Targeting FBN1 and BMP-8: The Potential Mechanism of SDF-1 in Acute Spinal Cord Injury Repair.

Abstract

Introduction: Acute Spinal Cord Injury (SCI) often causes motor and sensory deficits. SDF-1 promotes stem cell survival and proliferation, while FBN1 may impact repair mechanisms. This study investigates how SDF-1 promotes SCI treatment by inducing BMSC maturation through BMP-8-mediated FBN1 inhibition.

Methods: Bone marrow mesenchymal stem cells were induced to differentiate with BMP-8 and transfected with related plasmids (oe-NC, oe-SDF-1, oe-FBN1, si-BMP-8). CCK-8 and alizarin red staining were used to assess cell growth and differentiation. Western blotting was used to detect the levels of SDF-1, FBN1, and BMP-8. In a rat SCI model, cells with plasmids were injected, and motor recovery was assessed using BBB scoring. Immunofluorescence assay detected SDF-1 expression, while Western blotting was used to detect SDF-1, FBN1, and BMP-8.

Results: In cell experiments, BMP-8 induced successful differentiation of BMSCs. After overexpression of SDF-1, the proliferation and differentiation of BMSCs were increased. In animal experiments, the BBB score increased after overexpression of SDF-1.

Discussion: These findings suggest a potential therapeutic mechanism in which SDF-1 promotes spinal cord repair by modulating the BMP-8/FBN1 axis. The suppression of FBN1 appears to be a key step in enhancing BMSC function. Targeting this pathway could offer new strategies for regenerative treatment following SCI.

Conclusion: In acute spinal cord injury, SDF-1 enhances the differentiation of bone marrow mesenchymal stem cells induced by BMP-8 through the suppression of FBN1.