Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2018 Jan 5;32(4):1916–1932. doi: 10.1096/fj.201700826R

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© The Author(s)

This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0) (http://creativecommons.org/licenses/by-nc/4.0/) which permits noncommercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

PMC Copyright notice

Figure 4. — IKK2-DN^Camk2a mice exhibit prominent up-regulation of neuroinflammatory factors after trauma. A–E) Expression of proinflammatory genes 3 d after TBI. Most proinflammatory factors were significantly up-regulated in the cortical impact area of IKK2-DN^Camk2a mice, but not in IKK2-CA^Camk2a mice vs. control littermates. These factors include the complement factor C3 (A), the astroglial marker Gfap (B), the acute phase protein Lcn2 (C), the inflammatory cytokine Il1b (D), and the neuronal activity marker c-Fos (E). Expression levels measured by qPCR are presented relative to Hprt. Means ± sem (n = 4–6). *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001 [not significant (ns), 3 d after TBI between indicated groups, by 1-way-ANOVA followed by Bonferroni’s post hoc test]. F) Expression of astroglial and acute phase proteins after trauma. Representative immunoblot analysis and quantification of LCN2 and GFAP protein levels in brain lysates of 12-wk-old control and IKK2-DN^Camk2a mice 3 d after CHI. GAPDH was the loading control. Means ± sem (n = 3). *P < 0.05, **P < 0.01 (by 1-way ANOVA followed by Bonferroni’s post hoc test).

Figure 4. — IKK2-DN^Camk2a mice exhibit prominent up-regulation of neuroinflammatory factors after trauma. A–E) Expression of proinflammatory genes 3 d after TBI. Most proinflammatory factors were significantly up-regulated in the cortical impact area of IKK2-DN^Camk2a mice, but not in IKK2-CA^Camk2a mice vs. control littermates. These factors include the complement factor C3 (A), the astroglial marker Gfap (B), the acute phase protein Lcn2 (C), the inflammatory cytokine Il1b (D), and the neuronal activity marker c-Fos (E). Expression levels measured by qPCR are presented relative to Hprt. Means ± sem (n = 4–6). *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001 [not significant (ns), 3 d after TBI between indicated groups, by 1-way-ANOVA followed by Bonferroni’s post hoc test]. F) Expression of astroglial and acute phase proteins after trauma. Representative immunoblot analysis and quantification of LCN2 and GFAP protein levels in brain lysates of 12-wk-old control and IKK2-DN^Camk2a mice 3 d after CHI. GAPDH was the loading control. Means ± sem (n = 3). *P < 0.05, **P < 0.01 (by 1-way ANOVA followed by Bonferroni’s post hoc test).