Systemic and local cardiac inflammation after experimental long bone fracture, traumatic brain injury and combined trauma in mice

Figures

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  Figure 1. Systemic inflammation after experimental limb-, neuro- and combined trauma in mice. Mice received either closed tibia fracture (Fx) (light grey bars), traumatic brain injury (TBI) (dark grey bars), combined trauma (Fx ​+ ​TBI) (squared bars) or sham treatment (white bars). Blood plasma was analyzed after 6 and 24 ​h, respectively. Systemic levels of granulocyte-colony stimulating factor (G-CSF) in pg/ml (A), interleukin-6 (IL-6) in pg/ml (B), keratinocyte chemoattractant (KC) in pg/ml (C), interleukin-10 (IL-10) in pg/ml (D), monocyte chemotactic protein-1 (MCP-1) in pg/ml (E) and tumor necrosis factor (TNF) in pg/ml (F). Data are presented as mean ​± ​SEM. ∗p ​< ​0.05 was considered as statistically significant.

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  Figure 2. Cardiac injury after experimental limb-, neuro- and combined trauma in mice. Mice received either closed tibia fracture (Fx) (light grey bars), traumatic brain injury (TBI) (dark grey bars), combined trauma (Fx ​+ ​TBI) (squared bars) or sham treatment (white bars). Blood plasma and cardiac tissue were analyzed after 6 and 24 ​h, respectively. Systemic release of heart fatty acid binding protein (HFABP) in pg/ml (A) and of cardiac troponin I in pg/ml (B). mRNA expression (fold change) of cardiac troponin I in left ventricles (C) and of cardiac HFABP in left ventricles (D). Data are presented as mean ​± ​SEM. ∗p ​< ​0.05 was considered as statistically significant.

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  Figure 3. Local cardiac inflammation after experimental limb-, neuro- and combined trauma in mice. Mice received either closed tibia fracture (Fx) (light grey bars), traumatic brain injury (TBI) (dark grey bars), combined trauma (Fx ​+ ​TBI) (squared bars) or sham treatment (white bars). Cardiac tissue were analyzed after 6 and 24 ​h, respectively. mRNA expression (fold change) of toll-like receptor 4 (TLR4) (A), TLR9 (B), C5a receptor 1 (C5aR1) (C), interleukin-1β (IL-1β) (F) and tumor necrosis factor (TNF) (G). Protein expression (pixel density) of C5aR1 (D), C3a receptor (C3aR) (E) and nitrotyrosine (H). Data are presented as mean ​± ​SEM. ∗p ​< ​0.05 was considered as statistically significant.

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  Figure 4. Local cardiac alterations after experimental limb-, neuro- and combined trauma in mice. Mice received either closed tibia fracture (Fx) (light grey bars), traumatic brain injury (TBI) (dark grey bars), combined trauma (Fx ​+ ​TBI) (squared bars) or sham treatment (white bars). Cardiac tissue was analyzed after 6 and 24 ​h, respectively. mRNA expression (fold change) of glucose transporter 4 (GLUT4) (A), myocardial protein expression (fluorescence intensity) of GLUT4 (B), mRNA expression (fold change) of glucose transporter 2 (GLUT2) (C), myocardial protein expression (fluorescence intensity) of glucose transporter 1 (GLUT1) (D) and mRNA expression (fold change) of Connexin 43 (E). Representative images of Connexin 43 expression 24 ​h after Fx, TBI, Fx ​+ ​TBI or sham procedure in left ventricles of mice (F). The black arrows demonstrate the myocardial expression of Cx43. Data are presented as mean ​± ​SEM. ∗p ​< ​0.05 was considered as statistically significant.

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  Supplemental Figure 1. Myocardial tissue damage. Mice received either closed tibia fracture (Fx) (light grey bars), traumatic brain injury (TBI) (dark grey bars), combined trauma (Fx ​+ ​TBI) (squared bars) or sham treatment (white bars). Cardiac tissue was analyzed after 6 and 24 ​h, respectively. Myocardial tissue sections were stained by hematoxylin and eosin staining. Representative images of myocardial tissue 6 and 24 ​h after Fx, TBI, Fx ​+ ​TBI or sham procedure (A). Heart injury score of myocardial tissue (B). Data are presented as mean ​± ​SEM. ∗p ​< ​0.05 was considered as statistically significant.