Anti-FABP7 monoclonal antibody, clone 2I9

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.

Objectives - Carotid endarterectomy (CEA) is a recommended treatment in the prevention of ischemic stroke. However, this procedure may cause neurological complications caused by cerebrovascular damage. While YKL-40 is a proinflammatory protein, neurofilament light polypeptide (NEFL) and brain lipid-binding protein (FABP7) are structural components of the brain. The aim of the study was to investigate YKL-40, NEFL, and FABP7 in the serum of patients undergoing CEA. Materials and methods - The study included 25 participants who underwent CEA due to internal carotid artery stenosis. Blood samples were taken from each patient at three different intervals: prior to the surgery, 12 h after the surgery, and 48 h after the surgery. Serum levels of these brain damage markers were measured by enzyme-linked immunosorbent assay (ELISA). Results - The study showed that the serum YKL-40 level was significantly increased 48 h after CEA when compared to the level prior to surgery and also when compared to levels 12 h after surgery. There were no statistically significant differences in serum NEFL and FABP7 levels between all three recorded measurements. Conclusions - Data from our study showed that CEA affects serum YKL-40 but not NEFL and FABP7 levels. This implicates that YKL-40 may be a valuable serum marker of brain damage after CEA. However, the observed change in serum YKL-40 level in patients after CEA does not necessarily warrant a change in recommendations concerning the use of this treatment in patients with high-grade internal carotid artery stenosis.