Abnormal human chondrocyte morphology is related to increased levels of cell-associated IL-1β and disruption to pericellular collagen type VI.
Abnormal human chondrocyte morphology is related to increased levels of cell-associated IL-1β and disruption to pericellular collagen type VI.
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DOI：
10.1002/jor.21155
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发表时间：
2010-11
影响因子：
2.8
通讯作者：
Hall, Andrew C.
中科院分区：
文献类型：
--
作者：
Murray, Dianne H.;Bush, Peter G.;Brenkel, Ivan J.;Hall, Andrew C.
早期骨关节炎（OA）知之甚少，但异常的软骨细胞形态可能是重要的。我们研究了形态正常和异常软骨细胞中的IL-1β和细胞周VI型胶原。对人胫骨平台非退化（0/1级）区域（n = 21）外植体内的原位软骨细胞进行荧光标记和可视化[双光子激光扫描显微镜（2 PLSM）]。正常软骨细胞表现出“光滑”的膜表面，而异常细胞定义为表现出≥1个细胞质突起。通过细胞质突起/细胞的数量和平均长度对异常软骨细胞进行进一步分类。通过荧光免疫组织化学和共聚焦激光扫描显微镜（CLSM）观察单个软骨细胞相关的IL-1β或VI型胶原。荧光被量化为阳性体素的数目（即，具有高于基线的荧光的3D像素）/细胞。IL-1β相关荧光在正常和所有异常细胞之间增加，（99.7 ± 29.8 [11（72）] vs. 784 ± 382 [15（132）]; p = 0.04，阳性体素/细胞）和深部带（66.5 ± 29.4 [9（64）]对比795 ± 224 [9（56）]; p = 0.006）。突起数量/细胞（0-5）与IL-1β之间存在相关性（r2 = 0.988），特别是短突起（≤5 µm; p = 0.022）的增加。VI型胶原覆盖率和厚度随着突起的发展而降低（分别为p < 0.001和p = 0.005）。肉眼观察非退化软骨中的异常软骨细胞显示IL-1β显著增加和细胞周围VI型胶原丢失，这些变化可能导致软骨退化。© 2010骨科研究学会。由威利期刊公司出版J Orthop Res 28：1507-1514，2010
Early osteoarthritis (OA) is poorly understood, but abnormal chondrocyte morphology might be important. We studied IL-1β and pericellular collagen type VI in morphologically normal and abnormal chondrocytes. In situ chondrocytes within explants from nondegenerate (grade 0/1) areas of human tibial plateaus (n = 21) were fluorescently labeled and visualized [2-photon laser scanning microscopy (2PLSM)]. Normal chondrocytes exhibited a “smooth” membrane surface, whereas abnormal cells were defined as demonstrating ≥1 cytoplasmic process. Abnormal chondrocytes were further classified by number and average length of cytoplasmic processes/cell. IL-1β or collagen type VI associated with single chondrocytes were visualized by fluorescence immuno-histochemistry and confocal laser scanning microscopy (CLSM). Fluorescence was quantified as the number of positive voxels (i.e., 3D pixels with fluorescence above baseline)/cell. IL-1β-associated fluorescence increased between normal and all abnormal cells in the superficial (99.7 ± 29.8 [11 (72)] vs. 784 ± 382 [15 (132)]; p = 0.04, positive voxels/cell) and deep zones (66.5 ± 29.4 [9 (64)] vs. 795 ± 224 [9 (56)]; p = 0.006). There was a correlation (r2 = 0.988) between the number of processes/cell (0–5) and IL-1β, and an increase particularly with short processes (≤5 µm; p = 0.022). Collagen type VI coverage and thickness decreased (p < 0.001 and p = 0.005, respectively) with development of processes. Abnormal chondrocytes in macroscopically nondegenerate cartilage demonstrated a marked increase in IL-1β and loss of pericellular type VI collagen, changes that could lead to cartilage degeneration. © 2010 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 28:1507–1514, 2010
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