Injury‐induced sequential transformation of notochordal nucleus pulposus to chondrogenic and fibrocartilaginous phenotype in the mouse

Aggrecan Versican Intervertebral Disc Chondrogenesis Degeneration (medical)
DOI: 10.1002/path.2519 Publication Date: 2009-01-13T14:40:22Z
ABSTRACT
Intervertebral disc degeneration has been widely studied in different animal models. To test the hypothesis that needle puncture could induce progressive biochemical and molecular changes murine discs, we established a mouse tail model to investigate pathogenesis mechanism of puncture-induced degeneration. Caudal discs tails were punctured using 31G gauge at controlled depth under microscopic guidance. The progress was evaluated by radiographic analysis height, histological grading glycosaminoglycan (GAG) quantification pre-operation 1, 2, 6 12 weeks post-puncture. Gene protein expression extracellular matrix (ECM) analysed RT-PCR, situ hybridization immunohistochemistry. Histological study height revealed degenerative discs. Compared with control group, total GAG content decreased 40% (p < 0.05) aggrecan (Acan), decorin (Dcn) versican (Vcan; Cspg2) down-regulated A transient increase Col2a1-expressing cells elevation collagen II nucleus pulposus (NP) detected. Fibronectin (Fn1) up-regulated 50% deposition I NP observed This is first use an injury-induced mouse. involves transformation from notochordal chondrogenic eventually into fibrocartilaginous phenotype. have some similarity human degeneration, suggesting this may potentially be used future dissect pathways
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