LITAF Promotes Atherosclerotic Plaque Formation by Stimulating the NF-κB Inflammatory Pathway

• DOI: 10.1007/s11596-023-2802-x
• Publication Date: 2023-10-18T03:29:58Z
• Authors: Wei-juan Li; Wen-ping Zhou; Xu-yong Li; Xiao-li Jiang; Yun-chao Deng; Jie Shen; Han Xie; Gang Tan; Ling Huang; Hui Zhang
• Keywords: CD68; Oil Red O

Abstract Background Litaf protein is a newly discovered inflammatory protein, whether it is involved in the formation of atherosclerosis remains unclear; Methods Ten C57BL/6J mice and ten C57BL/6J mice with knockout of Litaf gene (C57BL/6J− Litaf−) were purchased from Animal Culture Center of Huazhong University of Science and Technology divided into two groups: control group and Litaf−/− group. Animals were given a normal diet and euthanized after 16-week culture. Mice, heart and whole aorta were isolated, and the aortic root of the mouse was taken for frozen sections; used for oil red staining and immunohistochemical staining (α-actin, CD68, Masson), and then compared the oil red staining area and the positive proportion of immunohistochemical staining in each group; at the same time, a sufficient amount of mouse blood was collected for extraction Plasma protein and RNA, monitoring the expression of inflammation-related proteins by Western and RT-PCR. Results Oil red staining of the aortic root sections of the mice in each group showed that the area of atherosclerotic plaques in Litaf−/− group was less than control group (P < 0.05). The aortic root sections of the mice in each group were immunohistochemical stained, and it can be found that the expression of α-actin and CD68 in Litaf−/− group was higher than that in the control group, while the results were opposite after Masson stainning(P < 0.05). The expressions of P65, IκB, and caspase3 were monitored by Western and RT-PCR. As shown in Figs. 2 and 3, the expressions of P65, IκB, and caspase3 in Litaf−/− group were lower than those in the control group (P < 0.05). Conclusions Litaf might participate in the formation of atherosclerosis through the NF-κB pathway and play a promoting role in the formation of atherosclerosis.