Matrix metalloproteinase 13 in the ligamentum flavum from lumbar spinal canal stenosis patients with and without diabetes mellitus

Guanyu Cui, Kota Watanabe, Yoshiteru Miyauchi, Naobumi Hosogane, Takashi Tsuji, Ken Ishii, Masaya Nakamura, Yoshiaki Toyama, Kazuhiro Chiba, Takeshi Miyamoto, Morio Matsumoto

研究成果: Article

12 引用 (Scopus)

抄録

Background: 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. Methods: 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. Results: 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 ± 0.61 vs. 0.05 ± 0.09, P = 0.002). The LF from the DM (+) LSCS patients was significantly thicker than that from the DM (-) LSCS patients (5.0 ± 0.9 vs. 3.1 ± 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). Conclusion: 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.

元の言語English
ページ(範囲)785-790
ページ数6
ジャーナルJournal of Orthopaedic Science
16
発行部数6
DOI
出版物ステータスPublished - 01-01-2011
外部発表Yes

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Ligamentum Flavum
Matrix Metalloproteinase 13
Spinal Stenosis
Spinal Canal
Diabetes Mellitus
Hypertrophy
Fibrosis
Fibrillar Collagens
Microfibrils
Elastic Tissue
Hematoxylin
Eosine Yellowish-(YS)

All Science Journal Classification (ASJC) codes

  • Orthopedics and Sports Medicine

これを引用

Cui, Guanyu ; Watanabe, Kota ; Miyauchi, Yoshiteru ; Hosogane, Naobumi ; Tsuji, Takashi ; Ishii, Ken ; Nakamura, Masaya ; Toyama, Yoshiaki ; Chiba, Kazuhiro ; Miyamoto, Takeshi ; Matsumoto, Morio. / Matrix metalloproteinase 13 in the ligamentum flavum from lumbar spinal canal stenosis patients with and without diabetes mellitus. :: Journal of Orthopaedic Science. 2011 ; 巻 16, 番号 6. pp. 785-790.
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title = "Matrix metalloproteinase 13 in the ligamentum flavum from lumbar spinal canal stenosis patients with and without diabetes mellitus",
abstract = "Background: 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. Methods: 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. Results: 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 ± 0.61 vs. 0.05 ± 0.09, P = 0.002). The LF from the DM (+) LSCS patients was significantly thicker than that from the DM (-) LSCS patients (5.0 ± 0.9 vs. 3.1 ± 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). Conclusion: 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.",
author = "Guanyu Cui and Kota Watanabe and Yoshiteru Miyauchi and Naobumi Hosogane and Takashi Tsuji and Ken Ishii and Masaya Nakamura and Yoshiaki Toyama and Kazuhiro Chiba and Takeshi Miyamoto and Morio Matsumoto",
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Cui, G, Watanabe, K, Miyauchi, Y, Hosogane, N, Tsuji, T, Ishii, K, Nakamura, M, Toyama, Y, Chiba, K, Miyamoto, T & Matsumoto, M 2011, 'Matrix metalloproteinase 13 in the ligamentum flavum from lumbar spinal canal stenosis patients with and without diabetes mellitus', Journal of Orthopaedic Science, 巻. 16, 番号 6, pp. 785-790. https://doi.org/10.1007/s00776-011-0135-2

Matrix metalloproteinase 13 in the ligamentum flavum from lumbar spinal canal stenosis patients with and without diabetes mellitus. / Cui, Guanyu; Watanabe, Kota; Miyauchi, Yoshiteru; Hosogane, Naobumi; Tsuji, Takashi; Ishii, Ken; Nakamura, Masaya; Toyama, Yoshiaki; Chiba, Kazuhiro; Miyamoto, Takeshi; Matsumoto, Morio.

:: Journal of Orthopaedic Science, 巻 16, 番号 6, 01.01.2011, p. 785-790.

研究成果: Article

TY - JOUR

T1 - Matrix metalloproteinase 13 in the ligamentum flavum from lumbar spinal canal stenosis patients with and without diabetes mellitus

AU - Cui, Guanyu

AU - Watanabe, Kota

AU - Miyauchi, Yoshiteru

AU - Hosogane, Naobumi

AU - Tsuji, Takashi

AU - Ishii, Ken

AU - Nakamura, Masaya

AU - Toyama, Yoshiaki

AU - Chiba, Kazuhiro

AU - Miyamoto, Takeshi

AU - Matsumoto, Morio

PY - 2011/1/1

Y1 - 2011/1/1

N2 - Background: 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. Methods: 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. Results: 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 ± 0.61 vs. 0.05 ± 0.09, P = 0.002). The LF from the DM (+) LSCS patients was significantly thicker than that from the DM (-) LSCS patients (5.0 ± 0.9 vs. 3.1 ± 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). Conclusion: 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.

AB - Background: 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. Methods: 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. Results: 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 ± 0.61 vs. 0.05 ± 0.09, P = 0.002). The LF from the DM (+) LSCS patients was significantly thicker than that from the DM (-) LSCS patients (5.0 ± 0.9 vs. 3.1 ± 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). Conclusion: 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.

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U2 - 10.1007/s00776-011-0135-2

DO - 10.1007/s00776-011-0135-2

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AN - SCOPUS:83055181403

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JO - Journal of Orthopaedic Science

JF - Journal of Orthopaedic Science

SN - 0949-2658

IS - 6

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