Expressions of membrane-type I matrix metalloproteinase, Ki-67 protein, and type II collagen by chondrocytes migrating from cartilage endplate into nucleus pulposus in rat intervertebral discs - A cartilage endplate-fracture model using an intervertebral disc organ culture
Expressions of membrane-type I matrix metalloproteinase, Ki-67 protein, and type II collagen by chondrocytes migrating from cartilage endplate into nucleus pulposus in rat intervertebral discs - A cartilage endplate-fracture model using an intervertebral disc organ culture
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DOI：
10.1097/01.brs.0000166155.48168.0e
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发表时间：
2005-06-15
期刊：
影响因子：
3
通讯作者：
An, HS
中科院分区：
文献类型：
--
作者：
Kim, KW;Ha, KY;An, HS
研究设计.免疫组化在器官培养的完整和软骨终板（CE）骨折的大鼠椎间盘（IVD）中进行。目的：证实软骨细胞从透明髓核（CE）迁移到髓核（NP）的相关生物学事件。最近发现，从脊索NP到纤维软骨NP的转变在兔IVD中是通过软骨细胞从CE迁移到NP外源性完成的。这一观察结果尚未在其他动物模型中进行研究，与软骨细胞迁移相关的生物学事件尚未在文献中阐明。从4周龄、6月龄、12月龄和18月龄Wistar大鼠中获得IVD，包括头部和尾部CE。为了加速软骨细胞迁移，将IVD的CE断裂并培养48小时。没有CE骨折的IVD被用作每个年龄组的对照。免疫组化法检测细胞迁移和细胞外基质消化的标志物膜型基质金属蛋白酶（MT 1-MMP）和增殖标志物Ki-67蛋白的表达，以及细胞周围II型胶原沉积（纤维软骨基质的标志物）。在对照组中，软骨细胞迁移仅限于沿着脊索NP的周边，并且NP内没有软骨细胞。然而，CE骨折组的所有IVD均显示软骨细胞从CE直接且更广泛地迁移到NP中。对照组和CE骨折组迁移的软骨细胞表达MT 1-MMP和Ki-67蛋白，并在NP中沉积II型胶原。本报告证明了在器官培养的大鼠IVD中软骨细胞从CE迁移到NP。这种现象在CE断裂的存在下加速。软骨细胞从CE迁移到NP表达MT 1-MMP和Ki-67蛋白，并沉积II型胶原。这些生物学策略可能使软骨细胞的透明CE迁移到异位NP区域，取代脊索细胞，并改变脊索组织成纤维软骨。这些结果表明，类似的生物学机制可能涉及在自然过渡从脊索NP的纤维软骨NP在其他动物模型，包括人类。
Study Design. Immunohistochemistry was performed in organ-cultured intact and cartilage endplate (CE)-fractured rat intervertebral discs (IVDs).Objectives. To demonstrate biologic events associated with migration of chondrocytes from hyaline CE into nucleus pulposus (NP).Summary of Background Data. It was recently revealed that the transition from a notochordal NP to a fibrocartilaginous NP in the rabbit IVD is accomplished exogenously by chondrocytes migrating from CEs into the NP. This observation has not been studied in other animal models, and the biologic events associated with chondrocyte migration have not been elucidated in the literature.Methods. IVDs including cranial and caudal CEs were obtained from 4-week, 6-month, 12-month, and 18-month old Wistar rats. To accelerate chondrocyte migration, CEs of IVDs were fractured and cultured for 48 hours. IVDs without CE-fracture were used as a control for each age group. Expressions of membrane-type I matrix metalloproteinase (MT1-MMP, as a marker for cell migration and extracellular matrix digestion) and Ki-67 protein ( as a proliferation marker) and pericellular deposition of type II collagen ( as a marker for fibrocartilaginous matrix) by the chondrocytes migrating from CE into NP were examined immunohistochemically.Results. In the control groups, chondrocyte migration limited only along the periphery of the notochordal NP and no chondrocytes were inside the NP proper. However, all the IVDs in the CE-fracture groups showed direct and more extensive migration of chondrocytes from CEs into the NP proper. The migrating chondrocytes in both control and CE-fracture groups expressed MT1-MMP and Ki-67 protein and deposited type II collagen in the NP.Conclusions. This report demonstrates the chondrocyte migration from CE into NP in the organ-cultured rat IVDs. This phenomenon is accelerated in the presence of CE fracture. The chondrocytes migrating from CEs into the NP expressed MT1-MMP and Ki-67 protein and deposited type II collagen. These biologic strategies probably enable chondrocytes of the hyaline CE to migrate into the ectopic NP region, replace notochordal cells, and change the notochordal tissue into fibrocartilage. These results suggest that similar biologic mechanisms may be involved in the natural transition from the notochordal NP to the fibrocartilaginous NP in other animal models, including human.