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

doi:10.3969/j.issn.2095-4344.2016.02.019

Abstract

Abstract:

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.

中国组织工程研究杂志出版内容重点：组织构建；骨细胞；软骨细胞；细胞培养；成纤维细胞；血管内皮细胞；骨质疏松；组织工程

Yang Zhe, Li Shu-wen. Notochordal cells maintain the proliferation and phenotype of chondrocyte-like cells in the disc nucleus pulposus[J]. Chinese Journal of Tissue Engineering Research, 2016, 20(2): 261-266.

Figures/Tables 1

References

[1] Hwang PY, Jing L, Michael KW,et al.N-Cadherin-Mediated Signaling Regulates Cell Phenotype for Nucleus Pulposus Cells of the Intervertebral Disc.Cell Mol Bioeng. 2015;8(1): 51-62.

[2] Han C,Zhu H.Research progress of nucleus pulposus cells phenotypic markers. Review Chinese.2011;25(7):867-870.

[3] 马可,胡祖鹏,齐宗华,等.退变椎间盘的细胞培养[J].中国组织工程研究与临床康复,2009,13(37):7249-7252.

[4] Hayes AJ, Ralphs JR.The response of foetal annulus fibrosus cells to growth factors: modulation of matrix synthesis by TGF-β1 and IGF-1.Histochem Cell Biol. 2011;136(2):163-175.

[5] Cappello R, Bird JL, Pfeiffer D, et al. Notochordal cell produce andassemble extracellular matrix in a distinct manner, which may beresponsible for the maintenance of healthy nucleus pulposus.Spine.2006;31(8):873-882.

[6] 赵献峰,刘浩,丰干均,等.脊索细胞促进髓核软骨样细胞增殖及表型维持[J].中国修复重建外科杂志,2008,22(8):939-943.

[7] Chen J,Yan W,Setton LA. Molecular phenotypes of noto -chordal cells purified from immature nucleus pulposus.Eur Spine J.2006;15(Suppl 3):S303-311.

[8] Wang S, Furmanek T, Kryvi H,et al. Transcriptome sequencing of Atlantic salmon (Salmo salar L.) notochord prior to development of the vertebrae provides clues to regulation of positional fate, chordoblast lineage and mineralisation.BMC Genomics.2014;15:141.

[9] Weiler C, Nerlich AG, Schaaf R,et al.Immunohistochemical identification of notochordal markers in cells in the aging human lumbar intervertebral disc.Eur Spine J.2010;19(10):1761-1770.

[10] Anderson DG, Izzo MW, Hall DJ,et al.Comparative gene expression profiling of normal and degenerative discs: analysis of a rabbit annular laceration model. Spine.2002;27:1291-1296.

[11] Oguz E,Tsai TT,Di Martino A,et al. Galectin-3 expression in the intervertebral disc: a useful marker of the notochord phenotype? Spine.2007;32:9-16.

[12] Ma K, Wu Y, Wang B,et al.Effect of a synthetic link N peptide nanofiber scaffold on the matrix deposition of aggrecan and type II collagen in rabbit notochordal cells.J Mater Sci Mater Med. 2013;24(2):405-415.

[13] Kim KW,Ha KY,Lee JS,et al.The apoptotic effects of oxidative stress and antiapoptotic effects of caspase inhibitors on rat notochordal cells. Spine (Phila Pa 1976).2007;32(22):2443-2448.

[14] Kourakis MJ, Reeves W, Newman-Smith E,et al.A one- dimensional model of PCP signaling: polarized cell behavior in the notochord of the ascidian Ciona.Dev Biol. 2014;395(1):120-130.

[15] Erwin WM.The Notochord, Notochordal cell and CTGF/CCN-2: ongoing activity from development through maturation.J Cell Commun Signal.2008;2(3-4):59-65.

[16] Purmessur D,Schek RM,Abbott RD,et al.Notochordal conditioned media from tissue increases proteoglycan accumulation and promotes a healthy nucleus pulposus phenotype in human mesenchymal stem cells. Arthritis Res Ther.2011;13(3):R81.

[17] Erwin WM,Islam D,Inman RD,et al.Notochordal cells protect nucleus pulposus cells from degradation and apoptosis:implications for the mechanisms of intervertebral disc degeneration. Arthritis Res Ther.2011;13(6):R215.

