TY - JOUR
T1 - Extracellular matrix proteins are time-dependent and regional-specific markers in experimental diffuse brain injury
AU - Griffiths, Daniel R.
AU - Jenkins, Taylor M.
AU - Addington, Caroline P.
AU - Stabenfeldt, Sarah E.
AU - Lifshitz, Jonathan
N1 - Publisher Copyright:
© 2020 The Authors. Brain and Behavior published by Wiley Periodicals LLC
PY - 2020/9/1
Y1 - 2020/9/1
N2 - Introduction: 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.
AB - Introduction: 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.
KW - S1BF
KW - extracellular matrix
KW - primary somatosensory barrel cortex
KW - protein
KW - traumatic brain injury
KW - ventral posterior medial
KW - ventral posterior medial thalamus
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U2 - 10.1002/brb3.1767
DO - 10.1002/brb3.1767
M3 - Article
C2 - 32705814
AN - SCOPUS:85088380564
SN - 2157-9032
VL - 10
JO - Brain and Behavior
JF - Brain and Behavior
IS - 9
M1 - e01767
ER -