2005 Fiscal Year Final Research Report Summary
Manifestation of HMGB-1 and Preventive Effect of Degeneration on Spinal Cord Following Acute Traumatic Injury.
| Project/Area Number |
16591499
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Orthopaedic surgery
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| Research Institution | Kagoshima University |
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Principal Investigator |
ARISHIMA Yoshiya Kagoshima Graduate School of Medical and Dental Sciences, Resaerch Associate, 大学院医歯学総合研究科, 助手 (90336339)
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| Co-Investigator(Kenkyū-buntansha) |
YONE Kazunori Kagoshima Graduate School of Medical and Dental Sciences, Professor, 大学院医歯学総合研究科, 教授 (40182844)
NAGAMINE Tomonori Kagoshima University, Hospital, Research Associate, 歯学部・歯学部附属病院, 助手 (10359979)
YOKOUCHI Masahiro Kagoshima Graduate School of Medical and Dental Sciences, Research Associate, 大学院医歯学総合研究科, 助手 (80359976)
HAYASHI Kyoji Kagoshima University, Hospital, Associate Professor, 歯学部・歯学部附属病院, 講師 (50325784)
KOMIYA Setsuro Kagoshima Graduate School of Medical and Dental Sciences, Professor, 大学院医歯学総合研究科, 教授 (30178371)
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| Project Period (FY) |
2004 – 2005
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| Keywords | Spinal Cord Injury / Apoptosis / Erythropoietin / HMGB-1 |
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| Research Abstract |
Several investigators have confirmed hat delayed neuronal and glial cell death caused by apoptosis formed functional disorders after acute traumatic spinal cord injury. However the mechanism in detail has been unclear. Recently several investigators have demonstrated that a nuclear protein, high mobility group box chromosomal protein 1 (HGMB-1) has a role of an inflammatory mediator in endotoxin shock. We studied the manifestation of HMGB-1 on acute traumatic spinal cord injury in rats, and examined the role of HMGB-1 in induction of apoptosis using immunohistochemical staining with the tumor necrosis factor a (TNF-α) and the terminal deoxynucleotidyl transferase mediated dUTP nick-end labeling (TUNEL) method.
Male Wistar rats were mounted on an apparatus to induce injury to the thoracic spinal cord by the static load technique. Immunohistochemical staining using anti HMGB-1 antibody, anti TNF-α antibody were performed and TUNEL staining was performed to detect of apoptosis. We also performed double-staining using anti HMGB-1 antibody with anti TNF-α antibody or anti active caspase-3 to confirm the appearance of those in the identical cells. And the appearance of the receptor for advanced glycation end products (RAGE) which is the specific receptor of HMGB-1 was also examined.
HMGB-1, TNF-α positive cells and TUNEL positive cells were seen in the maximum of forty-eight hours and seventy-two hours after injury in the models respectively. Double-staining showed that HMGB-1 with TNF-α or caspase-3 were demonstrated in the identical cells. HMGB-1 was positive in neurons or oligodendrocytes, but negative in astrocytes. HMGB-1 and RAGE were seen in the identical cells.
In this study, it was confirmed that HMGB-1 and TNF-α were seen in the identical cells, and the time of maximum appearance of it preceded that of TUNEL method. In conclusion, it was suggested that TNF-α has a role in the conduction of apoptosis in the relation with HMGB-1.
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