contribute to inflammation by expressing inflammatory cytokines. The present study suggests that apoptosis could not be silent in certain pathological situations.

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Effect of Glycyrrhizin on Apoptosis of Transplanted-L1210 cells in mice (글리시르히진이 생쥐에 이식된 L1210 세포의 아포프토시스에 미치는 영향)

  • Eun, Jae-Soon;Kwon, Jin;Oh, Chan-Ho
    • YAKHAK HOEJI
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    • v.42 no.3
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    • pp.324-329
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    • 1998
  • These experiments were conducted to investigate effects of glycyrrhizin (GL) on apoptosis of transplanted-L1210 cells in mice. GL induced apoptosis of transplanted-Ll2lO cells. GL increased nitric oxide production from peritoneal macrophages of L1210 cells-transplanted mice. NOC12, nitric oxide donor, induced apoptosis of L1210 cells in vitro. The apoptosis of L1210 cells were enhanced by co-culture of the peritoneal macrophages of GL-administered mice and L1210 cells in vitro, and was inhibited by L-NMMA. These results suggest that the apoptosis of transplanted-Ll2lO cells is partly induced by nitric oxide produced from peritoneal macrophages in GL-administered mice.

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Increased Expression of c-jun in the Bile Acid-Induced Apoptosis in Mouse F9 Teratocarcinoma Stem Cells

  • Baek, Jin-Hyen;Kang, Chang-Mo;Chung, Hae-Young;Park, Myung-Hwan;Kim, Kyu-Won
    • BMB Reports
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    • v.29 no.1
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    • pp.68-72
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    • 1996
  • Ursodeoxycholic acid (UDCA) and lithocholic acid (LCA), secondary bile acids, have been shown to have a cell differentiation activity in mouse F9 teratocarcinoma stem cells. Treatment with bile acids induced morphological changes, including cytoplasmic and nuclear membrane blebbing, aggregation of organelles, and chromatin condensation, corresponding to apoptosis. Moreover, the bile acids induced intemucleosomal DNA fragmentation, a hallmark of apoptosis. In addition, the expression of c-jun was increased, but that of c-myc and laminin was decreased during apoptosis induced by the bile acids in F9 cells. These results suggest that the bile acids can induce apoptosis in F9 cells. Furthermore, the c-jun expression may be related to the apoptosis induced by UDCA or LCA in F9 cells.

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Distinct Roles for JNK1 and JNK3 During TNF-α- or Etoposide-Induced Apoptosis in HeLa Cells

  • Ham, Young-Mi;Lim, Jin-Hee;Lee, Seung-Ki
    • Molecules and Cells
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    • v.28 no.6
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    • pp.509-513
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    • 2009
  • Here, we show that JNK1 and JNK3 have different roles in ${\alpha}-$ or etoposide-induced apoptosis in HeLa cells. Dominant negative JNK1 inhibited $TNF-{\alpha}-$ or etoposide-induced apoptosis, while dominant negative JNK3 promoted $TNF-{\alpha}-$ or etoposide-induced apoptosis. During $TNF-{\alpha}$-induced apoptosis, JNK1 was activated in a biphasic manner, exhibiting both transient and sustained activity, whereas JNK3 was activated early and in a transient manner. The role of JNK3 activation was an anti-apoptotic effect, while the role of JNK1 activation was a pro-apoptotic effect. These results suggest that the anti-apoptotic mechanism of JNK3 in $TNF-{\alpha}$-induced apoptosis originates before the apoptotic machinery is triggered.

Apigenin Sensitizes Huh-7 Human Hepatocellular Carcinoma Cells to TRAIL-induced Apoptosis

  • Kim, Eun-Young;Kim, An-Keun
    • Biomolecules & Therapeutics
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    • v.20 no.1
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    • pp.62-67
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    • 2012
  • TNF-related apoptosis-inducing ligand (TRAIL) is a promising agent for management of cancer because of its selective cytotoxicity to cancer cells. However, some cancer cells have resistance to TRAIL. Accordingly, novel treatment strategies are required to overcome TRAIL resistance. Here, we examined the synergistic apoptotic effect of apigenin in combination with TRAIL in Huh-7 cells. We found that combined treatment of TRAIL and apigenin markedly inhibited Huh-7 cell growth compared to either agent alone by inducing apoptosis. Combined treatment with apigenin and TRAIL induced chromatin condensation and the cleavage of poly (ADP-ribose) polymerase (PARP). In addition, enhanced apoptosis by TRAIL/apigenin combination was quantified by annexin V/PI flow cytometry analysis. Western blot analysis suggested that apigenin sensitizes cells to TRAIL-induced apoptosis by activating both intrinsic and extrinsic apoptotic pathway-related caspases. The augmented apoptotic effect by TRAIL/apigenin combination was accompanied by triggering mitochondria-dependent signaling pathway, as indicated by Bax/Bcl-2 ratio up-regulation. Our results demonstrate that combination of TRAIL and apigenin facilitates apoptosis in Huh-7 cells.

Cysteine Participates in Cell Proliferation by Inhibiting Caspase3-like Death Protease

  • Lee, Sang-Han;Hong, Soon-Duck
    • Journal of Life Science
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    • v.9 no.1
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    • pp.9-13
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    • 1999
  • Reduced thiols were important compounds for the maintenance of leukemia and lymphoma cell survival (and growth). In the course of examining the microenvirn-mental effects on lymphoma and leukemia cell growth, we found that cysteine suppressed apoptosis in these cells. In a present study, in order to investigate the role of cystein on the suppression of apoptotic cell death, we used CS21, P388, and L1210 cell lines. The addition of BSO, an inhibitor of glutathione synthase, induced apoptosis of these cells by blocking the cellular uptake of cysteine in CS21 cells. Although L1210 cells underwent apoptosis without thiol compounds, the addition of these compounds suppressed the apoptosis and promoted the growth or L1210 cells. When specific inhibitors of caspase3-like proteases, but not caspase1-like proteases, were activated during the L1210 cell apoptosis but the addition of thiol compounds suppressed the activation of caspase3-like proteases. These results suggest that reduced thiols including cysteine play an important role in the suppression of cell apoptosis by inhibiting the activation of caspase3-like proteases.

