Extracellular vesicles loaded with ApoB-100 protein affect the occurrence of coronary heart disease in patients after injury of spinal cord

Spinal cord injury (SCI) patients have an increased susceptibility to coronary heart disease (CHD) due to dysregulated lipid deposition. We conducted a comprehensive investigation to gain insights into the specific roles of Apolipoprotein B-100 (APOB-100) in the development of CHD in patients suffer...

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Bibliographic Details
Published in:International journal of biological macromolecules 2024-10, Vol.277 (Pt 4), p.134330, Article 134330
Main Authors: Wu, Chunshuai, Chen, Jiajia, Zhang, Jinlong, Hong, Hongxiang, Jiang, Jiawei, Ji, Chunyan, Li, Chaochen, Xia, Mingjie, Xu, Guanhua, Cui, Zhiming
Format: Article
Language:English
Subjects:
Adaptor Proteins, Vesicular Transport - genetics
Adaptor Proteins, Vesicular Transport - metabolism
Animals
APOB-100
Apolipoprotein B-100 - metabolism
Apoptosis
Coronary Disease - metabolism
Coronary Disease - pathology
Coronary heart disease
Disease Models, Animal
Extracellular vesicles
Extracellular Vesicles - metabolism
Female
Humans
Injury of spinal cord
Macrophages - metabolism
Male
Middle Aged
Neurons - metabolism
Rats
Rats, Sprague-Dawley
Sortilin
Spinal Cord Injuries - metabolism
Spinal Cord Injuries - pathology
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Summary:Spinal cord injury (SCI) patients have an increased susceptibility to coronary heart disease (CHD) due to dysregulated lipid deposition. We conducted a comprehensive investigation to gain insights into the specific roles of Apolipoprotein B-100 (APOB-100) in the development of CHD in patients suffering from SCI. First, we established an SCI rat model through semitransection. APOB-100 expression in plasma exosomes obtained from patients were determined. Subsequently, we found APOB-100 affected macrophage polarization when treating co-cultured neurons/macrophages lacking Sortilin with extracellular vesicles derived from SCI rats, where APOB-100 co-immunoprecipitated with Sortilin. Moreover, APOB-100 upregulation reduced neuronal cell viability and triggered apoptosis by upregulating Sortilin, leading to a decline in the Basso, Beattie, and Bresnahan (BBB) scale, exacerbation of neuron injury, increased macrophage infiltration, and elevated blood lipid-related indicators in SCI rats, which could be reversed by silencing Sortilin. In conclusion, APOB-100 from post-SCI patients' extracellular vesicles upregulates Sortilin, thereby endangering those patients to CHD.
ISSN:0141-8130
1879-0003
1879-0003
DOI:10.1016/j.ijbiomac.2024.134330