脊索细胞维持椎间盘髓核软骨样细胞增殖与表型的研究进展

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

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