Osteoarthritis in temporomandibular joint of Col2a1 mutant mice.
Osteoarthritis in temporomandibular joint of Col2a1 mutant mice.
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DOI：
10.1016/j.archoralbio.2013.02.008
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发表时间：
2013-09
影响因子：
3
通讯作者：
Seegmiller, R. E.
中科院分区：
文献类型：
--
作者：
Ricks, M. L.;Farrell, J. T.;Falk, D. J.;Holt, D. W.;Rees, M.;Carr, J.;Williams, T.;Nichols, B. A.;Bridgewater, L. C.;Reynolds, P. R.;Kooyman, D. L.;Seegmiller, R. E.
Col2a1 基因突变会导致不成比例的小肢症 (Dmm) 和先天性脊柱上皮发育不良 (sedc) 小鼠的膝关节软骨过早退化。本研究分析了 Col2a1 突变小鼠的颞下颌关节 (TMJ)，以提供 TMJ 骨关节炎 (OA) 的动物模型，从而可以更好地了解人类这种疾病的进展。在 2、6、9 和 12 个月时对 Dmm/+ 小鼠和对照小鼠进行比较。将颅骨固定，加工成石蜡切片，用番红-O/固绿染色，并用光学显微镜进行分析。使用 Mankin 评分程序对 OA 进行量化。进行了未折叠蛋白反应 (UPR) 测定，并使用免疫组织化学 (IHC) 测定已知的 OA 生物标志物。 Dmm/+ 颞下颌关节早在 6 个月大时就显示出髁软骨开裂。软骨细胞聚集，在基质中留下无细胞区域。在 Dmm/+ 小鼠中观察到 HtrA1、Ddr2 和 Mmp-13 的显着染色（p < 0.01）。我们检测到膝关节 UPR 上调，但 TMJ 未检测到。 Dmm/+ 小鼠的颞下颌关节会出现早发性骨关节炎。我们观察到与 OA 相关的生物标志物上调和髁软骨退化。 UPR 上调可能会加剧 OA 的发作。 Dmm/+ 小鼠 TMJ 是研究人类 OA 进展的可行模型。
Col2a1 gene mutations cause premature degeneration of knee articular cartilage in disproportionate micromelia (Dmm) and spondyloepiphesial dysplasia congenita (sedc) mice. The present study analyzes the temporomandibular joint (TMJ) in Col2a1 mutant mice in order to provide an animal model of TMJ osteoarthritis (OA) that may offer better understanding of the progression of this disease in humans. Dmm/+ mice and controls were compared at two, six, nine and 12 months. Craniums were fixed, processed to paraffin sections, stained with Safranin-O/Fast Green, and analyzed with light microscopy. OA was quantified using a Mankin scoring procedure. Unfolded protein response (UPR) assay was performed and immunohistochemistry (IHC) was used to assay for known OA biomarkers. Dmm/+ TMJs showed fissuring of condylar cartilage as early as 6 months of age. Chondrocytes were clustered, leaving acellular regions in the matrix. Significant staining of HtrA1, Ddr2 and Mmp-13 was observed in Dmm/+ mice (p< 0.01). We detected upregulation of the UPR in knee but not TMJ. Dmm/+ mice are subject to early-onset OA in the TMJ. We observed upregulation of biomarkers and condylar cartilage degradation concomitant with OA. An upregulated UPR may exacerbate the onset of OA. The Dmm/+ mouse TMJ is a viable model for the study of the progression of OA in humans.
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影响因子：
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作者：
AHMAD, NN;DIMASCIO, J;TASMAN, WS
通讯作者：
TASMAN, WS
影响因子：
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Baici, A
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LIPPIELLO, L;HALL, D;MANKIN, HJ
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MANKIN, HJ
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作者：
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通讯作者：
Landesberg, R
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作者：
Ghassemi-Nejad, S.;Kobezda, T.;Mikecz, K.
通讯作者：
Mikecz, K.