Caskey Robert C, Liechty Kenneth W
Department of General Surgery, University of Pennsylvania School of Medicine, Philadelphia, PA, USA.
Methods Mol Biol. 2013;1037:99-115. doi: 10.1007/978-1-62703-505-7_6.
There is a vast wealth of information to be gained by tracking both the fate and contribution of individual cell types to the wound healing response. This is particularly important in research focused on impaired healing, such as diabetic wound healing, where the number or function of one or more specific cell types may be abnormal and contribute to the observed healing derangements. Specifically, diabetic wounds have been shown to have an overactive inflammatory response and decreased angiogenesis. The ability to track specific cell types participating in these responses would dramatically improve our understanding of the cellular derangements in diabetic healing. In this chapter, we review two novel chimeric models based on the leptin deficient Db/Db mouse. The use of these models allows for the tracking of bone marrow derived inflammatory and progenitor cell populations as well as the determination of the molecular contributions of these cell populations to the wound healing response.
通过追踪个体细胞类型在伤口愈合反应中的命运和贡献，可以获得大量丰富的信息。这在专注于愈合受损的研究中尤为重要，例如糖尿病伤口愈合，其中一种或多种特定细胞类型的数量或功能可能异常，并导致观察到的愈合紊乱。具体而言，已证明糖尿病伤口具有过度活跃的炎症反应和血管生成减少。追踪参与这些反应的特定细胞类型的能力将极大地增进我们对糖尿病愈合中细胞紊乱的理解。在本章中，我们回顾了基于瘦素缺乏的Db/Db小鼠的两种新型嵌合模型。使用这些模型可以追踪骨髓来源的炎症细胞和祖细胞群体，并确定这些细胞群体对伤口愈合反应的分子贡献。
