Hypoxia inhibits pulmonary artery endothelial cell apoptosis via the e-selectin/biliverdin reductase pathway
Shasha SongZhi YiMin ZhangMin MaoLi FuXijuan ZhaoZizhen LiuJiayin GaoWeiwei CaoYumei LiuHengyuan ShiDaling Zhu
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Hypoxia
Biliverdin reductase
Deregulated apoptosis has been associated with many lung diseases. Although many studies have reported the apoptotic effects exhibited by silver nanoparticles (Ag-NPs) in various circumstances, the apoptosis mechanism of Ag-NPs is unclear. We investigated oxidative stress and apoptosis in human normal bronchial epithelial (BEAS-2B) cells to elucidate the role of p53 in apoptosis by Ag-NPs. First, dispersion and stability of Ag-NPs improved using bronchial epithelial cell growth medium with 5% fetal bovine serum. Then, we observed oxidative stress in BEAS-2B cells exposed to Ag-NPs. Second, we carried out a cell death assay to measure DNA fragmentation as a biomarker of apoptosis. BEAS-2B cells were treated with p53-specific short interfering RNA (siRNA) or p53 inhibitor (pifithrin-α) to investigate whether p53 is involved in apoptosis by Ag-NPs. As a result, Ag-NPs significantly enhanced DNA fragmentation dose-dependently and treatment with p53 siRNA or pifithrin-α prevented DNA fragmentation. We also found that apoptosis-related genes (caspase-3, Bax, and Bcl-2) were regulated by Ag-NPs, which was detected by mRNA and protein levels. These results suggest that Ag-NPs induced p53-mediated apoptosis in BEAS-2B cells. Our findings may contribute to understanding the potential roles of Ag-NPs in pulmonary disease.
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Cell death-inducing DFF45-like effector(CIDE) is a protein which has high affinity to DNA fragmentation factors.CIDEs were important apoptosis-relevent regulators,and play an important role in DNA degradation.If DNA were degadated incompletely,the apoptosis of cell is atypical,namely paraptosis.The research developments of CIDEs in cellular apoptosis was reviewed in the article.
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Apoptosis is usually accompanied by DNA fragmentation and up-regulation of reactive oxygen species, and it can be inhibited by overexpression of Bcl-2. Here, cadmium was found to induce apoptosis in BA/F3beta cells. MTT assay, Hochest 33258 staining, and transmission electron microscopy analysis were used to detect the apoptosis, however, neither DNA fragmentation nor up-regulation of reactive oxygen species were observed in this type of apoptosis. Furthermore, Bcl-2 overexpression had no effect on this type of apoptosis. In conclusion, these data suggested that cadmium induced a novel type of apoptosis in BA/F3beta cells.
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Previous studies have shown that pseudolaric acid B (PB) would cause apoptosis in human tumor cell lines. However, the mechanisms of PB induced apoptosis are still unclear. In the present study, the mechanisms of PB induced apoptosis in the human hepatocellular carcinoma Bel-7402 cell line were investigated by measuring cell viability, rate of apoptosis, cell cycle, detecting DNA fragmentation, and measuring caspase-3 activation. The results indicated that PB inhibited Bel-7402 cell viability and induced cell death by causing DNA fragmentation, up regulating the early and late apoptotic rates, activating caspase-3 protein, and detaining the cell cycle in the G2/M phases. Additionally, PB-induced apoptosis was a dose- and time-dependent manner. These observations suggest that PB-induced apoptosis occurs through a caspase-dependent pathway and detains the cell cycle in the G2/M phase.
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본 연구는 한국산 겨우살이 물 추출물과 이것에서 분리한 렉틴 성분을 실험적으로 간암을 유도한 흰쥐에게 투여하여 이들이 간 발암억제 효과 및 그 기전의 일부인 apoptosis와의 관련성을 조사하고자 하였다. 이를 위해 80～90 g 정도로 이유된 3주령 Sprague-Dawley종을 한국산 겨우살이 물 추출물투여(100 μg/kg BW), 렉틴의 투여(10 ng/kg BW)와 DEN 투여 여부에 따라 6군으로 나누어 발암물질 투여 1주일 후부터 주 2회 복강 투여하였다. 총 사육기간은 9주간이었고, 희생시킨 후 간조직을 분리하여 조직 병리학적 변화 측정을 위한 전암성 병변의 지표인 GST-P^+ foci의 수와 면적을 측정하였고, apopotosis와의 관련성을 조사하기 위하여 apoptosis 염색, DNA fragmentation 측정 및 Bcl-2, c-IAP2, caspase-9, caspase-3, fas-L의 발현정도 측정을 위한 western blotting을 실시하였다. 그 결과 다음과 같은 결론을 얻었다. (1) 체중은 발암물질에 의해 식이 섭취가 감소하는 것을 고려하여 제한섭취를 실시하였으므로 발암물질 투여에 따른 차이는 없었으며, 겨우살이 또는 렉틴의 투여에 따른 차이도 나타나지 않았다. 간 무게는 겨우살이, 렉틴의 투여에 따른 변화는 보이지 않았으나 발암물질 투여에 따라 유의적으로 증가하였고, 체중에 대한 상대적인 간 무게에 대한 결과도 간 무게의 결과와 유사하였다. 따라서 본 연구에 사용한 투여량의 한국산 겨우살이 물 추출물 및 렉틴이 간에 독성을 나타내는 농도가 아닌 것으로 보여진다. (2) GST-P^+ foci의 수, 면적과 PCNA은 겨우살이 물 추출물과 렉틴의 투여에 따라 모두 유의적으로 감소하였고, 겨우살이 물 추출물과 렉틴에 따른 차이는 보이지 않았다. (3) 조직화학적으로 apoptosis염색한 결과와 DNA fragmentation을 측정한 결과는 모두 apoptosis에 대한 증거가 나타나지 않았다. 그러나 western blot을 측정한 결과 apoptosis을 억제하는 것으로 알려진 단백질인 Bcl-2와 IAP2는 발암물질 투여에 의해 증가된 발현 정도가 겨우살이 물추출물이나 렉틴의 투여에 따른 차이를 보이지 않았으며, apoptosis를 촉진하는 단백질인 caspase-9, fas-L의 경우에는 발암물질 투여에 의해 증가된 발현 정도가 겨우살이 물 추출물 및 렉틴의 투여시 더욱 증가되었다.
