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Upregulation of membrane‐bound metalloendopeptidase neurolysin in a mouse model of focal brain ischemia
Author(s) -
Rashid Mamoon,
Yang Li,
Arumugam Thiruma V.,
Abbruscato Thomas J.,
Karamyan Vardan T.
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.852.6
Subject(s) - downregulation and upregulation , hippocampal formation , ischemia , microbiology and biotechnology , brain ischemia , forebrain , programmed cell death , neuroscience , pathology , chemistry , biology , medicine , central nervous system , biochemistry , gene , apoptosis
Membrane‐bound metalloendopeptidase neurolysin was recently identified as the non‐AT 1 , non‐AT 2 angiotensin binding site. Our previous study indicated dramatic over‐expression of this protein in membrane preparations of primary cortical neurons challenged in several in vitro models of cell death suggesting a possible role of neurolysin in neuronal survival. To further confirm the association between upregulation of neurolysin and neuronal cell death, in this work we studied the changes in density of membrane‐bound neurolysin in mouse transient middle cerebral artery occlusion model (60 min occlusion with ~75% local cerebral blood flow drop, followed by 24 h reperfusion). Brain parts were collected after documenting reperfusion injury by neurological scoring and TTC staining. Density of neurolsyin was estimated by radioligand binding assays in cerebral cortical, striatal, hippocampal and cerebellar membranes from ischemic hemispheres. Membrane preparations of the same brain parts from sham operated mice served as controls. Significant up‐regulation of neurolysin in membrane preparations of all forebrain regions from ischemic brains was observed. Density of neurolysin did not differ in cerebellar membranes of ischemic and control brains. These results confirm our in vitro observations further supporting a role of neurolsyin in neuronal cell death. Supported by TTUHSC SOP start‐up funds to VTK.