Upregulation of tissue inhibitor of metalloproteinase-1 contributes to restoration of the extracellular matrix in the rabbit basilar artery during cerebral vasospasm after subarachnoid hemorrhage

Ryota Kurogi, Yuichiro Kikkawa, Satoshi Matsuo, Akira Nakamizo, Masahiro Mizoguchi, Tomio Sasaki

研究成果: ジャーナルへの寄稿記事

4 引用 (Scopus)

抄録

Vascular remodeling caused by extracellular matrix (ECM) metabolism contributes to the development of cerebral vasospasm after subarachnoid hemorrhage (SAH). The balance between tissue inhibitor of metalloproteinases (TIMPs) and matrix metalloproteinases (MMPs) plays an important role in ECM remodeling. We investigated the mechanism of vascular remodeling following cerebral vasospasm in a rabbit double hemorrhage model. Rabbit basilar arteries were harvested on days 3, 5, and 7 after initial hemorrhage. TIMP-1, TIMP-2, MMP-2, and MMP-9 mRNA and protein expression were investigated with microarray analysis, quantitative real-time PCR, immunoblot analysis, and enzyme-linked immunosorbent assay (ELISA). The expression and localization of TIMP-1, TIMP-2, MMP-2, MMP-9, elastin, fibronectin, laminin, and collagens I, III, and IV were investigated with immuohistochemical staining. After SAH, TIMP-1 mRNA and protein expression were significantly increased on day 3 and then decreased to the control level on days 5 and 7. MMP-9 protein expression was significantly increased on day 7. TIMP-2 and MMP-2 mRNA and protein expression were significantly increased on day 7. Elastin, fibronectin, laminin, and collagens I, III, and IV protein expression was decreased on day 3 and then restored to control levels on day 7. Upregulation of TIMP-1 during the early phase of cerebral vasospasm may contribute to the recovery of the ECM during the late phase of cerebral vasospasm, resulting in a protective role of TIMP-1 from cerebral vasospasm. Moreover, the increase in arterial compliance by the decrease in ECM during the early phase of cerebral vasospasm may facilitate vasoconstriction of the cerebral artery.

元の言語英語
ページ(範囲)26-36
ページ数11
ジャーナルBrain Research
1616
DOI
出版物ステータス出版済み - 1 1 2015

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Intracranial Vasospasm
Basilar Artery
Tissue Inhibitor of Metalloproteinase-1
Subarachnoid Hemorrhage
Extracellular Matrix
Up-Regulation
Rabbits
Tissue Inhibitor of Metalloproteinase-2
Matrix Metalloproteinase 2
Matrix Metalloproteinase 9
Elastin
Laminin
Proteins
Fibronectins
Messenger RNA
Collagen
Hemorrhage
Tissue Inhibitor of Metalloproteinases
Cerebral Arteries
Microarray Analysis

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)
  • Molecular Biology
  • Clinical Neurology
  • Developmental Biology

これを引用

Upregulation of tissue inhibitor of metalloproteinase-1 contributes to restoration of the extracellular matrix in the rabbit basilar artery during cerebral vasospasm after subarachnoid hemorrhage. / Kurogi, Ryota; Kikkawa, Yuichiro; Matsuo, Satoshi; Nakamizo, Akira; Mizoguchi, Masahiro; Sasaki, Tomio.

:: Brain Research, 巻 1616, 01.01.2015, p. 26-36.

研究成果: ジャーナルへの寄稿記事

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abstract = "Vascular remodeling caused by extracellular matrix (ECM) metabolism contributes to the development of cerebral vasospasm after subarachnoid hemorrhage (SAH). The balance between tissue inhibitor of metalloproteinases (TIMPs) and matrix metalloproteinases (MMPs) plays an important role in ECM remodeling. We investigated the mechanism of vascular remodeling following cerebral vasospasm in a rabbit double hemorrhage model. Rabbit basilar arteries were harvested on days 3, 5, and 7 after initial hemorrhage. TIMP-1, TIMP-2, MMP-2, and MMP-9 mRNA and protein expression were investigated with microarray analysis, quantitative real-time PCR, immunoblot analysis, and enzyme-linked immunosorbent assay (ELISA). The expression and localization of TIMP-1, TIMP-2, MMP-2, MMP-9, elastin, fibronectin, laminin, and collagens I, III, and IV were investigated with immuohistochemical staining. After SAH, TIMP-1 mRNA and protein expression were significantly increased on day 3 and then decreased to the control level on days 5 and 7. MMP-9 protein expression was significantly increased on day 7. TIMP-2 and MMP-2 mRNA and protein expression were significantly increased on day 7. Elastin, fibronectin, laminin, and collagens I, III, and IV protein expression was decreased on day 3 and then restored to control levels on day 7. Upregulation of TIMP-1 during the early phase of cerebral vasospasm may contribute to the recovery of the ECM during the late phase of cerebral vasospasm, resulting in a protective role of TIMP-1 from cerebral vasospasm. Moreover, the increase in arterial compliance by the decrease in ECM during the early phase of cerebral vasospasm may facilitate vasoconstriction of the cerebral artery.",
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AU - Kikkawa, Yuichiro

AU - Matsuo, Satoshi

AU - Nakamizo, Akira

AU - Mizoguchi, Masahiro

AU - Sasaki, Tomio

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AB - Vascular remodeling caused by extracellular matrix (ECM) metabolism contributes to the development of cerebral vasospasm after subarachnoid hemorrhage (SAH). The balance between tissue inhibitor of metalloproteinases (TIMPs) and matrix metalloproteinases (MMPs) plays an important role in ECM remodeling. We investigated the mechanism of vascular remodeling following cerebral vasospasm in a rabbit double hemorrhage model. Rabbit basilar arteries were harvested on days 3, 5, and 7 after initial hemorrhage. TIMP-1, TIMP-2, MMP-2, and MMP-9 mRNA and protein expression were investigated with microarray analysis, quantitative real-time PCR, immunoblot analysis, and enzyme-linked immunosorbent assay (ELISA). The expression and localization of TIMP-1, TIMP-2, MMP-2, MMP-9, elastin, fibronectin, laminin, and collagens I, III, and IV were investigated with immuohistochemical staining. After SAH, TIMP-1 mRNA and protein expression were significantly increased on day 3 and then decreased to the control level on days 5 and 7. MMP-9 protein expression was significantly increased on day 7. TIMP-2 and MMP-2 mRNA and protein expression were significantly increased on day 7. Elastin, fibronectin, laminin, and collagens I, III, and IV protein expression was decreased on day 3 and then restored to control levels on day 7. Upregulation of TIMP-1 during the early phase of cerebral vasospasm may contribute to the recovery of the ECM during the late phase of cerebral vasospasm, resulting in a protective role of TIMP-1 from cerebral vasospasm. Moreover, the increase in arterial compliance by the decrease in ECM during the early phase of cerebral vasospasm may facilitate vasoconstriction of the cerebral artery.

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