Objective: TNFAIP8 and TIPE2 belong to TNFa-induced protein 8 (TNFAIP8/TIPE) family. They control apoptosis and direct leukocyte migration. Nucleus pulposus cell loss is a hallmark of intervertebral disc degeneration in response to injury, and inflammation may cause pain. Here, we examined the effects of TNFAIP8/TIPE2 deficiency on the intervertebral discs in mice with these genes deleted.
Design: Tail intervertebral discs in Tnfaip8 or Tipe2 single and double knockout mice ( Tnfaip8 -/- , Tipe2 -/- , and Tnfaip8/Tipe2 dko) , and wild-type controls were injured. The spine motion segments were stained with safranin O to reveal proteoglycans. Macrophages were identified by immunostaining, and selected inflammatory marker and collagen gene expression was examined by Real Time PCR.
Results: The injured tail intervertebral discs of Tnfaip -/- , Tipe2 -/- , and Tnfaip8/Tipe2 dko mice all displayed higher levels of proteoglycans than wild-type controls. Fewer macrophages were found in the injured intervertebral discs of Tipe2 -/- and Tnfaip8/Tipe2 dko mice than wild type. Il6 , Adam8 , and Col1 gene expression was downregulated in the injured intervertebral discs of Tnfip8/Tipe2 dko mice.
Conclusions: TNFAIP8 and TIPE2 loss of function ameliorated proteoglycan loss and inflammation in the injured intervertebral discs. They may serve as molecular targets to preserve disc structure and reduce inflammation.
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| http://dx.doi.org/10.1097/PHM.0000000000002488 | DOI Listing |
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