Wang Gaiping, Zhao Congcong, Chen Shasha, Li Xiaofang, Zhang Ling, Chang Cuifang, Xu Cunshuan
College of Life Science, Henan Normal University, No. 46, Construction East Road, Xinxiang, 453007, Henan, China.
State Key Laboratory Cultivation Base for Cell Differentiation Regulation, Henan Normal University, Xinxiang, 453007, Henan, China.
Mol Biol Rep. 2016 Dec;43(12):1371-1382. doi: 10.1007/s11033-016-4071-2. Epub 2016 Sep 1.
Osteopontin (OPN) is a member of Th1 cytokine secreted by activated lymphocytes and macrophages. However, it deserves to be studied whether OPN could promote cell activation or proliferation, and then facilitate hepatic self-repair during liver regeneration (LR). This study is designed to further reveal the effects of OPN on LR in vivo. Firstly, quantitative reverse transcription-PCR (qRT-PCR) and western blot (WB) were utilized to validate the expression profile of endogenous OPN in rat regenerating livers after partial hepatectomy (PH). Then OPN expression vector, two shRNA expression vectors and their respective test vectors were successfully constructed. Afterwards, test vectors were administrated into mouse livers via tail vein to find the more efficient shRNA. Furthermore, OPN expression vector and the more efficient shRNA expression vector were injected into rat regenerating livers, and then the changes in liver regeneration and hepatic microstructure were respectively detected by liver regeneration rate and HE staining, while the expressions of several marker genes were detected by qRT-PCR and WB. Endogenous OPN was strikingly up-regulated in both mRNA and protein level during LR, especially at 12 and 72 h after PH. The shRNA expression vector Opn(313) was found to be more efficient than Opn(887) in silencing the expression of Opn. Then OPN expression vector and Opn(313) were injected into rat remnant livers, and it showed that OPN overexpression aggravated hepatic necrosis and leukocytes infiltration, while OPN silencing inhibited liver regeneration rate and the expressions of PCNA and CCL2, but augmented that of BAX. In conclusion, OPN might enhance inflammation and cell proliferation, attenuate cell apoptosis, and ultimately facilitate liver regeneration at the termination stage of liver regeneration.
骨桥蛋白(OPN)是活化淋巴细胞和巨噬细胞分泌的Th1细胞因子成员。然而,OPN是否能促进细胞活化或增殖,进而在肝再生(LR)过程中促进肝脏自我修复,值得研究。本研究旨在进一步揭示OPN在体内对肝再生的影响。首先,利用定量逆转录聚合酶链反应(qRT-PCR)和蛋白质免疫印迹法(WB)验证部分肝切除(PH)后大鼠再生肝脏中内源性OPN的表达谱。然后成功构建了OPN表达载体、两种短发夹RNA(shRNA)表达载体及其各自的对照载体。之后,通过尾静脉将对照载体注入小鼠肝脏以寻找更有效的shRNA。此外,将OPN表达载体和更有效的shRNA表达载体注入大鼠再生肝脏,然后通过肝再生率和苏木精-伊红(HE)染色分别检测肝再生和肝脏微观结构的变化,同时通过qRT-PCR和WB检测几种标记基因的表达。在肝再生过程中,内源性OPN在mRNA和蛋白质水平均显著上调,尤其是在PH后12小时和72小时。发现shRNA表达载体Opn(313)在沉默Opn表达方面比Opn(887)更有效。然后将OPN表达载体和Opn(313)注入大鼠残余肝脏,结果显示OPN过表达加重了肝坏死和白细胞浸润,而OPN沉默则抑制了肝再生率以及增殖细胞核抗原(PCNA)和趋化因子CCL2的表达,但增加了凋亡相关蛋白BAX的表达。总之,OPN可能在肝再生的终末期增强炎症和细胞增殖,减轻细胞凋亡,最终促进肝再生。