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. Author manuscript; available in PMC: 2017 Jun 1.
Published in final edited form as: Biomaterials. 2016 Mar 18;91:166–181. doi: 10.1016/j.biomaterials.2016.03.014

Fig. 3. Interface between ECM hydrogel and host tissue.

Fig. 3

Concentrations >3 mg/mL resulted in an in situ gelation and retention within the lesion cavity producing an interface where the ECM hydrogel contacts with the host brain tissue. It is important to note two typical microenvironments within which ECM material can be found in these stroke-damaged brains: 1. The lesion cavity (yellow boxes); 2. Severely damaged tissue that is not part of the lesion core (white boxes). Higher concentrations of 4 and 8 mg/mL typically completely filled the cavity, but also displaced some damaged tissue. The 3 mg/mL also permeated into damaged tissue directly adjacent to the cavity. In areas of cortical tissue damage, some permeation of ECM could be seen. These areas were mostly void of neurons, but significant amounts of microglia were present directly interacting with some of the permeating ECM. (For interpretation of the references to color in this figure legend, the reader is referred to the web version of this article.)