Notochordal cells maintain the proliferation and phenotype of chondrocyte-like cells in the disc nucleus pulposus

Yang Zhe; Li Shu-wen

doi:10.3969/j.issn.2095-4344.2016.02.019

Abstract：BACKGROUND:The immature disc nucleus pulposus is composed of notochordal cels, but there is no notochordal cel in the mature human intervertebral disc, in which the notochordal cels are replaced by chondrocyte-like cels. It is very important to comprehend the disappearance of the notochordal cels; however, it is stil unknown at present. OBJECTIVE: To elaborate the feasibility of notochordal cels to maintain the proliferation and phenotype of chondrocyte-like cels and to induce the cartilage-like differentiation of bone marrow mesenchymal stem cels. METHODS: The first author used the computer to retrieve PubMed and Wanfang databases using the key words of “notochord cels; nucleus pulposus cels; identify” in English and Chinese, respectively. Totaly 9 896 relevant articles published from January 1999 to August 2015 were retrieved. Repetitive studies were excluded, and finaly 36 articles were in accordance with the inclusion criteria. RESULTS AND CONCLUSION:Now, the main functions of notochordal cels are to promote synthesis of extracelular matrix in the nucleus pulposus, induce directional differentiation of mesenchymal cels into nucleus pulposus cels or act as “seed cels” to form the nucleus pulposus cels. The presence and disappearance of notochordal cels is related to intervertebral disc degeneration. Cel apoptosis is involved in static compressionviadeath receptor signals, and then leads to intervertebral disc degeneration. fas ligand can mediate the reduction of notochordal cels, and hypoxia-inducible factor can induce spinal cord injury thereby triggering cel death and complete disappearance of nucleus pulposus. The measurement and verification of immune makers of notochordal cels, CK-8, CK-18 and galectin-3, can benefit to the identification and isolation of notochordal cels, and thereby help the studies on cel growth and differentiation, function and its mechanism of apoptosis.