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목적 : To investigate the production of the long pentraxin 3 (PTX3) in response to tunicamycin-induced endoplasmic reticulum (ER) stress, and its role in ER stress-associated cell death. PTX3 expression was evaluated in the human retinal pigment epithelial cell line, ARPE-19.
방법 : PTX3 production in ARPE-19 cells was analyzed in the absence or presence of tunicamycin treatment by enzyme-linked immunosorbent assay (ELISA). PTX3 protein and mRNA levels were estimated by western blot analysis and real-time reverse transcription-polymerase chain reaction (RT-PCR), respectively.. Protein and mRNA levels of CCAAT-enhancer-binding protein homologous protein (CHOP) and ARPE-19 cell viability were measured in the presence of tunicamycin-induced ER stress in control or PTX3 small hairpin RNA (shRNA)-transfected ARPE-19 cells.
결과 : The protein and mRNA levels of PTX3 were found to be significantly increased by tunicamycin treatment. PTX3 production was significantly decreased in inositol-requiring enzyme 1α (IRE1α shRNA-transfected ARPE-19 cells (501 ± 2.79 pg/mL) compared to control shRNA-transfected cells (1,310 ± 1.55 pg/mL). Furthermore, pretreatment with the NF-B inhibitor abolished tunicamycin-induced PTX3 production. Decreased cell viability and prolonged protein and mRNA expression of CHOP was observed under tunicamycin-induced ER stress in PTX3 shRNA transfected ARPE-19 cells.
결론 : These results suggest that PTX3 production increased in the presence of tunicamycin-induced ER stress. Therefore, PTX3 could be an important protector of ER stress-induced cell death in human retinal pigment epithelial cells. IRE1 and the NF-B signaling pathway may serve as potential targets for regulation of PTX3 expression in the retina. Therefore, their role in PTX3 expression needs to be further investigated.
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