@techreport{oai:kindai.repo.nii.ac.jp:00022168,
 author = {岡田, 清孝 and 河尾, 直之},
 month = {},
 note = {https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-18K06863/, 研究成果の概要（和文）：マウスのSTZ誘発糖尿病モデルとDex長期投与モデルでは、骨髄幹細胞異常とマクロファージ誘導の低下を伴う骨損傷後の修復遅延が認められた。この骨修復遅延には、線溶系の阻害因子であるPAI-1の関与が示唆された。また、STZモデルでは、血糖値の上昇と骨密度の低下が見られたが、Dex長期投与モデルでは正常範囲であった。両モデルにおける骨修復遅延に対するPAI-1の関与は、異なることが示唆された。研究成果の概要（英文）：We investigate the role of macrophages in diabetic delayed bone repair after femoral bone injury in streptozotocin (STZ)- or dexamethasone (Dex)-treated and plasminogen activator inhibitor-1 (PAI-1)-deficient female mice. STZ- or Dex-treatment induced a significant delay in bone repair after bone injury in wild-type mice. PAI-1 deficiency significantly blunted Dex-induced delayed bone repair in mice. STZ- or Dex-treatment significantly decreased the numbers of macrophages at the damaged site on day 2 after femoral bone injury in mice. On the other hand, PAI-1 deficiency significantly attenuated a decrease in the number of macrophages induced by STZ- or Dex-treatment at the damaged site on day 2 after bone injury in mice. PAI-1 is involved in delayed bone repair after bone injury induced by type 1 diabetes or glucocorticoid in mice. PAI-1 may influence early stage osteoblast differentiation and apoptosis during the osteoblastic restoration phase of the bone repair process., 研究種目：基盤研究(C);  研究期間：2018～2020;   課題番号：18K06863;   研究分野：医歯薬学;   科研費の分科・細目：, application/pdf},
 title = {糖尿病での骨損傷後の修復障害における骨髄幹細胞異常とマクロファージ機能の解明},
 year = {2021},
 yomi = {オカダ, キヨタカ and カワオ, ナオユキ}
}