生物
XBP1型
骨形态发生蛋白2
细胞生物学
牙周纤维
分子生物学
自噬
细胞凋亡
细胞生长
生物化学
基因
医学
牙科
RNA剪接
核糖核酸
体外
作者
Ziwei Cui,Ruoshan Qin,Jiarong Feng,Ling Yuan,Xin Zhou,Xiaodong Qin,Yanmin Li,Zhidong Zhang,Xiangyi He
出处
期刊:Tissue & Cell
[Elsevier]
日期:2023-08-01
卷期号:83: 102139-102139
被引量:2
标识
DOI:10.1016/j.tice.2023.102139
摘要
The endoplasmic reticulum stress (ERS) pathway, inositol-requiring enzyme-1 alpha-X-box binding protein-1 (IRE1α-XBP1), has been considered as a critical factor of human periodontal ligament cells (hPDLCs) in proliferation and osteogenesis. This study aimed to explore the effect and mechanism of XBP1s, which was cleaved by IRE1α on the proliferation and osteogenesis of hPDLCs.ERS model was induced by tunicamycin (TM); cell proliferation was assessed by CCK-8 assay; pLVX-XBP1s-hPDLCs cell line was established by lentivirus infaction; expression of ERS-related protein including eIF2α, GRP78, ATF4 and XBP1s, autophagy-related P62 and LC3, and apoptosis-related Bcl-2 and Caspase-3 were detected by Western Blot; expression of osteogenic genes was detected by RT-qPCR, and senescence of hPDLCs was explored by β-galactosidase staining. Furthermore, the interaction between XBP1s and human bone morphogenetic protein 2 (BMP2) was examined by immunofluorescence antibody test (IFAT).The results showed an increase in proliferation of hPDLCs from 0 to 24 h when ERS was induced by TM treatment (P < 0.05). XBP1s overexpression induced hPDLCs proliferation, upgraded autophagy and degraded apoptosis significantly (P < 0.05). In pLVX-XBP1s-hPDLCs, the ratio of senescent cells was markedly decreased after several passages (P < 0.05); After infection with pLVX-BMP2 lentiviral supernatant, IFAT result showed that XBP1s and BMP2 well co-located in the cytoplasm of pLVX-XBP1s-hPDLCs and PERK-ATF4 ERS branch was activated, meanwhile, there were obviously more mineralized nodules and mRNA expression of osteogenesis-related genes was continually up-regulated (P < 0.05).XBP1s promotes the proliferation via regulating the autophagy and apoptosis, and enhances expression of osteogenic genes in hPDLCs. The mechanisms in this regard need exploring further for periodontal tissue regeneration, functionalization and clinical applications.
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