Matrix metalloproteinase 13 in the ligamentum flavum from lumbar spinal canal stenosis patients with and without diabetes mellitus
Matrix metalloproteinase 13 in the ligamentum flavum from lumbar spinal canal stenosis patients with and without diabetes mellitus
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DOI：
10.1007/s00776-011-0135-2
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发表时间：
2011-11-01
影响因子：
1.7
通讯作者：
Matsumoto, Morio
中科院分区：
文献类型：
--
作者：
Cui, Guanyu;Watanabe, Kota;Matsumoto, Morio
腰椎管狭窄症（LSCS）是老年人最常见的脊柱疾病之一，而黄韧带（LF）肥大是导致LSCS的重要原因。基质金属蛋白酶13 （MMP13）可以降解纤维状胶原和弹性微原纤维，并参与炎症和纤维化。本研究的目的是比较LSCS合并糖尿病患者[DM(+)]与非糖尿病患者[DM (-)] LF中MMP13的表达情况，分析DM、MMP13表达与LF肥厚的关系。本研究分析了11例DM（+）和24例DM (-) LSCS患者的LFs。采用苏木精、伊红和马松三色染色对每个LF进行组织学分析。采用实时荧光定量PCR分析MMP13的表达情况。CT测量LF厚度。在DM (+) LSCS患者的LF中，弹性纤维比DM (-) LSCS患者更混乱，体积更小，而DM (+) LSCS患者的LF中纤维化组织比DM (-) LSCS患者更多。MMP13在DM (+) LSCS患者的LF中的表达显著升高（0.46 +/- A 0.61 vs. 0.05 +/- A 0.09, P = 0.002）。DM (+) LSCS患者的LF明显厚于DM (-) LSCS患者（5.0 +/- A 0.9 vs. 3.1 +/- A 0.8 mm, P < 0.01），且厚度与MMP13表达相关（相关系数= 0.43,P = 0.01， Pearson相关检验）。dm相关的MMP13表达可能是导致LF纤维化和肥大的因素之一。对这一过程机制的进一步研究可能会导致LF肥大的新疗法。
Lumbar spinal canal stenosis (LSCS) is one of the most common spinal disorders in the elderly, and ligamentum flavum (LF) hypertrophy is an important cause of LSCS. Matrix metalloproteinase 13 (MMP13) can degrade fibrillar collagens and elastic microfibrils, and is involved in inflammation and fibrosis. The purpose of this study was to compare the expression of MMP13 in the LF from LSCS patients with diabetes mellitus [DM (+)] with that in the LF from patients without DM [DM (-)] and to analyze the relationship among DM, MMP13 expression, and LF hypertrophy.LFs from 11 DM (+) and 24 DM (-) LSCS patients were analyzed in this study. Histology analysis using hematoxylin and eosin and Masson's trichrome stain was performed for each LF. The expression of MMP13 was analyzed by quantitative real-time PCR. The thickness of LF was measured by CT.In the LF from DM (+) LSCS patients, the elastic fibers were more disorganized and had lower volumes than in the LF from DM (-) LSCS patients, while more fibrotic tissue was observed in the LF from DM (+) than from DM (-) LSCS patients. MMP13 expression was significantly higher in the LF from DM (+) LSCS patients (0.46 +/- A 0.61 vs. 0.05 +/- A 0.09, P = 0.002). The LF from the DM (+) LSCS patients was significantly thicker than that from the DM (-) LSCS patients (5.0 +/- A 0.9 vs. 3.1 +/- A 0.8 mm, P < 0.01), and the thickness was correlated with the expression of MMP13 (correlation coefficient = 0.43, P = 0.01, Pearson's correlation test).DM-related MMP13 expression can be one of the factors contributing to fibrosis and hypertrophy of the LF. Further research on the mechanism of this process may lead to new therapies for LF hypertrophy.