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Platelet GPVI and CLEC-2 in skin wound healing
upper part of the scar in all groups (Figure 4F) and was notably lower in the DKO mice compared to WT and Gp6-/- mice (Figure 4G). There was no significant differ- ence in wound (myo)fibroblasts (Online Supplementary Figure S3E-G) and collagen content (Online Supplementary Figure S3H and I) between DKO mice and WT at day 3
and day 9 post injury.
These results indicate that the loss of vascular integrity
during the inflammatory phase increases extravasation of plasma proteins, including fibrinogen and clotting factors, into the wound of DKO mice. The increase in fibrinogen and fibrin deposition is associated with accelerated
A
B
DE
F
G
C
Figure 4. Lack of platelet immunoreceptor tyrosine-based activation motif (ITAM) receptors causes local and temporal bleeding leading to fibrin(ogen) deposition during inflammatory phase of wound repair. (A) Macroscopic images of inner side of skin wound at day 3 post injury (n=4-6). Dotted circle indicates wound area. Arrow points to dilated vessel. Arrowhead shows bleeding into surrounding skin. (B) Fibrinogen staining (brown) of skin wound at day 3 post injury. (C) Quantification of fibrinogen content at day 3 post injury (n=6). (D) Martius scarlet blue (MSB) staining of skin wound at day 3 post-injury. Red: old fibrin; blue: collagen; yellow: red blood cells/fresh fibrin. (E) Quantification of fibrin content in the wound at day 3 post injury (n=6-9). (F) MSB staining of wound scar at day 9 post injury. (G) Quantification of fibrin content in the scar at day 9 post injury (n=9-13). Graphs are presented as mean±Standard Error of Mean and analyzed by one-way ANOVA with Bonferroni’s multiple comparison test. *P<0.05; **P<0.01. Scale bar=200 μm.
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