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. Author manuscript; available in PMC: 2015 Sep 1.
Published in final edited form as: J Neurochem. 2014 Jul 4;130(5):626–641. doi: 10.1111/jnc.12781

Figure 1. Hsp110-/- mice sustain increased brain injury post-TBI.

Figure 1

WT (+/+) and hsp110-/- (-/-) mice were subjected to CCI or were sham-treated and analyzed 24 hours post-TBI.

(A) Brain water content was quantified from the ipsilateral cortex post-TBI. Data presented as mean+/-SD (n=5 mice). *p<0.05.

(B-C) The T2-weighted MR images were analyzed to determine the overall brain volume and corresponding edema volume for each imaged mouse. Consecutive images are presented as 1-8. Quantification of cerebral edema from the MRI data is presented in (C). Data presented as mean+/- SD. *p<0.05.

(D) Representative coronal brain sections stained with H&E at 24 hours post-TBI. Scale bars:200 μm.

(E-F) Apoptotic cells were stained in the cortex and hippocampal (Hippo) regions close to the injured site (-0.1mm to -1.58mm bregma). Scale bar:20μm. Quantification of the TUNEL-positive cells is presented in (F). Data are presented as mean+/-SD.**p<0.01.

(G-H) Immunoblotting analyses showing brain cell lysates of sham or TBI-treated mice using the indicated antibodies. β-Actin is loading control. Quantification of the immunoblots is presented in (H). Data are presented as mean+/-SD.*p<0.05,**p<0.01.

(I-J) IHC analyses showing increased GFAP (upper panel) and infiltrating CD11b (lower panel) immune cells post-TBI in the cortical area (-0.1mm to -0.94mm bregma). Scale Bars:20μm (upper); 10μm (lower panel). Quantification of the CD11b-positive cells post-TBI is presented. Data are presented as mean +/- SD. ** p<0.01.

In all panels, DAPI represents nuclei staining. In panels B to J, n=3-5 mice per group.