Intervertebral Disc Degeneration in a Percutaneous Mouse Tail Injury Model.
Intervertebral Disc Degeneration in a Percutaneous Mouse Tail Injury Model.
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DOI:
10.1097/phm.0000000000000818
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发表时间:
2018-03
影响因子:
3
通讯作者:
Zhang Y
中科院分区:
文献类型:
--
作者:
Tian Z;Ma X;Yasen M;Mauck RL;Qin L;Shofer FS;Smith LJ;Pacifici M;Enomoto-Iwamoto M;Zhang Y
Intervertebral disc (IVD) degenerates progressively with age and following injuries. In this study, we aimed to characterize early molecular events underlying disc degeneration using a mouse tail IVD injury model. We have established a transcutaneous minimally invasive approach to induce mouse tail IVD injury under fluoroscopic guidance. Morphological and molecular changes in the injured IVDs are compared with the baseline features of adjacent intact levels. Following needle puncture, tail IVDs exhibited time-dependent histological changes. The aggrecan neoepitope VDIPEN is evident from 2 days to 4 weeks post injury. A disintegrin and metalloproteinase domain-containing protein 8 (adam8) is a surface protease known to cleave fibronectin in the IVD. Gene expression of adam8 was elevated at all time points post injury, while the increase of C-X-C motif chemokine ligand (cxcl)-1 gene expression is statistically significant at 2 days and 2 weeks post injury. Type I collagen gene expression decreased initially at day 2, but increased at 2 weeks post injury, while no significant change in type II collagen gene expression was observed. The extracellular matrix gene expression pattern is consistent with fibrocartilage formation post injury. Mouse tail IVDs degenerate post needle puncture, as demonstrated by histological changes and aggrecan degradation. The minimally invasive tail IVD injury model should prove useful to investigators studying mechanisms of IVD degeneration and repair.