Abstract
IntroductionThe TNF‐α‐induced protein‐8 (TNFAIP8, also known as TIPE) family of molecules comprises four members: TNFAIP8 and TIPEs1‐3. Since the first description of these proteins, their roles in fine‐tuning inflammation and in directing leukocyte migration have been described in several organ systems. However, their relationship with intervertebral disc (IVD) is unknown.Materials and methodsHere, we describe the expression of TNFAIP8 family genes in the nucleus pulposus (NP) and annulus fibrosus (AF) of the normal adult murine IVD. We further describe the expression of these genes in the injured male and female murine IVD.Results Tnfaip8 gene expression was decreased, and Tipe1 gene expression was essentially unchanged, in response to injury. Tipe2 and Tipe3 gene expression was markedly elevated in response to IVD injury, along with those encoding known inflammatory markers (ie, Tnfa, Il6, Cxcl1, and Adam8). Additionally, sex‐related differences were also observed for some of these genes in intact and injured mouse IVDs. Future studies include examining tissue distribution of TNFAIP8 family proteins and identifying cells that produce them. In addition, examining mice that are deficient in TNFAIP8 molecules, in relation to gene expression, tissue morphology and mouse behavior, may further delineate the roles of these molecules in IVD inflammation and degeneration.
Highlights
The TNF-α-induced protein-8 (TNFAIP8, known as TIPE) family of molecules comprises four members: TNFAIP8 and TIPEs1-3
The TNFAIP8 family consists of four members, and recently has been found to regulate inflammatory processes, by interacting with inflammatory pathways and directing lymphocyte migration.[4,14]
We described gene expression in intact and injured intervertebral disc (IVD), which serves as baseline information for future mechanistic studies aimed at explaining potential roles of TNFAIP8 family members in homeostasis of the normal discs and their response to injury
Summary
Back pain related to intervertebral disc (IVD) degeneration costs billions of dollars in the U.S.1,2 Current treatments include surgical and nonsurgical approaches, and often result in incomplete symptom relief because the molecular relationships between back pain and IVD degeneration are still unclear. The mouse tail IVD injury model was established by Yang et al[23] and Martin et al.[24] We have recently refined the procedure using a percutaneous needle puncture approach, and have shown that needle injury results in a reproducible course of morphological and molecular changes consistent with IVD degeneration.[25,26] Among the four time points we studied,[26] reproducible changes in gene expression and histology occurred at 1 week post injury This time point was selected to examine TNFAIP8 family member gene expression. We have analyzed data from male and female mice separately in the present study
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