title: Overexpression of aquaporin‑1 aggravates hippocampal damage in mouse traumatic brain injury models.
abstract: 'Secondary insult' following primary traumatic brain injury (TBI), including ischemia and edema, may aggravate brain impairments and affect the outcomes. The hippocampus is particularly sensitive to ischemia or edema due to its selective vulnerability, as neural cells of the hippocampus may be more prone to abnormal function or cell death in response to ischemia and edema. Aquaporin‑1 (AQP‑1) was reported to be associated with cerebral edema; however, the expression and role of AQP‑1 in hippocampal edema following TBI have seldom been investigated. In the current study, BALB/c mouse closed craniocerebral injury models were established and the changes of AQP‑1 expression in hippocampi of mouse models following TBI were investigated. Neurological function and edema formation of the models were evaluated and the apoptotic hippocampal cells were then stained in situ and detected, followed by determination of AQP‑1 expression in the hippocampus using immunohistochemistry and western blot analysis. As a result, the majority of mice in the TBI group were severely injured and hippocampal edema was confirmed. The apoptotic cells increased significantly in the hippocampi of mice in the TBI group compared with those in the sham group (P<0.01) and the apoptotic rate increased gradually in a time‑dependent manner. The expression levels of AQP‑1 in the hippocampi of mice were markedly higher in the TBI group than in the sham group (P<0.05) at various time points and AQP‑1 expression levels peaked one day following TBI. These results indicate that upregulation of AQP‑1 may participate in edema formation and delayed cell death of the hippocampus following TBI and may also be a novel therapeutic target to protect the hippocampus from secondary injury following TBI.
authors.affiliation: Department of Neurosurgery, First Hospital of China Medical University, Shenyang, Liaoning 110001, P.R. China.
authors.forename: Bo
authors.initials: B
authors.lastname: Qiu
authors.affiliation: Department of Neurosurgery, First Hospital of China Medical University, Shenyang, Liaoning 110001, P.R. China.
authors.forename: Xinguo
authors.initials: X
authors.lastname: Li
authors.affiliation: Department of Pharmaceutics, School of Pharmacy, Fudan University, Shanghai 201203, P.R. China.
authors.forename: Xiyang
authors.initials: X
authors.lastname: Sun
authors.affiliation: Department of Neurosurgery, First Hospital of China Medical University, Shenyang, Liaoning 110001, P.R. China.
authors.forename: Yong
authors.initials: Y
authors.lastname: Wang
authors.affiliation: Department of Neurosurgery, First Hospital of China Medical University, Shenyang, Liaoning 110001, P.R. China.
authors.forename: Zhitao
authors.initials: Z
authors.lastname: Jing
authors.affiliation: Liaoning Centers for Diseases Control and Prevention, Shenyang, Liaoning 110005, P.R. China.
authors.forename: Xu
authors.initials: X
authors.lastname: Zhang
authors.affiliation: Department of Neurosurgery, First Hospital of China Medical University, Shenyang, Liaoning 110001, P.R. China.
authors.forename: Yunjie
authors.initials: Y
authors.lastname: Wang
mesh_terms: D000818:Animals; D017209:Apoptosis; D051398:Aquaporin 1 / Q000235:genetics* / Q000378:metabolism*; D001930:Brain Injuries / Q000378:metabolism* / Q000473:pathology; D004195:Disease Models, Animal; D004487:Edema / Q000209:etiology / Q000378:metabolism; D015870:Gene Expression; D006624:Hippocampus / Q000378:metabolism* / Q000473:pathology; D007150:Immunohistochemistry; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C
chemical_list: D051398:Aquaporin 1