VEGF vascularization pathway in human intervertebral disc does not change during the disc degeneration process View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2018-05-22

AUTHORS

Simona Capossela, Alessandro Bertolo, Kapila Gunasekera, Tobias Pötzel, Martin Baur, Jivko V. Stoyanov

ABSTRACT

OBJECTIVE: During degeneration of the intervertebral disc ingrowth of blood vessels and nerves into the disc are associated with back pain. Vascular endothelial growth factors promote vasculogenesis by binding to the membrane vascular endothelial growth factor receptor 1, while shorter soluble forms of this receptor can inhibit vascularization. We hypothesized that membrane and soluble receptor forms might change between stages of intervertebral disc degeneration. RESULTS: Expression of soluble and membrane forms of vascular endothelial growth factor receptor 1 in human degenerated intervertebral discs and healthy bovine caudal discs was assessed by qRT-PCR and immunoblot. Comparative microarray meta-analysis across disc degeneration grades showed that membrane and soluble forms of this receptor, together with other components of classic vascularization pathways, are constitutively expressed across human disc degeneration stages. Contrary to our hypothesis, we observed that expression of the classic vascularization pathway is stable across degeneration stages and we assume that soluble vascular endothelial growth factor receptor 1 does not contribute to prevent disc degeneration. However, we observed increased expression levels of genes involved in alternative vascularization signalling pathways in severely degenerated discs, suggesting that abnormal vascularization is part of the pathological progression of disc degeneration. More... »

PAGES

333

References to SciGraph publications

Identifiers

URI

http://scigraph.springernature.com/pub.10.1186/s13104-018-3441-3

DOI

http://dx.doi.org/10.1186/s13104-018-3441-3

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https://app.dimensions.ai/details/publication/pub.1104150754

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/29784013


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