title: Molecular pathology of pulmonary edema after injury in forensic autopsy cases.
abstract: The lung is vulnerable to trauma; pulmonary edema starts quickly as part of the systemic responses involved in shock. The present study investigated the molecular pathology of posttraumatic alveolar damage and responses involving pulmonary edema in forensic autopsy cases of injury (n = 66) compared with acute cardiac death cases (n = 13). Intrapulmonary mRNA and immunohistochemical expressions of matrix metalloproteinases (MMPs; MMP-2 and MMP-9), intercellular adhesion molecule-1, claudin-5, and aquaporins (AQPs, AQP-1 and AQP-5) were examined. Subacute injury deaths showed an increase in lung weight similar to that in acute cardiac death, but relative mRNA quantification using the Taqman real-time PCR assay demonstrated different findings among the causes of death; higher expressions were detected for all markers, except for AQP-5 in sharp instrument injury, for MMP-2 in blunt brain injury, and for MMP-9 in non-brain blunt injury, but these expression levels were lower in acute cardiac death. In immunostaining, only MMPs showed differences among the causes of death: MMP-2 expression was evident in most subacute deaths due to blunt brain injury and sharp instrument injury, whereas MMP-9 was intensely positive in those of non-brain blunt injury and sharp instrument injury. These findings suggest significant differences in the mechanism of pulmonary edema among fatal injuries and acute cardiac death, especially between blunt and sharp instrument injury. Systematic analysis of gene expressions using real-time PCR in combination with immunohistochemistry may be useful in evaluating pulmonary damage and responses after injury in death investigations, especially in connection with posttraumatic shock.
authors.affiliation: Department of Legal Medicine, Osaka City University Medical School, Asahi-machi 1-4-3, Abeno, 545-8585, Osaka, Japan. wangqi1980@live.com
authors.forename: Qi
authors.initials: Q
authors.lastname: Wang
authors.forename: Takaki
authors.initials: T
authors.lastname: Ishikawa
authors.forename: Tomomi
authors.initials: T
authors.lastname: Michiue
authors.forename: Bao-Li
authors.initials: BL
authors.lastname: Zhu
authors.forename: Da-Wei
authors.initials: DW
authors.lastname: Guan
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Maeda
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D051398:Aquaporin 1 / Q000032:analysis / Q000235:genetics; D051402:Aquaporin 5 / Q000032:analysis / Q000235:genetics*; D001344:Autopsy; D001930:Brain Injuries / Q000235:genetics / Q000473:pathology; D002423:Cause of Death; D062507:Claudin-5 / Q000032:analysis / Q000235:genetics; D016757:Death, Sudden, Cardiac / Q000473:pathology; D003937:Diagnosis, Differential; D005260:Female; D015870:Gene Expression / Q000235:genetics; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000032:analysis / Q000235:genetics; D008168:Lung / Q000473:pathology*; D055370:Lung Injury / Q000235:genetics* / Q000473:pathology*; D008297:Male; D020778:Matrix Metalloproteinase 2 / Q000032:analysis / Q000235:genetics; D020780:Matrix Metalloproteinase 9 / Q000032:analysis / Q000235:genetics; D008875:Middle Aged; D009929:Organ Size; D057089:Pathology, Molecular / Q000379:methods*; D011654:Pulmonary Edema / Q000473:pathology*; D012333:RNA, Messenger / Q000032:analysis*; D060888:Real-Time Polymerase Chain Reaction / Q000379:methods; D012774:Shock, Traumatic / Q000235:genetics* / Q000473:pathology*; D055815:Young Adult
chemical_list: C496020:AQP1 protein, human; C496036:AQP5 protein, human; D051402:Aquaporin 5; C107466:CLDN5 protein, human; D062507:Claudin-5; D012333:RNA, Messenger; D018799:Intercellular Adhesion Molecule-1; D051398:Aquaporin 1; D020778:Matrix Metalloproteinase 2; D020780:Matrix Metalloproteinase 9