Silencing of long noncoding RNA MEG3 enhances cerebral protection of dexmedetomidine against hypoxic‐ischemic brain damage in neonatal mice by binding to miR‐129‐5p

2018 ◽  
Vol 120 (5) ◽  
pp. 7978-7988 ◽  
Author(s):  
Xiu‐Min Zhou ◽  
Jie Liu ◽  
Ying Wang ◽  
Man‐He Zhang
Keyword(s):  
Brain Damage ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Cerebral Protection ◽  
Ischemic Brain Damage ◽  
Ischemic Brain ◽  
Neonatal Mice

scholarly journals Cell-specific roles of GRK2 in onset and severity of hypoxic-ischemic brain damage in neonatal mice

2010 ◽  
Vol 24 (3) ◽  
pp. 420-426 ◽  
Author(s):  
Cora H. Nijboer ◽  
Cobi J. Heijnen ◽  
Hanneke L.D.M. Willemen ◽  
Floris Groenendaal ◽  
Gerald W. Dorn ◽  
...  
Keyword(s):  
Brain Damage ◽  
Ischemic Brain Damage ◽  
Ischemic Brain ◽  
Neonatal Mice

scholarly journals Effects of MicroRNA-592-5p on Hippocampal Neuron Injury Following Hypoxic-Ischemic Brain Damage in Neonatal Mice - Involvement of PGD2/DP and PTGDR

2018 ◽  
Vol 45 (2) ◽  
pp. 458-473 ◽  
Author(s):  
Li-Qun Sun ◽  
Gong-Liang Guo ◽  
Sai Zhang ◽  
Li-Li  Yang
Keyword(s):  
Cell Cycle ◽  
Mouse Model ◽  
Signaling Pathway ◽  
Brain Damage ◽  
Target Gene ◽  
Ischemic Brain Damage ◽  
Ischemic Brain ◽  
Expression Levels ◽  
Neonatal Mice ◽  
Group A

Background/Aims: This study aimed to explore the effect of microRNA-592-5p (miR-592-5p) on hypoxic-ischemic brain damage (HIBD)-induced hippocampal neuronal injury in a neonatal mouse model relative to the involvement of one target gene, PTGDR, and the PGD2/ DP signaling pathway. Methods: A total of 30 neonatal mice aged 7 days were randomly selected to establish an HIBD mouse model. Hippocampal neuronal cells were transfected into a control group, a blank group, a negative control (NC) group, an miR-592-5p mimics group, an miR-592-5p inhibitors group, an siRNA-PTGDR group and an miR-592-5p inhibitors + siRNA-PTGDR group. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and Western blot analyses were performed to detect the expression levels of miR-592-5p, PTGDR, DP2, Bcl-2 and Bax in tissues and cells. Cell proliferation, cell cycle and apoptosis were detected by MTT assay and flow cytometry, respectively. Results: The expression levels of miR-592-5p and Bcl-2 decreased, while the expression levels of PTGDR, DP2 and Bax increased in the HIBD group. PTGDR is a target gene of miR-592-2p. Compared with the NC and blank groups, the expression levels of PTGDR, DP2 and Bax decreased, while the expression levels of miR-592-5p and Bcl-2 increased in the miR-592-5p mimics group. The siRNA-PTGDR group showed the same trend as that observed in the miR-592-5p mimics group, except with no difference in miR-592-5p expression. The miR-592-5p inhibitors group showed an opposite gene expression trend compared to that in the miR-592-5p mimics group. The S phase of the cell cycle was prolonged, the G1 phase was reduced, proliferation was increased, and the apoptosis rate was decreased in the siRNA-PTGDR and miR-592-5p mimics groups. Opposite trends for cell cycle, proliferation and apoptosis were observed in the miR-592-5p inhibitors group. Conclusions: Our study suggests that miR-592-5p upregulation protects against hippocampal neuronal injury caused by HIBD by targeting PTGDR and inhibiting the PGD2/DP signaling pathway.

Studies on cerebral protection of digoxin against hypoxic–ischemic brain damage in neonatal rats

Neuroreport ◽  
2016 ◽  
Vol 27 (12) ◽  
pp. 906-915 ◽  
Author(s):  
Kaiwei Peng ◽  
Danfeng Tan ◽  
Miao He ◽  
Dandan Guo ◽  
Juan Huang ◽  
...  
Keyword(s):  
Brain Damage ◽  
Cerebral Protection ◽  
Neonatal Rats ◽  
Ischemic Brain Damage ◽  
Ischemic Brain

scholarly journals Long Noncoding RNA Fos Downstream Transcript Is Developmentally Dispensable but Vital for Shaping the Poststroke Functional Outcome

Stroke ◽  
2021 ◽  
Author(s):  
Suresh L. Mehta ◽  
Anil K. Chokkalla ◽  
TaeHee Kim ◽  
Saivenkateshkomal Bathula ◽  
Bharath Chelluboina ◽  
...  
Keyword(s):  
Functional Outcome ◽  
Rna Sequencing ◽  
Brain Damage ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Focal Ischemia ◽  
Developmental Expression ◽  
Lesion Volume ◽  
Sequencing Analysis ◽  
Ischemic Brain

Background and Purpose: Stroke induces the expression of several long noncoding RNAs in the brain. However, their functional significance in poststroke outcome is poorly understood. We recently observed that a brain-specific long noncoding RNA called Fos downstream transcript (FosDT) is induced rapidly in the rodent brain following focal ischemia. Using FosDT knockout rats, we presently evaluated the role of FosDT in poststroke brain damage. Methods: FosDT knockout rats were generated using CRISPR-Cas9 genome editing on a Sprague-Dawley background. Male and female FosDT −/− and FosDT +/+ cohorts were subjected to transient middle cerebral artery occlusion. Postischemic sensorimotor deficits were evaluated between days 1 and 7 and lesion volume on day 7 of reperfusion. The developmental expression profile of FosDT was determined with real-time polymerase chain reaction and mechanistic implications of FosDT in the ischemic brain were conducted with RNA-sequencing analysis and immunostaining of pathological markers. Results: FosDT expression is developmentally regulated, with the adult cerebral cortex showing significantly higher FosDT expression than neonates. FosDT −/− rats did not show any anomalies in growth and development, fertility, brain cytoarchitecture, and cerebral vasculature. However, when subjected to transient focal ischemia, FosDT −/− rats of both sexes showed enhanced sensorimotor recovery and reduced brain damage. RNA-sequencing analysis showed that improved poststroke functional outcome in FosDT −/− rats is partially associated with curtailed induction of inflammatory genes, reduced apoptosis, mitochondrial dysfunction, and oxidative stress. Conclusions: Our study shows that FosDT is developmentally dispensable, mechanistically important, and a functionally promising target to reduce ischemic brain damage and facilitate neurological recovery.

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