Gruber H E, Ingram J A, Hanley E N
Department of Orthopaedic Surgery, Carolinas Medical Center, PO Box 32861, Charlotte, North Carolina 28232, USA.
Biotech Histochem. 2005 May-Aug;80(3-4):157-62. doi: 10.1080/10520290500387607.
Matrix metalloproteinases (MMPs) degrade components of the extracellular matrix of the disc, but the presence of MMP-19 has not been explored. In other tissues, MMP-19 is known to act in proteolysis of the insulin-like growth factor (IGF) binding protein-3, thereby exposing this protein to make it available to influence cell behavior. MMP-19 also has been shown to inhibit capillary-like formation and thus play a role in the avascular nature of the disc. Using immunohistochemistry, normal discs from six subjects aged newborn through 10 years and 20 disc specimens from control donors or surgical patients aged 15-76 (mean age 40.2 years) were examined for immunolocalization of MMP-19; six Thompson grade I discs, five Thompson grade II, eight Thompson grade III, five Thompson grade IV, and one Thompson grade V discs were analyzed. The results indicate that in discs from young subjects, MMP-19 was uniformly localized in the outer annulus. In discs from adult donors and surgical patients, outer and inner annulus cells only occasionally showed MMP-19 localization. The greatest expression of MMP-19 was observed in young discs, and little expression was seen in older or degenerating discs. Because MMP-19 has been shown to regulate IGF-mediated proliferation in other tissues, its decline in the aging/degenerating disc may contribute to the age-related decrease in disc cell numbers.
基质金属蛋白酶(MMPs)可降解椎间盘细胞外基质的成分,但MMP - 19的存在情况尚未得到研究。在其他组织中,已知MMP - 19可作用于胰岛素样生长因子(IGF)结合蛋白 - 3的蛋白水解过程,从而使该蛋白得以暴露,进而影响细胞行为。MMP - 19还被证明可抑制毛细血管样结构的形成,因此在椎间盘的无血管特性中发挥作用。利用免疫组织化学方法,对6名年龄从新生儿到10岁受试者的正常椎间盘以及20份来自15 - 76岁(平均年龄40.2岁)对照供体或手术患者的椎间盘标本进行了MMP - 19免疫定位检查;分析了6个汤普森I级椎间盘、5个汤普森II级、8个汤普森III级、5个汤普森IV级和1个汤普森V级椎间盘。结果表明,在年轻受试者的椎间盘中,MMP - 19均匀定位于外环。在成年供体和手术患者的椎间盘中,外环和内环细胞仅偶尔显示MMP - 19定位。MMP - 19在年轻椎间盘中表达最高,而在老年或退变椎间盘中表达很少。由于MMP - 19已被证明在其他组织中可调节IGF介导的增殖,其在老化/退变椎间盘中的减少可能导致与年龄相关的椎间盘细胞数量下降。