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Low levels of Bax inhibitor-1 gene expression increase tunicamycin-induced apoptosis in human neuroblastoma SY5Y cells.

Wu D, Wang P, Wang S - Neural Regen Res (2012)

Bottom Line: In control SH-SY5Y cells, tunicamycin treatment induced endoplasmic reticulum stress-mediated apoptosis; however, after Bax inhibitor-1 gene knockdown, cell survival rates were significantly decreased and the degree of apoptosis was significantly increased following tunicamycin treatment.In addition, chromatin condensation and apparent apoptotic phenomena, such as marginalization and cytoplasmic vesicles, were observed.Our findings indicate that Bax inhibitor-1 can delay apoptosis induced by endoplasmic reticulum stress.

View Article: PubMed Central - PubMed

Affiliation: Department of Medical Genetics, School of Basic Medical Sciences, Peking University, Beijing 100191, China.

ABSTRACT
A human SH-SY5Y neuroblastoma cell line with a low level of Bax inhibitor-1 expression was established by lentivirus-mediated RNA interference and fluorescence-activated cell sorting. In control SH-SY5Y cells, tunicamycin treatment induced endoplasmic reticulum stress-mediated apoptosis; however, after Bax inhibitor-1 gene knockdown, cell survival rates were significantly decreased and the degree of apoptosis was significantly increased following tunicamycin treatment. In addition, chromatin condensation and apparent apoptotic phenomena, such as marginalization and cytoplasmic vesicles, were observed. Our findings indicate that Bax inhibitor-1 can delay apoptosis induced by endoplasmic reticulum stress.

No MeSH data available.


Related in: MedlinePlus

Effect of Bax inhibitor-1 on tunicamycin (TUN)-induced cell apoptosis.Cell apoptosis was detected using the Annexin V-FITC kit after treatment with 10 μg/mL TUN (TUN10) for 24 hours. Data (%) are expressed as mean ± SD from three independent experiments.aP < 0.05, vs. 0 μg/mL TUN-treated cells (TUN0); bP < 0.05, vs. SY5Y/B cells (one-way analysis of variance).
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Figure 4: Effect of Bax inhibitor-1 on tunicamycin (TUN)-induced cell apoptosis.Cell apoptosis was detected using the Annexin V-FITC kit after treatment with 10 μg/mL TUN (TUN10) for 24 hours. Data (%) are expressed as mean ± SD from three independent experiments.aP < 0.05, vs. 0 μg/mL TUN-treated cells (TUN0); bP < 0.05, vs. SY5Y/B cells (one-way analysis of variance).

Mentions: TUN-induced cell apoptosis was detected in both SY5Y/B and SY5Y/P cells, but the rate of apoptosis was increased in SY5Y/B cells compared with SY5Y/P cells. After treatment with 10 μg/mL TUN for 24 hours, cell apoptosis increased 24% in SY5Y/B cells compared with 14% in SY5Y/P cells (P < 0.05; Figure 4). These results suggested that inhibition of BI-1 expression in SH-SY5Y cells significantly increased sensitivity to TUN-mediated PCD upon ER stress signaling.


Low levels of Bax inhibitor-1 gene expression increase tunicamycin-induced apoptosis in human neuroblastoma SY5Y cells.

Wu D, Wang P, Wang S - Neural Regen Res (2012)

Effect of Bax inhibitor-1 on tunicamycin (TUN)-induced cell apoptosis.Cell apoptosis was detected using the Annexin V-FITC kit after treatment with 10 μg/mL TUN (TUN10) for 24 hours. Data (%) are expressed as mean ± SD from three independent experiments.aP < 0.05, vs. 0 μg/mL TUN-treated cells (TUN0); bP < 0.05, vs. SY5Y/B cells (one-way analysis of variance).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4308804&req=5

Figure 4: Effect of Bax inhibitor-1 on tunicamycin (TUN)-induced cell apoptosis.Cell apoptosis was detected using the Annexin V-FITC kit after treatment with 10 μg/mL TUN (TUN10) for 24 hours. Data (%) are expressed as mean ± SD from three independent experiments.aP < 0.05, vs. 0 μg/mL TUN-treated cells (TUN0); bP < 0.05, vs. SY5Y/B cells (one-way analysis of variance).
Mentions: TUN-induced cell apoptosis was detected in both SY5Y/B and SY5Y/P cells, but the rate of apoptosis was increased in SY5Y/B cells compared with SY5Y/P cells. After treatment with 10 μg/mL TUN for 24 hours, cell apoptosis increased 24% in SY5Y/B cells compared with 14% in SY5Y/P cells (P < 0.05; Figure 4). These results suggested that inhibition of BI-1 expression in SH-SY5Y cells significantly increased sensitivity to TUN-mediated PCD upon ER stress signaling.

Bottom Line: In control SH-SY5Y cells, tunicamycin treatment induced endoplasmic reticulum stress-mediated apoptosis; however, after Bax inhibitor-1 gene knockdown, cell survival rates were significantly decreased and the degree of apoptosis was significantly increased following tunicamycin treatment.In addition, chromatin condensation and apparent apoptotic phenomena, such as marginalization and cytoplasmic vesicles, were observed.Our findings indicate that Bax inhibitor-1 can delay apoptosis induced by endoplasmic reticulum stress.

View Article: PubMed Central - PubMed

Affiliation: Department of Medical Genetics, School of Basic Medical Sciences, Peking University, Beijing 100191, China.

ABSTRACT
A human SH-SY5Y neuroblastoma cell line with a low level of Bax inhibitor-1 expression was established by lentivirus-mediated RNA interference and fluorescence-activated cell sorting. In control SH-SY5Y cells, tunicamycin treatment induced endoplasmic reticulum stress-mediated apoptosis; however, after Bax inhibitor-1 gene knockdown, cell survival rates were significantly decreased and the degree of apoptosis was significantly increased following tunicamycin treatment. In addition, chromatin condensation and apparent apoptotic phenomena, such as marginalization and cytoplasmic vesicles, were observed. Our findings indicate that Bax inhibitor-1 can delay apoptosis induced by endoplasmic reticulum stress.

No MeSH data available.


Related in: MedlinePlus