Open AccessConstant compression decreases vascular bud and VEGFA expression in a rabbit vertebral endplate ex vivo culture model
Author(s) -
Jia-Wen Zhan,
Shang-Quan Wang,
Minshan Feng,
Xu Wei,
Jie Yu,
Xunlu Yin,
Tao Han,
Liguo Zhu
Publication year - 2020
Publication title -
plos one
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.99
H-Index - 332
ISSN - 1932-6203
DOI - 10.1371/journal.pone.0234747
Subject(s) - vascular endothelial growth factor a , ex vivo , intervertebral disc , western blot , immunohistochemistry , compression (physics) , angiogenesis , aggrecan , pathology , lumbar , in vivo , vascular endothelial growth factor , anatomy , andrology , biology , chemistry , medicine , vegf receptors , materials science , biochemistry , osteoarthritis , cancer research , genetics , composite material , alternative medicine , gene , articular cartilage
Summary of background data The vascular buds in the vertebral endplate (VEP) are the structural foundation of nutrient exchange in the intervertebral disc (IVD). VEGF is closely related to angiogenesis in the endplate and intervertebral disc degeneration (IDD). Objective To investigate the effects of static load on vascular buds and VEGF expression in the VEP and to further clarify the relation between IDD and VEGF. Methods IVD motion segments were harvested from rabbit lumbar spines and cultured under no-loading conditions (controls) or in custom-made apparatuses under a constant compressive load (0.5 MPa) for up to 14 days. Tissue integrity and the number of vascular buds were determined, and the concentrations and expression of Aggrecan, COL2a1, and VEGFA in the VEPs were assessed after 3, 7, and 14 days of culturing and then compared with those of fresh tissues. Results Under the constant compression, the morphological integrity of the VEPs was gradually disrupted, and immunohistochemistry results showed a significant decrease in the levels of Agg and COL2a1. During the static load, the number of vascular buds in the VEPs was gradually reduced from the early stage of culture, and ELISA showed that the constant compressive load caused a significant decrease in the VEGFA and VEGFR2 protein concentrations, which were consistent with the immunohistochemistry results. Western blot and RT-PCR results also showed that the loading state caused a significant decrease in VEGFA expression compared with that of fresh and control samples. Conclusions Constant compression caused degeneration of the VEP as well as a decreased number of vascular buds, thereby accelerating disc degeneration. VEGFA is involved in this process. We anticipate that regulating the expression of VEGFA may improve the condition of the lesions to the vascular buds in the endplates, thus enhancing the nutritional supply function in IVD and providing new therapeutic targets and strategies for the effective prevention and treatment of IDD.