Hyperglycemia induces abnormal gene expression in hematopoietic stem cells and their progeny in diabetic neuropathy. Issue 6 (25th February 2014)

• Record Type: Journal Article
• Authors: Katagi, Miwako; Terashima, Tomoya; Okano, Junko; Urabe, Hiroshi; Nakae, Yuki; Ogawa, Nobuhiro; Udagawa, Jun; Maegawa, Hiroshi; Matsumura, Kazuhiro; Chan, Lawrence; Kojima, Hideto
• Is Part Of: FEBS letters. Volume 588:Issue 6(2014)
• Page Start: 1080
• Page End: 1086
• Publication Date: 2014-02-25
• Subjects: Neuropathy -- Hyperglycemia -- Hematopoietic stem cell -- Cell–cell fusion -- Stem cell abnormalities; Biochemistry -- Periodicals; Biophysics -- Periodicals; Molecular biology -- Periodicals; Biochimie -- Périodiques; Biochemistry; Biophysics; Molecular biology; Periodicals; 572.05
• DOI: 10.1016/j.febslet.2014.02.030
• Languages: English
• ISSNs: 0014-5793

Abstract

Abstract : Diabetic peripheral neuropathy is a major chronic diabetic complication. We have previously shown that in type 1 diabetic streptozotocin‐treated mice, insulin‐ and TNF‐α co‐expressing bone marrow‐derived cells (BMDCs) induced by hyperglycemia travel to nerve tissues where they fuse with nerve cells, causing premature apoptosis and nerve dysfunction. Here we show that similar BMDCs also occur in type 2 diabetic high‐fat diet (HFD) mice. Furthermore, we found that hyperglycemia induces the co‐expression of insulin and TNF‐α in c‐kit + Sca‐1 + lineage − (KSL) progenitor cells, which maintain the same expression pattern in the progeny, which in turn participates in the fusion with neurons when transferred to normoglycemic animals. Abstract : Hyperglycemia induces bone marrow stem cell abnormalities. Insulin‐ and TNF‐α‐positive cells appear among KSL cells in hyperglycemic mice. Progeny of KSL cells exposed to hyperglycemia fuse with normal DRG neurons.