Deng You-Ping, Liu Ying-Juan, Yang Zhan-Qiu, Wang Yan-Jun, He Bing-Yan, Liu Pin
Department of Pediatrics, Zhongnan Hospital, Wuhan University, Wuhan, Hubei 430071, P.R. China.
Medical Research Center, Zhongnan Hospital, Wuhan University, Wuhan, Hubei 430071, P.R. China.
Exp Ther Med. 2017 Jul;14(1):753-758. doi: 10.3892/etm.2017.4533. Epub 2017 Jun 1.
Human bocavirus (HBoV) is classified in the genus within the Parvoviridae family, first identified from children with respiratory diseases. Previous studies have investigated the stimulating effect of HBoV on cell apoptosis and autophagy. In the present study, human bronchial epithelial cells (HBECs) were utilized to examine the mechanism of HBoV recombination expressing vector (pWHL-1) on the promotion of cell apoptosis and autophagy. The results from the present study indicated that pWHL-1 inhibited the proliferation of HBECs in a time-dependent manner. Additionally, pWHL-1induced apoptosis, as substantiated by an increased apoptotic rate and presence of autophagosomes. Following pWHL-1 transfection, proliferating cell nuclear antigen, caspase-3 and B cell lymphoma 2 (Bcl-2) protein expression levels were decreased, with the exception of Bcl-2 associated × (Bax) protein, which increased. mRNA and protein expression levels of microtubule-associated protein 1A/1B-light chain 3 (LC3) II and autophagy protein 5 were increased in pWHL-1-transfected HBECs, whereas, the mRNA and protein levels of LC3I and sequestosome 1 were decreased. Notably, pWHL-1 also enhanced the activation of p53 and inhibited AKT activation in HBECs. Results from the present study suggest that pWHL-1 induces apoptosis and autophagy, thus providing a novel insight into the effect of HBoV and its uses in respiratory diseases.
人博卡病毒（HBoV）属于细小病毒科中的一个属，最初是从患有呼吸道疾病的儿童中鉴定出来的。先前的研究已经探讨了HBoV对细胞凋亡和自噬的刺激作用。在本研究中，利用人支气管上皮细胞（HBECs）来研究HBoV重组表达载体（pWHL-1）促进细胞凋亡和自噬的机制。本研究结果表明，pWHL-1以时间依赖性方式抑制HBECs的增殖。此外，pWHL-1诱导细胞凋亡，这通过凋亡率增加和自噬体的存在得到证实。pWHL-1转染后，增殖细胞核抗原、半胱天冬酶-3和B细胞淋巴瘤2（Bcl-2）蛋白表达水平降低，但Bcl-2相关X蛋白（Bax）除外，其表达增加。在pWHL-1转染的HBECs中，微管相关蛋白1A/1B轻链3（LC3）II和自噬蛋白5的mRNA和蛋白表达水平增加，而LC3I和聚集体蛋白1的mRNA和蛋白水平降低。值得注意的是，pWHL-1还增强了p53的激活并抑制了HBECs中AKT的激活。本研究结果表明，pWHL-1诱导细胞凋亡和自噬，从而为HBoV的作用及其在呼吸道疾病中的应用提供了新的见解。
