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. Author manuscript; available in PMC: 2018 Aug 1.
Published in final edited form as: Nanomedicine. 2017 Apr 17;13(6):1925–1932. doi: 10.1016/j.nano.2017.04.004

Figure 4. Investigation of mechanisms of injury-induced accumulation of CGKRK.

Figure 4

A) CGKRK was mixed with EDTA-treated blood and administered intravesically. Low magnification images (10x objective) show the lumen, urothelial and muscular layers. Blood did not induce the binding in the absence of injury, suggesting that bleeding caused by the injury per se is not responsible for the widespread binding; B) Mice were pretreated with anti-inflammatory agent dexamethasone prior to injury. Pretreatment did not block injury-induced binding of CGKRK; C) chemical disruption of the urothelium barrier with ethanol resulted in widespread accumulation of CGKRK, suggesting that loss of the barrier’s function is required for CGKRK binding. Low magnification = 2x objective; high magnification = 20x objective (cropped image). An asterisk marks bladder lumen in all images. A dotted line delineates the urothelium/lumen boundary. Size bar = 200 μm.