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Title 

COMP-angiopoietin-1 promotes wound healing through enhanced angiogenesis, lymphangiogenesis, and blood flow in a diabetic mouse model

Authors 

C H ChoH K SungK T KimH G CheonG T OhHyo Jeong HongO J YooG Y Koh

Publisher 

National Academy of Sciences

Issue Date 

2006

Citation 

Proceedings of the National Academy of Sciences of the United States of America, vol. 103, no. 13, pp. 4946-4951

Keywords 

cutaneous wounddiabetesgrowth factornitric oxidetherapeutic proteinangiopoietin 1angiopoietin receptorbeta galactosidasebovine serum albumincartilage oligomeric matrix protein

Abstract 

Microvascular dysfunction is a major cause of impaired wound healing seen in diabetic patients. Therefore, reestablishment of structural and functional microvasculature could be beneficial to promote wound healing in these patients. Angiopoietin-1 (Ang1) is a specific growth factor functioning to generate a stable and functional vasculature through the Tie2 and Tie1 receptors. Here we determined the effectiveness of cartilage oligomeric matrix protein (COMP)-Ang1, a soluble, stable, and potent form of Ang1, on promotion of healing in cutaneous wounds of diabetic mice. An excisional full-thickness wound was made in the dorsal side of the tail of diabetic (db/db) mice, and mice were then treated systemically with adenovirus (Ade) encoding COMP-Ang1 or with control virus encoding β-gal (Ade-β-gal) or treated topically with recombinant COMP-Ang1 protein or BSA. Time course observations revealed that mice treated with Ade-COMP-Ang1 or COMP-Ang1 protein showed accelerated wound closure and epidermal and dermal regeneration, enhanced angiogenesis and lymphangiogenesis, and higher blood flow in the wound region compared with mice treated with control virus or BSA. COMP-Ang1 promotion of wound closure and angiogenesis was not dependent on endothelial nitric oxide synthase or inducible nitric oxide synthase alone. Taken together, these findings indicate that COMP-Ang1 can promote wound healing in diabetes through enhanced angiogenesis, lymphangiogenesis, and blood flow.

ISSN 

0027-8424

Link 

http://dx.doi.org/10.1073/pnas.0506352103

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2019-05-02


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