HAX1 is associated with neuronal apoptosis and astrocyte proliferation after spinal cord injury. (October 2018)

• Record Type: Journal Article
• Authors: Lu, Xiongsong; Xue, Pengfei; Fu, Luyu; Zhang, Jinlong; Jiang, Jiawei; Guo, Xiaofeng; Bao, Guofeng; Xu, Guanhua; Sun, Yuyu; Chen, Jiajia; Cui, Zhiming
• Is Part Of: Tissue & cell. Volume 54(2018)
• Page Start: 1
• Page End: 9
• Publication Date: 2018-10
• Subjects: HAX-1 -- Spinal cord injury -- Neuronal apoptosis -- Astrocyte proliferation; Cytology -- Periodicals; 571.5
• DOI: 10.1016/j.tice.2018.07.001
• Languages: English
• ISSNs: 0040-8166

Abstract

Highlights: There are few reports about HAX1 in spinal cord injury. We found the expression of HAX1 in the pathological process of spinal cord injury earlier. HAX1 plays a dual role in spinal cord injury and is likely to have broad research prospects. Some preliminary research objectives are also proposed, which will provide some directions for future research. Abstract: HS1-associated protein X-1 (HAX1) is a class of multifunctional protein, participated in various physiological processes such as cell apoptosis, proliferation and motility. However, the HAX1 expression and function in the spinal cord injury (SCI) pathological process have not been investigated. In our current research, the rat model of SCI was established, and then we explored the possible role of HAX1 after SCI. The results of western blot indicated that HAX1 was present in sham operated control group and significantly elevated at 3 days post SCI, then declined gradually. Immunohistochemical studies indicated HAX1 expression was enhanced significantly in white and gray matter at 3 days post SCI compared with sham operated group. Double immunofluorescence staining showed the proportion of cells, double-labeled HAX1 and neurons, astrocytes, increased significantly at 3 days post SCI. In addition, co-localization of HAX1/active caspase-3 and HAX1/PCNA was tested in cells. Furthermore, over-expression of HAX1 inhibited neuronal apoptosis in vitro, and in astrocytes HAX1 silencing could down-regulate PCNA expression post LPS treatment. Meanwhile, CCK8 assay showed that knockdown of HAX1 could inhibit the astrocyte proliferation. In summary, our data indicated that HAX1 might play significant roles in pathological process of neuronal apoptosis and astrocyte proliferation during SCI.