دورية أكاديمية

Inhibition of Let7c microRNA is neuroprotective in a rat intracerebral hemorrhage model.

التفاصيل البيبلوغرافية
العنوان: Inhibition of Let7c microRNA is neuroprotective in a rat intracerebral hemorrhage model.
المؤلفون: Jeong-Min Kim, Soon-Tae Lee, Kon Chu, Keun-Hwa Jung, Jin Hee Kim, Jung-Suk Yu, Soyun Kim, So Hee Kim, Dong-Kyu Park, Jangsup Moon, Jaejun Ban, Manho Kim, Sang Kun Lee, Jae-Kyu Roh
المصدر: PLoS ONE, Vol 9, Iss 6, p e97946 (2014)
بيانات النشر: Public Library of Science (PLoS), 2014.
سنة النشر: 2014
المجموعة: LCC:Medicine
LCC:Science
مصطلحات موضوعية: Medicine, Science
الوصف: Intracerebral hemorrhage (ICH) is a devastating neurological disease with a grave prognosis. We evaluated microRNA (miRNA) expression after ICH and evaluated Let7c as a therapeutic target. We harvested hemorrhagic brain 24 hours after collagenase induced ICH in the rat. Microarray analysis was performed to compare the miRNAs expression pattern between hemorrhagic hemisphere and contralateral hemisphere. An in vitro thrombin toxicity model and blood injection ICH model were also used to evaluate miRNA expression. We selected miRNA for the therapeutic target study after reviewing target gene databases and their expression. The antagonistic sequence of the selected miRNA (antagomir) was used to evaluate its therapeutic potential in the in vitro thrombin toxicity and in vivo ICH models. Among 1,088 miRNAs analyzed, let7c was induced in the thrombin and ICH models. Let7c antagomir treatment increased cell survival in the in vitro thrombin injury model and improved neurological function at 4 weeks after ICH. Let7c antagomir decreased perihematoma edema, apoptotic cell death and inflammation around hematoma. Let7c antagomir also induced insulin like growth factor receptor 1 (IGF1R) protein and phosphorylated serine threonine kinase after ICH. This study shows a distinct miRNA expression pattern after ICH. The let7c antagomir reduced cell death and edema and enhanced neurological recovery at least in part by activating the IGF1R pro-survival pathway. This suggests blocking let7c might be a potential therapeutic target in ICH.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 1932-6203
Relation: http://europepmc.org/articles/PMC4068982?pdf=render; https://doaj.org/toc/1932-6203
DOI: 10.1371/journal.pone.0097946
URL الوصول: https://doaj.org/article/d41a767694064161b4d06b236e2496ac
رقم الأكسشن: edsdoj.41a767694064161b4d06b236e2496ac
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:19326203
DOI:10.1371/journal.pone.0097946