Limitations of the db/db mouse in translational wound healing research: Is the NONcNZO10 polygenic mouse model superior?

被引:53
作者
Fang, Robert C. [1 ]
Kryger, Zol B. [1 ]
Buck, Donald W., II [1 ]
De La Garza, Mauricio [1 ]
Galiano, Robert D. [1 ]
Mustoe, Thomas A. [1 ]
机构
[1] Northwestern Univ, Feinberg Sch Med, Div Plast & Reconstruct Surg, Lab Wound Repair & Regenerat Med, Chicago, IL 60611 USA
关键词
DIABETES-MELLITUS; MURINE MODEL; MICE; OBESITY; LEPTIN; STREPTOZOTOCIN; PATHOGENESIS; DIABESITY; RECEPTOR; FUTURE;
D O I
10.1111/j.1524-475X.2010.00634.x
中图分类号
Q2 [细胞生物学];
学科分类号
071013 [干细胞生物学];
摘要
Murine models have provided valuable insights into the pathogenesis of both diabetes and chronic wounds. However, only a few published reports to date have investigated wound healing differences among the differing diabetic mouse models. The goal of the present study was to further define the wound healing deficiency phenotypes of streptozotocin-induced (STZ-induced), Akita, and db/db diabetic mice in comparison with a promising new polygenic strain of Type 2 diabetes (NONcNZO10) by using three specific wound models that targeted different critical processes in the pathogenesis of chronic wounds. Incisional, excisional, and ischemia/reperfusion wound models were established on mice of each strain. Wound healing parameters including tensile strength, epithelial gap, and wound necrosis were evaluated. In contrast to the other diabetic mice, the NONcNZO10 strain was found to have significant wound healing impairments in all wound healing models. Not only do the NONcNZO10 mice appear to better model human Type 2 diabetes, these provocative findings suggest that the mice may show more clinically relevant wound healing deficiencies than previous diabetic mouse models.
引用
收藏
页码:605 / 613
页数:9
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