[18] Kim JH, Moon HJ, Lee JH,et al.Rabbit notochordal cells modulate the expression of inflammatory mediators by human annulus fibrosus cells cocultured with activated macrophage-like THP-1 cells.Spine (Phila Pa 1976). 2012;37(22):1856-1864.

[19] Aguiar DJ, Johnson SL, Oegema TR.Notochordal cells interact with nucleus pulposus cells: regulation of proteoglycan synthesis.Exp Cell Res.1999;246(1):129-137.

[20] Erwin WM.The enigma that is the nucleus pulposus cell: the search goes on.Arthritis Res Ther. 2010;12(3):118.

[21] Erwin WM, Ashman K, O'Donnel P,et al.Nucleus pulposus notochord cells secrete connective tissue growth factor and up-regulate proteoglycan expression by intervertebral disc chondrocytes.Arthritis Rheum.2006;54(12):3859-3867.

[22] Purmessur D, Cornejo MC, Cho SK,et al. Notochordal cell-derived therapeutic strategies fordiscogenic back pain. Global Spine J.2013;3(3):201-218.

[23] Guehring T,Urban JP,Cui Z,et al.Noninvasive 3D vital imaging and characterization of notochordal cells of the intervertebral disc by femtosecond near-infrared two-photon laser scanning microscopy and spatial-volume rendering.Microsc Res Tech. 2008;71(4):298-304.

[24] Yamamoto M, Morita R, Mizoguchi T,et al.Mib-Jag1-Notch signalling regulates patterning and structural roles of the notochord by controlling cell-fate decisions.Development. 2010;137(15):2527-2537.

[25] Cornejo MC, Cho SK, Giannarelli C, et al.Soluble factors from the notochordal-rich intervertebral disc inhibit endothelial cell invasion and vessel formation in the presence and absence of pro-inflammatory cytokines. Osteoarthritis Cartilage. 2015; 23(3):487-496.

[26] Won HY, Park JB, Park EY,et al.Effect of hyperglycemia on apoptosis of notochordal cells and intervertebral disc degeneration in diabetic rats.J Neurosurg Spine.2009;11(6): 741-748.

[27] Yurube T, Hirata H, Kakutani K,et al.Notochordal cell disappearance and modes of apoptotic cell death in a rat tail static compression-induced disc degeneration model. Arthritis Res Ther.2014;16(1):R31.

[28] Erwin M.Canonical Wnt signaling and caveolae play a role in intervertebral disc degeneration; the continuing saga of the mysterious notochordal cell. Arthritis Res Ther.2013;15(2):113.

[29] Inui Y,Nishida K,Doita M, et al.Fas-ligand expression on nucleus pulposus begins in developing embryo.Spine (Phila Pa 1976). 2004;29(21):2365-2369.

[30] Kim JW,Park SH,Park SS,et al.Fetus-in-fetu in the cranium of a 4-month-old boy: histopathology and short tandem repeat polymorphism-based genotyping. Case report.J Neurosurg Pediatr.2008;1(5):410-414.

[31] Ma K, Shao Z, Wang B,et al.Promotion effect of notochordal cells conditioned medium on proliferation and differentiation of bone marrow mesenchymal stem cells.Zhongguo Xiu Fu Chong Jian Wai Ke Za Zhi.2012;26(5):601-606.

[32] Merceron C, Mangiavini L, Robling A, et al.Loss of HIF-1α in the Notochord Results in Cell Death and Complete Disappearance of the Nucleus Pulposus.PLoS One.2014; 9(10): e110768.

[33] Park EY, Park JB. High glucose-induced oxidative stress promotes autophagy through mitochondrial damage in rat notochordal cells. Int Orthop.2013;37(12):2507-2514.

[34] Jiang L, Yuan F, Dong J.Comment on Park et al.High glucose-induced oxidative stress promotes autophagy through mitochondrial damage in rat notochordal cells.Int Orthop. 2014;38(3):675-676.

[35] Ferrari L, Pistocchi A, Libera L,et al.Riva P FAS/FASL are dysregulated in chordoma and their loss-of-function impairs zebrafish notochord formation.Oncotarget.2014;5(14):5712-5724.