Impact Of Lentivirus-mediated MiR-155Targeting MMP16on Intervertebral Disc Degeneration In Mice Anular Needle-puncture Model

Background and objective：Molecular mechanisms of disc degeneration has not clarify these years, but the roleof matrix metalloproteinases in the degenerative process has been widely recognized thatalmost everything can degrade the extracellular matrix of nucleus pulposus. Studies haveshown that MicroRNAs can inhibit matrix metalloproteinase mRNA to control itsexpression. Our previous study found that miR-155in degenerative intervertebral disccells was significantly reduced, and miR-155has been shown to regulate matrixmetalloproteinase16that MMP-16, so we assume that miR-155by MMP-16inregulation play a role in disc degeneration. In this experiment, we use acupuncturethrough modeling method to establish the model of disc degeneration, the abovedegenerative process in the experience card. This is the first time in the experiencecertificate MMP-16role in disc degeneration process, its purpose is explained by the roleof miR-155in the regulation of MMP-16in disc degeneration. Methods：We selected55patients with clinically disc degeneration Pfirrmann grade II to IVgrade, surgical removal of the real-time PCR technology use within30minutes of itsnucleus quantitative analysis, and use the same method to take five corpses normal discquantitative analysis for comparison. Select90C57mice were prepared by discdegeneration models were using acupuncture. Judged by in situ hybridization andreal-time PCR technology miR-155as to whether the regulation of MMP-16andlentivirus can stably transfected into mouse models of disc degeneration, and throughradiographic and histological assessment test disc back varying degrees. Use changes inHE staining and immunohistochemical techniques to detect extracellular matrix.Results：Through this experiment can be found miR-155expression in mice reduces discdegeneration, by upregulating the expression of miR-155overexpression can suppressthe expression of MMP-16, MMP-16can contribute to disc degeneration, MMP-16candegradation of the extracellular matrix of type II collagen and aggrecan, lentivirus canstably transfected nucleus pulposus cells C57mice.Conclusion：The first in vivo experiments in vivo validation miR-155regulates the expression ofMMP-16is further validation of its effect on disc degeneration process. More intuitiveand powerful proof of the important role of miR-155and MMP-16for disc degeneration.Regulated miR-155can inhibit the expression of MMP-16, and thus can reduce thedegradation of the matrix outside the nucleus pulposus cells of type II collagen andaggrecan, thus providing a new target for the prevention and treatment of intervertebraldisc degeneration in the future.