Oxidative stress tolerance of early stage diabetic endothelial progenitor cell

• Published in: Regenerative therapy Vol. 1; no. C; pp. 38 - 44
• Main Authors: Sukmawati, Dewi, Fujimura, Satoshi, Jitsukawa, Sachie, Ito-Hirano, Rie, Ishii, Takamasa, Sato, Tadayuki, Hayashi, Ayato, Itoh, Seigo, Mizuno, Hiroshi, Daida, Hiroyuki, Tanaka, Rica
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 01-06-2015; Japanese Society for Regenerative Medicine; Elsevier
• Subjects: Anti-oxidative enzymes; Bone marrow-derived endothelial progenitor cells; Diabetes; Original; Oxidative stress; Oxidative stress; QQc; BM-EPC; EPC-CFU; BM-KSL; dEPC-CFU; Bone marrow-derived endothelial progenitor cells; tEPC-CFU; Anti-oxidative enzymes; pEPC-CFU; DM BM-KSL; Diabetes; EPC-CFA; BM-EPC, bone marrow-derived endothelial progenitor cells; pEPC-CFU, primitive/small EPC-CFU; EPC-CFA, endothelial progenitor cell colony forming assay; dEPC-CFU, definitive/large EPC-CFU; tEPC-CFU, total EPC-CFU; EPC-CFU, endothelial progenitor cell colony forming unit; DM BM-KSL, diabetic BM-KSL; BM-KSL, bone marrow derived-c-Kit+Sca-1+Lin; QQc, quality and quantity culture system
• ISSN: 2352-3204; 2352-3204
• DOI: 10.1016/j.reth.2014.11.001

One of the causes for poor vasculogenesis of diabetes mellitus (DM) is known to rise from the dysfunction of bone marrow-derived endothelial progenitor cells (BM EPCs). However, the origin of its cause is less understood. We aimed to investigate the effect of oxidative stress in early stage of diabetic BM-EPC and whether its vasculogenic dysfunction is caused by oxidative stress.
Bone marrow c-Kit+Sca-1+Lin− (BM-KSL) cells were sorted from control and streptozotocin-induced diabetic C57BL6J mice by flow cytometry. BM-KSLs were then assessed for vasculogenic potential (colony forming assay; EPC-CFA), accumulation of intracellular ROS (CM-H2DCFDA), carbonylated protein (ELISA), anti-oxidative enzymes expression (RT-qPCR) and catalase activity (Amplex Red).
Compared to control, DM BM-KSL had significantly lower EPC-CFUs in both definitive EPC-CFU and total EPC-CFU (p < 0.05). Interestingly, the oxidative stress level of DM BM-KSL was comparable and was not significantly different to control followed by increased in anti-oxidative enzymes expression and catalase activity.
Primitive BM-EPCs showed vasculogenic dysfunction in early diabetes. However the oxidative stress is not denoted as the major initiating factor of its cause. Our results suggest that primitive BM-KSL cell has the ability to compensate oxidative stress levels in early diabetes by increasing the expression of anti-oxidative enzymes.
•Primitive BM-EPC showed EPC-CFU dysfunction in early diabetes.•Primitive BM-EPC has the ability to withstand oxidative stress in early diabetes.•Early diabetic BM-EPC increased anti-oxidative expression to compensate oxidative stress.