eLife · 2020
A delayed fractionated dose RTS,S AS01 vaccine regimen mediates protection via improved T follicular helper and B cell responses.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Pallikkuth Suresh, Chaudhury Sidhartha, Lu Pinyi, Pan Li, Jongert Erik, Wille-Reece Ulrike, Pahwa Savita
Аннотация
INTRODUCTION: Cerebral ischemia-reperfusion (CI/R) injury commonly occurs in ischemic stroke (IS) patients. The study examined the role of long non-coding RNA (lncRNA) TINCR in a middle cerebral artery occlusion and reperfusion (MCAO/R) induced rat model and oxygen-glucose deprivation/re-oxygenation (OGD/R) induced neuron cell models.
MATERIAL AND METHODS: Rats were treated with MCAO/R to induce IS animal models and neural stem cells (NSCs) were treated with OGD/R to establish cell models. The neurological function, cerebral infarction area, and inflammation of rats were evaluated. Cell proliferation, migration and apoptosis were assessed. Target association between TINCR and miR-125b-5p was verified. Based on the competing endogenous RNA (ceRNA) regulatory network, the rescue experiments were done in NSCs via cell transfection.
RESULTS: In MCAO/R rats, downregulated expression of lncRNA TINCR was tested, accompanied by neurological dysfunction and cerebral infarction. TINCR overexpression in rats led to the recovery of neurological dysfunction and cerebral infarction, while inflammation and apoptosis were inhibited. In accordance with in vivo experiment results, declined TINCR was also tested in OGD/R treated NSCs. The rescue experiments demonstrated that TINCR overexpression promoted NSC proliferation and migration, but suppressed cell apoptosis and inflammation. TINCR serves as a ceRNA of miR-125b-5p, and miR-125b-5p abolished the protective role of TINCR in OGD/R cell models.
CONCLUSIONS: LncRNA TINCR attenuated CI/R injury through competitively binding to miR-125b-5p.
MATERIAL AND METHODS: Rats were treated with MCAO/R to induce IS animal models and neural stem cells (NSCs) were treated with OGD/R to establish cell models. The neurological function, cerebral infarction area, and inflammation of rats were evaluated. Cell proliferation, migration and apoptosis were assessed. Target association between TINCR and miR-125b-5p was verified. Based on the competing endogenous RNA (ceRNA) regulatory network, the rescue experiments were done in NSCs via cell transfection.
RESULTS: In MCAO/R rats, downregulated expression of lncRNA TINCR was tested, accompanied by neurological dysfunction and cerebral infarction. TINCR overexpression in rats led to the recovery of neurological dysfunction and cerebral infarction, while inflammation and apoptosis were inhibited. In accordance with in vivo experiment results, declined TINCR was also tested in OGD/R treated NSCs. The rescue experiments demonstrated that TINCR overexpression promoted NSC proliferation and migration, but suppressed cell apoptosis and inflammation. TINCR serves as a ceRNA of miR-125b-5p, and miR-125b-5p abolished the protective role of TINCR in OGD/R cell models.
CONCLUSIONS: LncRNA TINCR attenuated CI/R injury through competitively binding to miR-125b-5p.