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Journal Article

Citation

Zhao D, Ishikawa T, Quan L, Li DR, Michiue T, Yoshida C, Komatu A, Chen JH, Zhu BL, Maeda H. Forensic Sci. Int. 2008; 177(2-3): 176-183.

Affiliation

Department of Legal Medicine, Osaka City University Medical School, Asahi-machi 1-4-3, Abeno, Osaka 545-8585, Japan. legalmed@med.osaka-cu.ac.jp

Copyright

(Copyright © 2008, Elsevier Publishing)

DOI

10.1016/j.forsciint.2007.12.004

PMID

18243616

Abstract

Glucose transporter 1 (GLUT1) and vascular endothelial growth factor (VEGF) have been established as being responsible for cellular adaptation to oxygen deficiency in tissue ischemia and hypoxia mediated by hypoxia-inducible factor 1. We hypothesized that mRNA quantification of these factors in autopsy tissue specimens could have diagnostic significance for investigating the pathology of death, especially after injury. Various cases (total, n=119; less than 48h postmortem) were examined, including fatal blunt injury (n=71) and sharp instrument injury (n=18), as well as asphyxia (strangulation/hanging, n=12) and acute myocardial infarction/ischemia (n=18) as controls. Quantification of mRNA by TaqMan real-time RT-PCR and immunostaining were performed for GLUT1 and VEGF in lung, kidney, and skeletal muscle specimens. The postmortem interval showed no significant influence on the relative quantification of mRNA during the early postmortem period. Characteristic results were found in blunt injury cases: both GLUT1 and VEGF mRNAs decreased in the lung but increased in the skeletal muscle depending on survival time. In the kidney, subacute deaths showed higher GLUT1 mRNA levels compared with acute deaths from blunt injury, but no significant change was found for VEGF mRNA. Immunohistochemistry showed visually predominant GLUT1 immunoreactivity in the renal cortex for cases with a longer survival time, coincident with the results at the mRNA level. Tissue-specific differences in mRNA quantification of GLUT1 and VEGF shed light on tissue ischemia/hypoxia and subsequent tissue-dependent pathophysiological changes leading to death after injury.


Language: en

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