@article{oai:shiga-med.repo.nii.ac.jp:00003867,
 author = {樫, 美和子 and 寺島, 智也 and 大橋, 夏子 and 中江, 由希 and 山田, 茜 and 仲川, 孝彦 and 宮澤, 伊都子 and 前川, 聡 and 岡野, 純子 and 鈴木, 義久 and 藤野, 和典 and 江口, 豊 and 小島, 秀人 and KATAGI, Miwako and TERASHIMA, Tomoya and OHASHI, Natsuko and NAKAE, Yuki and YAMADA, Akane and NAKAGAWA, Takahiko and MIYAZAWA, Itsuko and MAEGAWA, Hiroshi and OKANO, Junko and SUZUKI, Yoshihisa and FUJINO, Kazunori and EGUCHI, Yutaka and KUSHIMA, Ryoji},
 issue = {1},
 journal = {Communications Biology},
 month = {May},
 note = {pdf, Journal Article, Diabetic neuropathy is an incurable disease. We previously identified a mechanism by which aberrant bone marrow-derived cells (BMDCs) pathologically expressing proinsulin/TNF-α fuse with residential neurons to impair neuronal function. Here, we show that CD106-positive cells represent a significant fraction of short-term hematopoietic stem cells (ST-HSCs) that contribute to the development of diabetic neuropathy in mice. The important role for these cells is supported by the fact that transplantation of either whole HSCs or CD106-positive ST-HSCs from diabetic mice to non-diabetic mice produces diabetic neuronal dysfunction in the recipient mice via cell fusion. Furthermore, we show that transient episodic hyperglycemia produced by glucose injections leads to abnormal fusion of pathological ST-HSCs with residential neurons, reproducing neuropathy in nondiabetic mice. In conclusion, we have identified hyperglycemia-induced aberrant CD106-positive ST-HSCs underlie the development of diabetic neuropathy. Aberrant CD106-positive ST-HSCs constitute a novel therapeutic target for the treatment of diabetic neuropathy.},
 title = {Malfunctioning CD106-positive, short-term hematopoietic stem cells trigger diabetic neuropathy in mice by cell fusion.},
 volume = {4},
 year = {2021}
}