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Development of Apoptosis Model and Bioimmune Responses in Experimental Animal I. Induction and Indicator of Apoptosis and Hepatic Tumorigenesis (실험동물에서 Apoptosis의 모델개발과 생체면역반응 및 형태학적 특징 I. Apoptosis 및 Hepatic Tumorigenesis의 유도 및 관련지표의 검색)

  • 강정부;하우송;김지경
    • Journal of Veterinary Clinics
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    • v.16 no.1
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    • pp.100-107
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    • 1999
  • Apoptosis is now widely recognized as a common form of cell death and represents mechanism of cell clearance in many physiological situations where deletion of cells is required. In vivo administration of bacterial lipopolysaccharide (LPS) to Balb/c mice induced DNA fragmentation in the thymus. DNA fragmentation in the thymus was roughly dependent on the dose of LPS injected and reached the peak 18 hours after injection. This apoptosis in the thymus might be mediated due to LPS stimulant. DEN (diethylnitrosamine) has been shown to cause liver cancer in experimental animals and humans. The hepatic tumorigenesis was induced by ad libitum feeding of DEN only. It was suggested that DEN induced hepatic tumorgenesis in rat is a good reproducible model for studying biochemical and pathophysiological changes associated with the development of hepatic tumorigenesis and apoptosis.

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Antiapoptotic Fusion Protein Delivery Systems

  • Tan, Cheau Yih;Kim, Yong-Hee
    • Macromolecular Research
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    • v.16 no.6
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    • pp.481-488
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    • 2008
  • Apoptosis is a natural cell suicide mechanism to maintain homeostasis. However, many of the diseases encountered today are caused by aberrant apoptosis where excessive apoptosis leads to neurodegenerative disorders, ischemic heart disease, autoimmune disorders, infectious diseases, etc. A variety of antiapoptotic agents have been reported to interfere with the apoptosis pathway. These agents can be potential drug candidates for the treatment or prevention of diseases caused by dysregulated apoptosis. Obviously, world-wide pharmaceutical and biotechnology companies are gearing up to develop antiapoptotic drugs with some products being commercially available. Polymeric drug delivery systems are essential to their success. Recent R&D efforts have focused on the chemical or bioconjugation of antiapoptotic proteins with the protein transduction domain (PTD) for higher cellular uptake with antibodies for specific targeting as well as with polymers to enhance the protein stability and prolonged effect with success observed both in vivo and in vitro. All these different fusion antiapoptotic proteins provide promising results for the treatment of dysregulated apoptosis diseases.

A Phospholipase C-Dependent Intracellular $Ca^{2+}$ Release Pathway Mediates the Capsaicin-Induced Apoptosis in HepG2 Human Hepatoma Cells 73

  • Kim Jung-Ae;Kang Young Shin;Lee Yong Soo
    • Archives of Pharmacal Research
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    • v.28 no.1
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    • pp.73-80
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    • 2005
  • The effect of capsaicin on apoptotic cell death was investigated in HepG2 human hepatoma cells. Capsaicin induced apoptosis in time- and dose-dependent manners. Capsaicin induced a rapid and sustained increase in intracellular $Ca^{2+}$ concentration, and BAPTA, an intracellular $Ca^{2+}$ chelator, significantly inhibited capsaicin-induced apoptosis. The capsaicin-induced increase in the intracellular $Ca^{2+}$ and apoptosis were not significantly affected by the extracellular $Ca^{2+}$ chelation with EGTA, whereas blockers of intracellular $Ca^{2+}$ release (dantrolene) and phospholipase C inhibitors, U-73122 and manoalide, profoundly reduced the capsaicin effects. Interestingly, treatment with the vanilloid receptor antagonist, capsazepine, did not inhibit either the increased capsaicin-induced $Ca^{2+}$ or apoptosis. Collectively, these results suggest that the capsaicin-induced apoptosis in the HepG2 cells may result from the activation of a PLC-dependent intracellular $Ca^{2+}$ release pathway, and it is further suggested that capsaicin may be valuable for the therapeutic intervention of human hepatomas.

Stigmasterol isolated from marine microalgae Navicula incerta induces apoptosis in human hepatoma HepG2 cells

  • Kim, Young-Sang;Li, Xi-Feng;Kang, Kyong-Hwa;Ryu, BoMi;Kim, Se Kwon
    • BMB Reports
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    • v.47 no.8
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    • pp.433-438
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    • 2014
  • Plant sterols have shown potent anti-proliferative effects and apoptosis induction against breast and prostate cancers. However, the effect of sterols against hepatic cancer has not been investigated. In the present study, we assessed whether the stigmasterol isolated from Navicula incerta possesses apoptosis inductive effect in hepatocarcimona (HepG2) cells. According to the results, Stigmasterol has up-regulated the expression of pro-apoptotic gene expressions (Bax, p53) while down-regulating the anti-apoptotic genes (Bcl-2). Probably via mitochondrial apoptosis signaling pathway. With the induction of apoptosis caspase-8, 9 were activated. The DNA damage and increase in apoptotic cell numbers were observed through Hoechst staining, annexin V staining and cell cycle analysis. According to these results, we can suggest that the stigmasterol shows potent apoptosis inductive effects and has the potential to be tested as an anti-cancer therapeutic against liver cancer.