Brain injury induces HIF-1α-dependent transcriptional activation of LRRK2 that exacerbates brain damage
Leucine-rich repeat kinase 2 ( LRRK2 ), originally identified as a causative genetic factor in Parkinson’s disease, is now associated with a number of pathologies. Here, we show that brain injury induces a robust expression of endogenous LRRK2 and suggest a role of LRRK2 after injury. We found that...
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Published in | Cell death & disease Vol. 9; no. 11; pp. 1125 - 19 |
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Main Authors | , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
London
Nature Publishing Group UK
12.11.2018
Springer Nature B.V |
Subjects | |
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Abstract | Leucine-rich repeat kinase 2
(
LRRK2
), originally identified as a causative genetic factor in Parkinson’s disease, is now associated with a number of pathologies. Here, we show that brain injury induces a robust expression of endogenous LRRK2 and suggest a role of LRRK2 after injury. We found that various in vitro and in vivo models of traumatic brain injury (TBI) markedly enhanced LRRK2 expression in neurons and also increased the level of hypoxia-inducible factor (HIF)-1α. Luciferase reporter assay and chromatin immunoprecipitation revealed direct binding of HIF-1α in LRRK2 proximal promoter. We also found that HIF-1α-dependent transcriptional induction of
LRRK2
exacerbated neuronal cell death following injury. Furthermore, application of G1023, a specific, brain-permeable inhibitor of LRRK2, substantially prevented brain tissue damage, cell death, and inflammatory response and alleviated motor and cognitive defects induced by controlled cortical impact injury. Together, these results suggest HIF-1α-LRRK2 axis as a potential therapeutic target for brain injury. |
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AbstractList | Leucine-rich repeat kinase 2 (LRRK2), originally identified as a causative genetic factor in Parkinson’s disease, is now associated with a number of pathologies. Here, we show that brain injury induces a robust expression of endogenous LRRK2 and suggest a role of LRRK2 after injury. We found that various in vitro and in vivo models of traumatic brain injury (TBI) markedly enhanced LRRK2 expression in neurons and also increased the level of hypoxia-inducible factor (HIF)-1α. Luciferase reporter assay and chromatin immunoprecipitation revealed direct binding of HIF-1α in LRRK2 proximal promoter. We also found that HIF-1α-dependent transcriptional induction of LRRK2 exacerbated neuronal cell death following injury. Furthermore, application of G1023, a specific, brain-permeable inhibitor of LRRK2, substantially prevented brain tissue damage, cell death, and inflammatory response and alleviated motor and cognitive defects induced by controlled cortical impact injury. Together, these results suggest HIF-1α-LRRK2 axis as a potential therapeutic target for brain injury. Abstract Leucine-rich repeat kinase 2 ( LRRK2 ), originally identified as a causative genetic factor in Parkinson’s disease, is now associated with a number of pathologies. Here, we show that brain injury induces a robust expression of endogenous LRRK2 and suggest a role of LRRK2 after injury. We found that various in vitro and in vivo models of traumatic brain injury (TBI) markedly enhanced LRRK2 expression in neurons and also increased the level of hypoxia-inducible factor (HIF)-1α. Luciferase reporter assay and chromatin immunoprecipitation revealed direct binding of HIF-1α in LRRK2 proximal promoter. We also found that HIF-1α-dependent transcriptional induction of LRRK2 exacerbated neuronal cell death following injury. Furthermore, application of G1023, a specific, brain-permeable inhibitor of LRRK2, substantially prevented brain tissue damage, cell death, and inflammatory response and alleviated motor and cognitive defects induced by controlled cortical impact injury. Together, these results suggest HIF-1α-LRRK2 axis as a potential therapeutic target for brain injury. Leucine-rich repeat kinase 2 ( LRRK2 ), originally identified as a causative genetic factor in Parkinson’s disease, is now associated with a number of pathologies. Here, we show that brain injury induces a robust expression of endogenous LRRK2 and suggest a role of LRRK2 after injury. We found that