2009•PubMedRequires access

[Mechanism of inhibition of apoptosis of human umbilical vein endothelial cells induced by oxidized-low density lipoprotein by erythropoietin].

Xiao-fang Yang, Jian Xiong, Zhilu Wang, Yan Li, Zhe-tong Xu, Lijun Cui, Feng Wang, Lili Tan, Li Zhang

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Abstract

OBJECTIVE: To explore the protective effect of erythropoietin (EPO) against oxidized-low density lipoprotein (ox-LDL)-induced apoptosis in human umbilical vein endothelial cells (HUVECs) in an ox-LDL induced apoptosis model. METHODS: Third-sixth passage of cultured HUVECs were used, and they were divided into two groups. The cells were pretreated with different concentrations (6.25, 50, 100 kU/L) of recombinant human erythropoietin (rhEPO) for 24 hours, then they were exposed to ox-LDL (100 mg/L) for 48 hours; another group of cells were pretreated with antisense to 0.5 micromol/L LOX-1 mRNA or 0.5 micromol/L sense for 24 hours, and then HUVECs were exposed to ox-LDL (100 mg/L) for 12 hours. Apoptosis was assessed by the apoptosis ratio, cell viability, and Bcl-2/Bax ratio. RESULTS: As compared to untreated controls, pretreatment with rhEPO led to increased cell survival of HUVECs and decreased cell apoptosis in a dose-dependent manner (all P<0.05). Consistently, the Bcl-2/Bax ratios were also increased in a similar fashion. The ratio of apoptosis protein Bcl-2/Bax was increased in the antisense LOX-1 mRNA group than that of ox-LDL group (P<0.05), but the one in the sense LOX-1 mRNA group was not significantly different from that of ox-LDL group. CONCLUSION: The ox-LDL can induce apoptosis in HUVECs by regulating LOX-1 mRNA, and rhEPO can increase Bcl-2/Bax ratio and inhibit ox-LDL-induced apoptosis of HUVECs.

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What this paper is about

OBJECTIVE: To explore the protective effect of erythropoietin (EPO) against oxidized-low density lipoprotein (ox-LDL)-induced apoptosis in human umbilical vein endothelial cells (HUVECs) in an ox-LDL induced apoptosis model. METHODS: Third-sixth passage of cultured HUVECs were used, and they were divided into two groups. The cells were pretreated with different concentrations (6.25, 50, 100 kU/L) of recombinant human erythropoietin (rhEPO) for 24 hours, then they were exposed to ox-LDL (100 mg/L) for 48 hours; another group of cells were pretreated with antisense to 0.5 micromol/L LOX-1 mRNA or 0.5 micromol/L sense for 24 hours, and then HUVECs were exposed to ox-LDL (100 mg/L) for 12 hours. Apoptosis was assessed by the apoptosis ratio, cell viability, and Bcl-2/Bax ratio. RESULTS: As compared to untreated controls, pretreatment with rhEPO led to increased cell survival of HUVECs and decreased cell apoptosis in a dose-dependent manner (all P<0.05). Consistently, the Bcl-2/Bax ratios were also increased in a similar fashion. The ratio of apoptosis protein Bcl-2/Bax was increased in the antisense LOX-1 mRNA group than that of ox-LDL group (P<0.05), but the one in the sense LOX-1 mRNA group was not significantly different from that of ox-LDL group. CONCLUSION: The ox-LDL can induce apoptosis in HUVECs by regulating LOX-1 mRNA, and rhEPO can increase Bcl-2/Bax ratio and inhibit ox-LDL-induced apoptosis of HUVECs.

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Available abstract

OBJECTIVE: To explore the protective effect of erythropoietin (EPO) against oxidized-low density lipoprotein (ox-LDL)-induced apoptosis in human umbilical vein endothelial cells (HUVECs) in an ox-LDL induced apoptosis model. METHODS: Third-sixth passage of cultured HUVECs were used, and they were divided into two groups. The cells were pretreated with different concentrations (6.25, 50, 100 kU/L) of recombinant human erythropoietin (rhEPO) for 24 hours, then they were exposed to ox-LDL (100 mg/L) for 48 hours; another group of cells were pretreated with antisense to 0.5 micromol/L LOX-1 mRNA or 0.5 micromol/L sense for 24 hours, and then HUVECs were exposed to ox-LDL (100 mg/L) for 12 hours. Apoptosis was assessed by the apoptosis ratio, cell viability, and Bcl-2/Bax ratio. RESULTS: As compared to untreated controls, pretreatment with rhEPO led to increased cell survival of HUVECs and decreased cell apoptosis in a dose-dependent manner (all P<0.05). Consistently, the Bcl-2/Bax ratios were also increased in a similar fashion. The ratio of apoptosis protein Bcl-2/Bax was increased in the antisense LOX-1 mRNA group than that of ox-LDL group (P<0.05), but the one in the sense LOX-1 mRNA group was not significantly different from that of ox-LDL group. CONCLUSION: The ox-LDL can induce apoptosis in HUVECs by regulating LOX-1 mRNA, and rhEPO can increase Bcl-2/Bax ratio and inhibit ox-LDL-induced apoptosis of HUVECs.

Key concepts: Apoptosis, Umbilical vein, Erythropoietin, Medicine, Human umbilical vein endothelial cell, Messenger RNA, Lipoprotein, Molecular biology

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