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논문 기본 정보

자료유형
학술저널
저자정보
Malcolm E. Dombrowski (University of Pittsburgh) Adam S. Olsen (University of Pittsburgh) Nicholas Vaudreuil (University of Pittsburgh) Brandon K. Couch (University of Pittsburgh) Qing Dong (University of Pittsburgh) Michelle Tucci (University of Mississippi Medical Center) Joon Y. Lee (University of Pittsburgh) Nam V. Vo (University of Pittsburgh) Gwendolyn Sowa (University of Pittsburgh)
저널정보
대한척추신경외과학회 Neurospine 대한척추신경외과학회지 제17권 제1호
발행연도
2020.1
수록면
69 - 76 (8page)

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Objective: Rabbit annulus fibrosus (AF) cells were exposed to isolated or combined mechanical and inflammatory stress to examine the expression of neuropeptide Y (NPY). This study aims to explore the ability of AF cells to produce NPY in response to mechanical and inflammatory stress. Methods: Lumbar AF cells of 6- to 8-month-old female New Zealand white rabbits were harvested and exposed to combinations of inflammatory (interleukin-1β) and mechanical (6% or 18%) tensile stress using the Flexcell System. NPY concentrations were measured in the media via enzyme-linked immunosorbent assay. The presence of NPY receptor-type 1 (NPY-1R) in AF cells of rabbit intervertebral discs was also analyzed via immunohistochemistry and immunofluorescence. Results: Exposure to inflammatory stimuli showed a significant increase in the amount of NPY expression compared to control AF cells. Mechanical strain alone did not result in a significant difference in NPY expression. While combined inflammatory and mechanical stress did not demonstrate an increase in NPY expression at low (6%) levels of strain, at 18% strain, there was a large—though not statistically significant—increase in NPY expression under conditions of inflammatory stress. Lastly, immunofluorescence and immunohistochemistry of AF cells and tissue, respectively, demonstrated the presence of NPY-1R. Conclusion: These findings demonstrate that rabbit AF cells are capable of expressing NPY, and expression is enhanced in response to inflammatory and mechanical stress. Because both inflammatory and mechanical stress contribute to intervertebral disc degeneration (IDD), this observation raises the potential of a mechanistic link between low back pain and IDD.

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