• ホーム
  • 検索結果
  • The Tissue Fibrinolytic System Contributes to the Induction of Macrophage Function and CCL3 during Bone Repair in Mice.

The Tissue Fibrinolytic System Contributes to the Induction of Macrophage Function and CCL3 during Bone Repair in Mice.

PloS one (2015-04-22)
Naoyuki Kawao, Yukinori Tamura, Yoshitaka Horiuchi, Katsumi Okumoto, Masato Yano, Kiyotaka Okada, Osamu Matsuo, Hiroshi Kaji
要旨

Macrophages play crucial roles in repair process of various tissues. However, the details in the role of macrophages during bone repair still remains unknown. Herein, we examined the contribution of the tissue fibrinolytic system to the macrophage functions in bone repair after femoral bone defect by using male mice deficient in plasminogen (Plg-/-), urokinase-type plasminogen activator (uPA-/-) or tissue-type plasminogen activator (tPA-/-) genes and their wild-type littermates. Bone repair of the femur was delayed in uPA-/- mice until day 6, compared with wild-type (uPA+/+) mice. Number of Osterix-positive cells and vessel formation were decreased in uPA-/- mice at the bone injury site on day 4, compared with those in uPA+/+ mice. Number of macrophages and their phagocytosis at the bone injury site were reduced in uPA-/- and Plg-/-, but not in tPA-/- mice on day 4. Although uPA or plasminogen deficiency did not affect the levels of cytokines, including TNF-α, IL-1β, IL-6, IL-4 and IFN-γ mRNA in the damaged femur, the elevation in CCL3 mRNA levels was suppressed in uPA-/- and Plg-/-, but not in tPA-/- mice. Neutralization of CCL3 antagonized macrophage recruitment to the site of bone injury and delayed bone repair in uPA+/+, but not in uPA-/- mice. Our results provide novel evidence that the tissue fibrinolytic system contributes to the induction of macrophage recruitment and CCL3 at the bone injury site, thereby, leading to the enhancement of the repair process.

材料
製品番号
ブランド
製品内容

Sigma-Aldrich
モノクローナル抗VEGF抗体 マウス宿主抗体, clone 3F7, purified immunoglobulin, buffered aqueous solution
Sigma-Aldrich
抗血管内皮増殖因子抗体 ヤギ宿主抗体, IgG fraction of antiserum, lyophilized powder
Sigma-Aldrich
モノクロナール抗血管内皮増殖因子 マウス宿主抗体, clone 26503, purified immunoglobulin, lyophilized powder
Sigma-Aldrich
Anti-PECAM-1 antibody produced in rabbit, affinity isolated antibody
Sigma-Aldrich
抗血管内皮増殖因子抗体 ヤギ宿主抗体, affinity isolated antibody, lyophilized powder
Sigma-Aldrich
ANTI-CD31(C-TERMINAL) antibody produced in rabbit, purified immunoglobulin, buffered aqueous solution
Sigma-Aldrich
Anti-ADGRE1 antibody produced in rabbit, Prestige Antibodies® Powered by Atlas Antibodies, affinity isolated antibody, buffered aqueous glycerol solution
Sigma-Aldrich
モノクローナル抗PECAM1抗体 マウス宿主抗体, clone MEM-05, purified immunoglobulin, buffered aqueous solution
Sigma-Aldrich
Monoclonal Anti-PECAM1, (C-terminal) antibody produced in mouse, clone 4E3-1D9, purified immunoglobulin, buffered aqueous solution
Sigma-Aldrich
Monoclonal Anti-SP7 antibody produced in mouse, clone 1C11, purified immunoglobulin, buffered aqueous solution
Sigma-Aldrich
抗PECAM1抗体 マウス宿主抗体, purified immunoglobulin, buffered aqueous solution
Sigma-Aldrich
Anti-EMR1 antibody produced in rabbit, affinity isolated antibody
Sigma-Aldrich
Anti-SP7, (N-terminal) antibody produced in rabbit, affinity isolated antibody
Sigma-Aldrich
Anti-SP7 antibody produced in rabbit, affinity isolated antibody
Sigma-Aldrich
モノクロナール抗PECAM1 マウス宿主抗体, clone 1D2-1A5, purified immunoglobulin, buffered aqueous solution
Sigma-Aldrich
Monoclonal Anti-SP7 antibody produced in mouse, clone 2G6, purified immunoglobulin, buffered aqueous solution
Sigma-Aldrich
Anti-VEGFA antibody produced in goat, affinity isolated antibody, buffered aqueous solution

ソーシャルメディア

LinkedIn icon
Twitter icon
Facebook Icon
Instagram Icon

Merck

研究、開発、製造

私たちは、バイオテクノロジーと医薬品の研究&開発および製造のソリューションとサービスを提供する、グローバルなライフサイエンス業界のリーディングサプライヤーです。

© 2021 Merck KGaA, Darmstadt, Germany and/or its affiliates.All Rights Reserved.

当ウェブサイトのいかなる内容についても、許可なく複写することを禁じます。