Open AccessExtracellular matrix proteins are time‐dependent and regional‐specific markers in experimental diffuse brain injury
Author(s) -
Griffiths Daniel R.,
Jenkins Taylor M.,
Addington Caroline P.,
Stabenfeldt Sarah E.,
Lifshitz Jonathan
Publication year - 2020
Publication title -
brain and behavior
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.915
H-Index - 41
ISSN - 2162-3279
DOI - 10.1002/brb3.1767
Subject(s) - fibronectin , extracellular matrix , reelin , laminin , hippocampus , traumatic brain injury , neuroinflammation , cortex (anatomy) , tenascin , pathology , thalamus , medicine , hippocampal formation , neuroscience , endocrinology , biology , microbiology and biotechnology , inflammation , psychiatry
The extracellular matrix (ECM) provides structural support for neuronal, glial, and vascular components of the brain, and regulates intercellular signaling required for cellular morphogenesis, differentiation and homeostasis. We hypothesize that the pathophysiology of diffuse brain injury impacts the ECM in a multi‐dimensional way across brain regions and over time, which could facilitate damage and repair processes. Methods Experimental diffuse TBI was induced in male Sprague‐Dawley rats (325–375 g) by midline fluid percussion injury (FPI); uninjured sham rats serve as controls. Tissue from the cortex, thalamus, and hippocampus was collected at 15 min, 1, 2, 6, and 18 hr postinjury as well as 1, 3, 7, and 14 days postinjury. All samples were quantified by Western blot for glycoproteins: fibronectin, laminin, reelin, and tenascin‐C. Band intensities were normalized to sham and relative to β‐actin. Results In the cortex, fibronectin decreased significantly at 15 min, 1 hr, and 2 hr postinjury, while tenascin‐C decreased significantly at 7 and 14 days postinjury. In the thalamus, reelin decreased significantly at 2 hr, 3 and 14 days postinjury. In the hippocampus, tenascin‐C increased significantly at 15 min and 7 days postinjury. Conclusion Acute changes in the levels of these glycoproteins suggest involvement in circuit dismantling, whereas postacute levels may indicate a restorative or regenerative response associated with recovery from TBI.