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ヘムオキシゲナーゼ1欠損と全身性慢性炎症に対する防御機構の破綻
https://doi.org/10.24517/00051048
https://doi.org/10.24517/00051048182d6a2b-0f60-4dd1-bfae-dd038255c042
名前 / ファイル | ライセンス | アクション |
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ME-PR-KOIZUMI-S-kaken 2008-14p.pdf (734.4 kB)
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Item type | 報告書 / Research Paper(1) | |||||
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公開日 | 2018-06-14 | |||||
タイトル | ||||||
タイトル | ヘムオキシゲナーゼ1欠損と全身性慢性炎症に対する防御機構の破綻 | |||||
タイトル | ||||||
言語 | en | |||||
タイトル | Heme oxygenase-1 deficiency and failure of human defense mechanisms against generalized chronic inflammation | |||||
言語 | ||||||
言語 | jpn | |||||
資源タイプ | ||||||
資源タイプ識別子 | http://purl.org/coar/resource_type/c_18ws | |||||
資源タイプ | research report | |||||
ID登録 | ||||||
ID登録 | 10.24517/00051048 | |||||
ID登録タイプ | JaLC | |||||
著者 |
小泉, 晶一
× 小泉, 晶一 |
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著者別表示 |
Koizumi, Shoichi
× Koizumi, Shoichi |
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書誌情報 |
平成19(2007)年度 科学研究費補助金 基盤研究(B) 研究成果報告書 en : 2007 Fiscal Year Final Research Report 巻 2005-2007, p. 14p., 発行日 2008-03 |
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出版者 | ||||||
出版者 | 金沢大学医薬保健研究域医学系 | |||||
抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | ヘムオキシゲナーゼ1(HO-1)はヘムを一酸化炭素(CO)とビリルビンとフェリチン(Feより誘導される)に代謝する律則酵素である。われわれが世界で初めて発見した「ヒトHO-1欠損」症例(1999)は2歳頃からの全身性慢性炎症が増悪し,6歳で死亡した。本症例のこれまでの詳細な病態解析とin vitro実験的研究によって、HO-1の、生体へのストレス防御因子としての役割を解明し、下記の研究成果を得た。 (1)患児の生検材料やリンパ球細胞株でHO-1の発現が認めらないことと、HO-1遺伝子の異常から本疾患が確立された。 (2)HO-1欠損症の臨床特徴は、主として造血系単球と血管内皮細胞及び腎尿細管細胞の障害に起因する。 (3)HO-1欠損症では、外因性酸化ストレスによって、全身性炎症と凝固線溶系の著しい亢進を惹起し、ストレスが長期に継続すると、免疫系や凝固線溶系が消耗、破壊される。 (4)単球細胞表面抗原の異常、貪食能の低下が認められた。また、CD16high/CCR2-の細胞亜群にHO-1発現が強く、この細胞群の動態は細菌性感染症とウイルス性感染症で異なっていることから、単球のHO-1発現が各種感染症の病態表現に深くかかわっていることが示唆された。さらに、単球のHb/Hp/CD163コンプレックスがHO-1誘導と強く相関することがわかった。 (5)各種腎疾患の生検材料、及びin vitro細胞株の検討から、HO-1は腎尿細管上皮がストレス防御に有効に働いていることが強く示唆された。さらに尿沈さ細胞中のHO-1濃度測定は、腎尿細管傷害を観察する非侵襲的な方法として有用であろうと思われた。 (6)以上、HO-1欠損症の詳細な検討は、システミックな炎症発症における新しい病態機序の解明に役立ち、そして、新しい治療法の開発に繋がるかの知れない。 |
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抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | Heme oxygenase (HO) is the rate-limiting enzyme that adds an oxygen molecule to the porphyrin ring of heme, thereby catalyzing the oxidation of heme to biliverdin/ bilirubin, free iron, and carbon monoxide (CO). By producing these metabolites, HO plays a crucial role in humans as a defense factor against a variety of oxidative stresses. The first case of human HO - 1 deficiency was reported by Yachie, et. Al. in our laboratory in 1999. A series of clinical and laboratory investigation of the patient with HO-1 deficiency revealed that (1) The boy completely lacked HO-1, genetically having a two-base-pair deletion in exon 3 of the paternal allele of the gene and a deletion of exon 2 of the maternal allele with genomic exon-deletion (1,730bp) mediated by Alu-Alu, recombination. (2) Dysfunction of both monocytes and endothelial cells was remarkably demonstrated. (2) External continuous stresses triggered excessive systemic inflammatory reactions and marked abnormalities of the coagulation/ fibrinolysis system, resulting finally in exhaustion of immune and coagulation system. (3) Morphological abnormality of monocytes and significant reduction of their surface molecules resulted in a markedly impaired phagocytosis of monocytes. Furthermore, the selective expansion of a CD16+++, CCR2- subpopulation of monocytes that preferentially produced HO-1 mRNA was shown during the acute phase of infections including both bacterial and viral infections. HO-1 production by alveolar macrophages in childhood pulmonary hypertension correlated with overexpression of CD1G3 surface molecules was also demonstrated. (4) Progressive renal tubulointerstitial injury was remarkable in the patient with HO-1 deficiency. Enhanced production of HO-lin proximal tubular epithelial cells as compared with mesangial cells was shown in variety of renal biopsy specimen as well as in vitro experiment. Recently HO-1 production by urinary tract cells and evaluation of tubulointestinal injury of the kidney was investigated by MA analysis of urinary sediments. Detailed analysis of HO-I deficiency may offer a valuable tool to understand the pathogenesis of and to develop a novel therapeutic approach to systemic inflammatory illnesses. | |||||
内容記述 | ||||||
内容記述タイプ | Other | |||||
内容記述 | 研究課題/領域番号:17390298, 研究期間(年度):2005-2007 | |||||
内容記述 | ||||||
内容記述タイプ | Other | |||||
内容記述 | 出典:「ヘムオキシゲナーゼ1欠損と全身性慢性炎症に対する防御機構の破綻」研究成果報告書 課題番号17390298 (KAKEN:科学研究費助成事業データベース(国立情報学研究所)) 本文データは著者版報告書より作成 |
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著者版フラグ | ||||||
出版タイプ | AM | |||||
出版タイプResource | http://purl.org/coar/version/c_ab4af688f83e57aa | |||||
関連URI | ||||||
識別子タイプ | URI | |||||
関連識別子 | https://kaken.nii.ac.jp/search/?qm=50019973 | |||||
関連名称 | https://kaken.nii.ac.jp/search/?qm=50019973 | |||||
関連URI | ||||||
識別子タイプ | URI | |||||
関連識別子 | https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-17390298/ | |||||
関連名称 | https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-17390298/ | |||||
関連URI | ||||||
識別子タイプ | URI | |||||
関連識別子 | https://kaken.nii.ac.jp/report/KAKENHI-PROJECT-17390298/173902982007kenkyu_seika_hokoku_gaiyo/ | |||||
関連名称 | https://kaken.nii.ac.jp/report/KAKENHI-PROJECT-17390298/173902982007kenkyu_seika_hokoku_gaiyo/ |