Fig. 5: Hydrogel FBR severity is determined by the extent of acute neural tissue damage at the material interface, which is associated with axonal damage, APP accumulation, and amyloid formation. | Nature Communications

Fig. 5: Hydrogel FBR severity is determined by the extent of acute neural tissue damage at the material interface, which is associated with axonal damage, APP accumulation, and amyloid formation.

From: Foreign body responses in mouse central nervous system mimic natural wound responses and alter biomaterial functions

Fig. 5

a Detail images of the material–tissue interface for DCHMO and DCHK at 48 h after injection. ALDH1L1-tdT reporter and GFAP identify host astrocytes and the loss of these cells demarcates regions of host tissue damage. At 48 h, CD13-positive cells in this damaged tissue region predominately label actively remodeling vasculature. b Quantification of radial thickness of tissue damage around DCHMO and DCHK (n = 9 mice per group). ***P = 0.0001 Welch’s (unequal variance) two-tailed t test (t = 6.56, df = 8.74). c, d Detail images for DCHMO, DCHK, and L-NIO-induced stroke at acute (48 h, 48 h), subacute (1 week, 1wk), and chronic (6 weeks, 6wk) timepoints after injection, comparing staining for amyloid precursor protein (APP) c or amyloid-beta (Aβ) d with GFAP and CD13. e Images show Aβ, Iba-1, and CD13 at the interface of DCHMO, DCHK, and DCHMM with host tissue at 1 week after injection. f Quantification of Aβ at 1 week after DCHMO, DCHK and DCHMM. NS or *P = 0.0153 and =0.0227 for DCHMO versus DCHK and DCHMM, respectively, one-way ANOVA with Bonferroni, n = 4 mice per group. All graphs shows mean ± s.e.m with individual data points superimposed. G hydrogels, ax axons.

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