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Malfunctioning CD106-positive, short-term hematopoietic stem cells trigger diabetic neuropathy in mice by cell fusion.

KATAGI Miwako 40732459 TERASHIMA Tomoya 40378485 OHASHI Natsuko 60816776 NAKAE Yuki 40638186 YAMADA Akane NAKAGAWA Takahiko 60641595 MIYAZAWA Itsuko 20649305 0000-0001-6310-7225 MAEGAWA Hiroshi 00209363 0000-0002-4611-8149 OKANO Junko 50447968 SUZUKI Yoshihisa 30243025 FUJINO Kazunori 70402716 EGUCHI Yutaka 00263054 KUSHIMA Ryoji 40252382 滋賀医科大学

2021.05.21

概要

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 develop- ment of diabetic neuropathy. Aberrant CD106-positive ST-HSCs constitute a novel ther- apeutic target for the treatment of diabetic neuropathy.

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