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Anti-inflammatory effect of platelet-rich plasma on nucleus pulposus cells with response of TNF-α and IL-1.

Cited 66 time in Web of Science Cited 74 time in Scopus
Authors

Kim, Ho-Joong; Yeom, Jin S.; Koh, Yong-Gon; Yeo, Jee-Eun; Kang, Kyoung-Tak; Kang, Young-Mi; Chang, Bong-Soon; Lee, Choon-Ki

Issue Date
2014-04
Publisher
Wiley Periodicals
Citation
Journal of Orthopaedic Research Vol.32 No.4, pp. 551-556
Keywords
의약학platelet-rich plasmanucleus pulposus cellinterleukin-1tumor necrosis factor-α
Abstract
The purpose of this study was to investigate the anti-inflammatory effect of platelet-rich plasma (PRP) with collagen matrix on human nucleus pulposus (NP) cell in response to pro-inflammatory cytokines such as tumor necrosis factor-alpha (TNF-α) and interleukin-1 (IL-1). NP cells from human disks were cultured in a monolayer and maintained in the collagen matrix prior to the addition of recombinant human IL-1 and TNF-α. After applying IL-1 and TNF-α, PRP prepared by using a commercially available platelet concentration system was added. The response was investigated using real-time PCR for mRNA expression of type II collagen, aggrecan, matrix metalloproteinase-3 (MMP-3), and cyclooxygenase-2 (COX-2). The combination of IL-1β and TNF-α led to decrease of matrix synthesis gene expression such as collagen type II and aggrecan and increase of the degradation gene expression of COX-2 and MMP-3, compared to the control. Consecutive PRP exposure significantly recovered the down-regulated gene expression of collagen type II and aggrecan and significantly reduced the increased MMP-3 and COX-2 gene expression, compared to that of control groups with pro-inflammatory cytokines. The administration of PRP with collagen matrix markedly suppressed cytokine-induced pro-inflammatory degrading enzymes and mediators in the NP cell. It also rescued gene expression concerning matrix synthesis, thereby stabilizing NP cell differentiation.
ISSN
0736-0266 (print)
1554-527X (online)
Language
English
URI
https://hdl.handle.net/10371/91405
DOI
https://doi.org/10.1002/jor.22532
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