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Role of Lipocalin-2 in Thrombin-Induced Brain Injury

Stroke (1970), 2016-04, Vol.47 (4), p.1078-1084 [Peer Reviewed Journal]

2016 American Heart Association, Inc. ;ISSN: 0039-2499 ;EISSN: 1524-4628 ;DOI: 10.1161/STROKEAHA.115.012153 ;PMID: 26869387

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Title:
Role of Lipocalin-2 in Thrombin-Induced Brain Injury
Author: Mao, Shanshan ; Xi, Guohua ; Keep, Richard F ; Hua, Ya
Subjects: Acute-Phase Proteins - genetics ; Acute-Phase Proteins - metabolism ; Animals ; Brain - drug effects ; Brain - metabolism ; Brain - pathology ; Brain Edema - chemically induced ; Brain Edema - metabolism ; Brain Edema - pathology ; Cell Death - drug effects ; Cerebral Hemorrhage - chemically induced ; Cerebral Hemorrhage - metabolism ; Cerebral Hemorrhage - pathology ; Lipocalin-2 ; Lipocalins - genetics ; Lipocalins - metabolism ; Magnetic Resonance Imaging ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Oncogene Proteins - genetics ; Oncogene Proteins - metabolism ; Receptor, PAR-1 - metabolism ; Thrombin ; Up-Regulation - drug effects
Is Part Of: Stroke (1970), 2016-04, Vol.47 (4), p.1078-1084
Description: BACKGROUND AND PURPOSE—Thrombin and lipocalin-2 (LCN2) contribute to intracerebral hemorrhage–induced brain injury. Thrombin-induced brain damage is partially through a thrombin receptor, protease-activated receptor-1. LCN2 is involved in cellular iron transport and neuroinflammation. This study investigated the role of LCN2 in thrombin-induced brain injury. METHODS—There were 3 parts in this study. First, male adult C57BL/6 wild-type or LCN2 knockout (LCN2 KO) mice had an intracaudate injection of thrombin (0.4 U) or saline. Second, LCN2 KO mice had an injection of thrombin (0.4 U) with recombinant mouse LCN2 protein (1 μg) into the right caudate. Third, protease-activated receptor-1 KO or wild-type mice had an intracaudate injection of thrombin or saline. All mice had T2-weighted magnetic resonance imaging and behavioral tests. Brains were used for histology, immunohistochemistry, and Western blotting. RESULTS—Intracerebral thrombin injection caused LCN2 upregulation and brain injury in mice. Thrombin-induced brain swelling, blood–brain barrier disruption, neuronal death, and neurological deficits were markedly less in LCN2 KO mice (P<0.05) and were exacerbated by exogenous LCN2 coinjection. In addition, thrombin injection resulted in less LCN2 expression and brain injury in protease-activated receptor-1 KO mice. CONCLUSIONS—Thrombin upregulates LCN2 through protease-activated receptor-1 activation and causes brain damage.
Publisher: United States: American Heart Association, Inc
Language: English
Identifier: ISSN: 0039-2499
EISSN: 1524-4628
DOI: 10.1161/STROKEAHA.115.012153
PMID: 26869387
Source: MEDLINE
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Role of Lipocalin-2 in Thrombin-Induced Brain Injury

2016 American Heart Association, Inc. ;ISSN: 0039-2499 ;EISSN: 1524-4628 ;DOI: 10.1161/STROKEAHA.115.012153 ;PMID: 26869387

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