various in vitro and in vivo models of traumatic brain injury (TBI) markedly enhanced LRRK2 expression in neurons and also increased the level of hypoxia-inducible factor (HIF)-1α. Luciferase reporter assay and chromatin immunoprecipitation revealed direct binding of HIF-1α in LRRK2 proximal promoter. We also found that HIF-1α-dependent transcriptional induction of LRRK2 exacerbated neuronal cell death following injury. Furthermore, application of G1023, a specific, brain-permeable inhibitor of LRRK2, substantially prevented brain tissue damage, cell death, and inflammatory response and alleviated motor and cognitive defects induced by controlled cortical impact injury. Together, these results suggest HIF-1α-LRRK2 axis as a potential therapeutic target for brain injury. |
ArticleNumber | 1125 |
Author | Bae, Jinhyun Bu, Youngmin Ko, Eunhwa Her, Song Ryu, Hoon Bae, Yun-Hee Joo, Hyejin Choi, Hwan Geun Lee, Byoung Dae Hur, Eun-Mi Hyeon, Seung Jae |
Author_xml | – sequence: 1 givenname: Yun-Hee surname: Bae fullname: Bae, Yun-Hee organization: Department of Neuroscience, Graduate School, Kyung Hee University – sequence: 2 givenname: Hyejin surname: Joo fullname: Joo, Hyejin organization: Department of Science in Korean medicine, Graduate School, Kyung Hee University – sequence: 3 givenname: Jinhyun surname: Bae fullname: Bae, Jinhyun organization: Department of Herbal Pharmacology, College of Korean Medicine, Kyung Hee University – sequence: 4 givenname: Seung Jae surname: Hyeon fullname: Hyeon, Seung Jae organization: Center for Neuroscience, Brain Science Institute, Korea Institute of Science and Technology – sequence: 5 givenname: Song surname: Her fullname: Her, Song organization: Korea Basic Science Institute – sequence: 6 givenname: Eunhwa surname: Ko fullname: Ko, Eunhwa organization: New Drug development center, Daegu-Gyeongbuk Medical Innovation Foundation – sequence: 7 givenname: Hwan Geun surname: Choi fullname: Choi, Hwan Geun organization: New Drug development center, Daegu-Gyeongbuk Medical Innovation Foundation – sequence: 8 givenname: Hoon surname: Ryu fullname: Ryu, Hoon organization: Center for Neuroscience, Brain Science Institute, Korea Institute of Science and Technology, Veteran’s Affairs Boston Healthcare System, Boston University Alzheimer’s Disease Center and Department of Neurology, Boston University School of Medicine – sequence: 9 givenname: Eun-Mi surname: Hur fullname: Hur, Eun-Mi organization: Department of Neuroscience, College of Veterinary Medicine, Research Institute for Veterinary Science, and BK21 PLUS Program for Creative Veterinary Science Research, Seoul National University – sequence: 10 givenname: Youngmin surname: Bu fullname: Bu, Youngmin email: ymbu@khu.ac.kr organization: Department of Herbal Pharmacology, College of Korean Medicine, Kyung Hee University – sequence: 11 givenname: Byoung Dae surname: Lee fullname: Lee, Byoung Dae email: bdaelee@khu.ac.kr organization: Department of Neuroscience, Graduate School, Kyung Hee University, Department of Physiology, Kyung Hee University School of Medicine |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/30420654$$D View this record in MEDLINE/PubMed |
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Snippet | Leucine-rich repeat kinase 2
(
LRRK2
), originally identified as a causative genetic factor in Parkinson’s disease, is now associated with a number of... Leucine-rich repeat kinase 2 (LRRK2), originally identified as a causative genetic factor in Parkinson's disease, is now associated with a number of... Abstract Leucine-rich repeat kinase 2 ( LRRK2 ), originally identified as a causative genetic factor in Parkinson’s disease, is now associated with a number of... Leucine-rich repeat kinase 2 (LRRK2), originally identified as a causative genetic factor in Parkinson’s disease, is now associated with a number of... |
SourceID | pubmedcentral proquest crossref pubmed springer |
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Title | Brain injury induces HIF-1α-dependent transcriptional activation of LRRK2 that exacerbates brain damage |
URI | https://link.springer.com/article/10.1038/s41419-018-1180-y https://www.ncbi.nlm.nih.gov/pubmed/30420654 https://www.proquest.com/docview/2132254624 https://search.proquest.com/docview/2132735761 https://pubmed.ncbi.nlm.nih.gov/PMC6232134 |
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