Cystatin C, a protease inhibitor, in degenerating rat hippocampal neurons following transient forebrain ischemia

• Published in: Brain research Vol. 691; no. 1; pp. 1 - 8
• Main Authors: Palm, Donald E., Knuckey, Neville W., Primiano, Michael J., Spangenberger, Anthony G., Johanson, Conrad E.
• Format: Journal Article
• Language: English
• Published: London Elsevier B.V 11.09.1995; Amsterdam Elsevier; New York, NY
• Subjects: Animals; Astrocytes - physiology; Biological and medical sciences; CA1; Cerebrospinal Fluid Proteins - physiology; Choroid plexus; CSF; Cystatin C; Cystatins - physiology; Cysteine protease inhibitor; Cysteine Proteinase Inhibitors - physiology; Delayed neuronal death; Hippocampus - cytology; Hippocampus - physiology; Immunohistochemistry; Ischemic Attack, Transient - physiopathology; Male; Medical sciences; Nerve Degeneration - physiology; Nerve Tissue Proteins - physiology; Neurology; Prosencephalon - blood supply; Pyramidal Cells - cytology; Pyramidal Cells - physiology; Rats; Rats, Sprague-Dawley; Vascular diseases and vascular malformations of the nervous system; γ-Trace protein; Choroid plexus; Delayed neuronal death; CA1; Cysteine protease inhibitor; γ-Trace protein; CSF; Cystatin; Nervous system diseases; Rat; Enzyme; Cysteine endopeptidases; Rodentia; Central nervous system; Enzyme inhibitor; Cardiovascular disease; Cerebrospinal fluid; Cerebral disorder; Vascular disease; Vertebrata; Experimental disease; Mammalia; Ischemia; Animal; Central nervous system disease; Hydrolases; Proteinases; Cerebrovascular disease; Hippocampus; Brain (vertebrata)
• ISSN: 0006-8993; 1872-6240
• DOI: 10.1016/0006-8993(95)00520-Z

Cystatin C, a cysteine protease inhibitor produced by the choroid plexus and found in CSF at high concentrations, may have an important role in brain injury. We used the two-vessel occlusion model with hypotension to induce transient forebrain ischemia (TFI) in rats for 10 min and then examined cystatin C immuno-like reactivity (CC-IR) after 1, 3, 7 and 14 days of recovery. Our results reveal that CC-IR was minimal or absent in the hippocampus of normal and 1 day post-ischemic animals. However, CC-IR was present in CA1 pyramidal cells and a small number of reactive glia of the stratum radiatum (SR) and stratum oriens (SO) at 3, 7 and 14 days post-ischemia. Histological assessment of the hippocampus indicates that CC-IR was localized in morphologically degenerative neurons. This distinct temporal expression of cystatin C in the rat hippocampus is concurrent with delayed neuronal death following TFI. Thus, these results indicate that cystatin C and/or its substrates may be important components of the post-ischemic neurodegenerative and repair process.