C1QBP promotes apoptosis of goat fetal turbinate cells via inhibiting the expression of TRIM5 or TNFSF10

Qiuyun Li ¹ Yixing Dan ¹ zhengding Tang ² Yupeng Ren ² Huanrong Zhang ¹ Falong Yang ² Jiangjiang Zhu ¹ Hua Xiang ^2*

• ¹ Southwest Minzu University, Chengdu, China
• ² 西南民族大学, ChengDu, China

Background]. Infectious ecthyma is a severe and highly contagious disease caused by ORF virus (ORFV). The virus is responsible for significant economic losses in the goat industry and threatens humans. Regarding complement component 1, q subcomponent binding protein (C1QBP), we previously showed that C1QBP can interact with ORFV129. However, the role of C1QBP in regulating the apoptosis of goat fetal turbinate cells is unknown. [Methods]. After pcDNA3.1-C1QBP and siRNA were transfected into goat fetal turbinate cells (GFTCs), the expression of C1QBP was detected by western blot and cell cycle and apoptosis using flow cytometry. The expression of cycle-related genes cyclin-dependent protein kinase 2 (CDK2) and cyclin-dependent kinase inhibitors 1A (p21) and apoptosis-related genes cysteinyl aspartate specific proteinase 3(Caspase 3), cysteinyl aspartate specific proteinase 7 (Caspase 7), p53, poly (ADP-ribose) polymerase 1 (PARP1), B-Cell lymphoma-2 Like-11 (BCL2L11), B-cell lymphoma 2 associated X protein (Bax) and B-cell lymphoma 2 (Bcl-2) were tested by real-time quantitative PCR (RT-qPCR). The effect of MTT on the proliferation of GFTCs was detected. The localization of C1QBP in GFTCs was detected by inverted fluorescence microscope. Finally, transcriptome sequencing was performed and validated by siRNA treatment knockdown of C1QBP, and screening two genes tripartite motif containing 5 (TRIM5) and tumor necrosis factor superfamilymember10 (TNFSF10) with significant changes in expression levels and relevance to cell apoptosis, and to verify their roles in C1QBP-induced cell apoptosis. [Results]. Knockdown of C1QBP significantly increased cell viability; cells remained in the G0/G1 phase and reduced apoptosis. Knockdown of C1QBP reduced the mRNA expression of CDK2, p21, Caspase3, Caspase7, Bax, PARP1, BCL2L11 and p53, up regulated the mRNA expression of the Bcl-2. Except for Bcl-2, The opposite effect was observed when C1QBP was overexpressed in GFTCs and the mRNA levels of Bcl-2 had noThe full text is 8587 words；Five figures, two supplementary pictures; Two table, three supplementary forms.