Up‐regulation of tissue‐type transglutaminase after traumatic 
brain injury

• Published in: Journal of neurochemistry Vol. 80; no. 4; pp. 579 - 588
• Main Authors: Tolentino, Paul J., DeFord, S. Michelle, Notterpek, Lucia, Glenn, Christopher C., Pike, Brian R., Wang, Kevin K. W., Hayes, Ronald L.
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Science, Ltd 01.02.2002; Blackwell
• Subjects: Animals; Biological and medical sciences; Blotting, Northern; Blotting, Western; Brain Injuries - enzymology; Calibration; Cerebral Cortex - enzymology; Cerebral Cortex - injuries; Disease Models, Animal; GTP-Binding Proteins - genetics; GTP-Binding Proteins - metabolism; Hippocampus - enzymology; Hippocampus - injuries; Injuries of the nervous system and the skull. Diseases due to physical agents; Isoenzymes - genetics; Isoenzymes - metabolism; Linear Models; Male; Medical sciences; Polymerase Chain Reaction; quantitative PCR; Rats; Rats, Sprague-Dawley; RNA, Messenger - metabolism; transglutaminase; Transglutaminases - genetics; Transglutaminases - metabolism; Traumas. Diseases due to physical agents; traumatic brain injury; Up-Regulation; Nervous system diseases; Cerebral cortex; Rat; Enzyme; Transferases; Rodentia; Gene expression; Aminoacyltransferases; Trauma; Cerebral disorder; Vertebrata; Mammalia; Animal; Central nervous system disease; Protein-glutamine γ-glutamyltransferase
• ISSN: 0022-3042; 1471-4159
• DOI: 10.1046/j.0022-3042.2001.00726.x

Tissue‐type transglutaminase (tTG, EC 2.3.2.13) has been implicated in various disease paradigms including neurodegenerative disease. In these studies, tTG induction after traumatic brain injury was studied using a rat cortical impact model. Using western blots, two forms of tTG protein expression were identified – a ∼79‐kDa primary form (tTG‐L) and a less abundant ∼70‐kDa form (tTG‐S). Both forms of tTG protein were elevated after injury. In ipsilateral cortex, peak induction of tTG‐L protein [561% ± 80% of control (n = 5)] was observed five days after injury, with expression remaining elevated after two weeks. Peak induction of tTG‐S protein [302% ± 81% of control (n = 5)] was observed three days after injury. Lesser tTG protein induction was observed in hippocampus. Northern blot analysis demonstrated two tTG transcripts in the ipsilateral cortex with peak induction of tTG‐L mRNA three days after injury. However, tTG‐S mRNA was not identified in control samples and only faintly detected in injured tissue. To facilitate analysis of low abundance transcripts in smaller tissue samples, a semiquantitative real‐time PCR strategy was used. Semi‐quantitative PCR analysis of tTG‐L mRNA induction in ipsilateral cortex (peak after three days; 414% ± 21% of control, n= 3) confirmed tTG‐L mRNA induction determined by northern blot (410% of control).