Abstract:
:The astrocyte-endothelial cell interaction is crucial for normal brain homeostasis and blood-brain barrier (BBB) disruption in pathological conditions. However, the mechanism by which astrocytes control BBB integrity, especially after traumatic brain injury (TBI), remains unclear. Here, we present evidence that astrocyte-derived fatty acid-binding protein 7 (FABP7), a differentiation- and migration-associated molecule, may function as a modulator of BBB permeability in a rat weight-drop model of TBI. Immunohistochemical analysis revealed that TBI induced increased expression of FABP7 in astrocytes, accompanied by caveolin-1 (Cav-1) upregulation in endothelial cells. Administration of recombinant FABP7 significantly ameliorated TBI-induced neurological deficits, brain edema, and BBB permeability, concomitant with upregulation of endothelial Cav-1 and tight junction protein expression, while FABP7 knockdown resulted in the opposite effects. Furthermore, pretreatment with daidzein, a specific inhibitor of Cav-1, reversed the inhibitory effects of recombinant FABP7 on matrix metalloproteinase (MMP)-2/9 expression and abolished its BBB protection after TBI. Altogether, these findings suggest that astrocyte-derived FABP7 upregulation may represent an endogenous protective response to BBB disruption partly mediated through a Cav-1/MMP signaling pathway following TBI.
journal_name
Exp Neuroljournal_title
Experimental neurologyauthors
Rui Q,Ni H,Lin X,Zhu X,Li D,Liu H,Chen Gdoi
10.1016/j.expneurol.2019.113044subject
Has Abstractpub_date
2019-12-01 00:00:00pages
113044eissn
0014-4886issn
1090-2430pii
S0014-4886(19)30193-1journal_volume
322pub_type
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