HUCMNCs protect vascular endothelium and prevent ISR after endovascular interventional therapy for vascular diseases in T2DM rabbits

HUCMNCs protect vascular endothelium and prevent ISR after endovascular interventional therapy... The therapeutic effect of transplantation of human umbilical cord blood cell-derived mononuclear cells (HUCMNCs) on treating in-stent restenosis (ISR) after endovascular interventional therapy (EIT) was evaluated in preclinical rabbit model of type 2 diabetes mellitus (T2DM)-related peripheral artery disease (PAD). HUCMNCs were transplanted to T2DM rabbits subjected to femoral artery occlusion surgery and received EIT. Serum concentration of soluble vascular endothelial cadherin (VE-cad) and plasma concentration of lipoprotein-associated phospholipase A2 (Lp-PLA2) were determined with enzyme-linked immunosorbent assay before and after the transplantation. The injury and the recovery of right femoral artery at stenting site were evaluated with Hematoxylin and Eosin (HE) staining. HUCMNCs purified from umbilical cord blood were 100% CD45+ and 96.5% CD34− with round or oval morphology and adherent growth pattern. The soluble VE-cad and Lp-PLA2 were significantly attenuated after HUCMNC transplantation. The intimal area and the ratio between intimal area and medium film area in the dilated occlusion site were also dramatically decreased 4 weeks after receiving HUCMNCs. HUCMNC transplantation is effective in protecting vascular endothelial function and preventing ISR after EIT in T2DM rabbits suffering from PAD. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Molecular and Cellular Biochemistry Springer Journals

HUCMNCs protect vascular endothelium and prevent ISR after endovascular interventional therapy for vascular diseases in T2DM rabbits

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Publisher
Springer US
Copyright
Copyright © 2017 by Springer Science+Business Media New York
Subject
Life Sciences; Biochemistry, general; Medical Biochemistry; Oncology; Cardiology
ISSN
0300-8177
eISSN
1573-4919
D.O.I.
10.1007/s11010-017-3024-y
Publisher site
See Article on Publisher Site

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