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Objective
To investigate the effect of eicosapentaenoic acid(EPA) on the apoptosis of human colon cancer SW480 cells and the mechanisms.
Methods
Mitochondrial membrane potential was detected, the quantity of cytochrome C was analyzed by Elisa kit, and the expression of cleaved caspase-9 and caspase-3 was detected by Western Blot.
Results
After treatment with EPA(0μg/mL, 42.1μg/mL, 84.2μg/mL, 168.4μg/mL), the mitochondrial membrane potential(Δψm) of SW480 cells were declined(P<0.05), the values were (99.71±0.04)%, (95.04±0.10)%, (88.65±0.41)% and (73.60±1.20)%(t=5.161, 6.302, 4.601, 5.198, all P<0.05). The quantity of cytochrome C in cytosol was increased significantly compared with no treatment group, and the values were (12.8±1.2)ng/mL, (115.5±3.5)ng/mL, (290.5±5.2)ng/mL and (262.0±12.5)ng/mL in different EPA treatment groups(t=6.345, 6.013, 5.846, 4.613, all P<0.01). The expression of cleaved caspase-9 and caspase-3 were significantly increased.
Conclusion
EPA inhibits SW480 cells growth and induces apoptosis in a dose dependent manner.This action may be mediated by mitochondria-mediated intrinsic apoptosis pathway, cytochrome C release, and caspase-9 and caspase-3 activation.
Key words:
Colon tumor; Twenty carbon five acid; SW480 cells; Cell apoptosis
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Agarose gel electrophoresis
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AIM: To compare hypoxia and hypoxia reoxygenation induced apoptosis of cardiomyocytes and to investigate the role of apoptosis in cardiomyocytes injury caused by hypoxia/reoxygenation. METHODS: Cultured neonatal rat cardiomyocytes were divided into two groups.Both groups were cultured in an incubator of 950 ml/L N 2 and 50 ml/L CO 2 for 16, 32 and 48 h. Cells of one group were put into normal incubation for 6 h after hypoxia to form the cell models of hypoxia reoxygenation injury. Morphological changes in apoptotic cardiomyocytes were measured by TUNEL staining. Apoptosis rates were measured by flow cytometer. RESULTS: Positive cells were detected by TUNEL staining. Apoptotis rates of cardiomyocytes measured by flow cytometer after hypoxia for 16,32 and 48 h were (2.9±0.5)%,(6.2±0.8)% and (26.6±3 0)% respectively.The apoptosis rates of cells undergoing hypoxia for 16,32 and 48 h followed by reoxygenation for 6 h were (5.5±0.7)%,(11.0±1.1)% and (14.2±1.6)% respectively. CONCLUSION: The apoptosis rates of cardiomyocytes increased with time of hypoxia.Reoxygenation could worsen cardiomyocytes injury,as compared with hypoxia.
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Aim To study the role of hypoxiainduced apoptosis in neonatal rat cardiomyocyte and the protection effect of nitric oxide(NO). Methods Neonatal rat cardiomyocytes were cultured in an incubator of 950 mL/L N 2 and 50 mL/L CO 2 for 16, 32 and 48 h to create cell models of hypoxia injury and detect apoptosis. And NO donor SNAP at 100 μ mol/L was added to the models. Apoptosis was detected in the hypoxia cells without or with No treatment. Results After hypoxia of 16, 32 and 48 h,the apoptosis rates of cardiomyocytes were 29% ± 05% , 62% ± 08% and 266% ± 30% , respectively. Whereas the apoptosis rates of cells treated with SNAP were 02% ± 03% , 34% ± 04% and 118% ± 12% , respectively. Conclusion Apoptosis is the main form of hypoxia injury in cardiomyocytes; NO protect cardiomyocytes from apoptosis induced by hypoxia.
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