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Background: Neonatal hypoxic-ischemic encephalopathy (HIE) represents as a major cause of neonatal morbidity and mortality. However, the underlying molecular mechanisms in brain damage are still not fully elucidated. This study was conducted to determine the specific potential molecular mechanism in the hypoxic-ischemic induced cerebral injury.
Methods: Here, hypoxic-ischemic (HI) animal models were established and primary cortical neurons were subjected to oxygen-glucose deprivation (OGD) to mimic HIE model in-vivo and in-vitro. The HI-induced neurological injury was evaluated by Zea-longa scores, Triphenyte-trazoliumchloride (TTC) staining the Terminal Deoxynucleotidyl Transferased Utp Nick End Labeling (TUNEL) and immunofluorescent staining. Then the expression of Cytochrome c oxidase subunit 5a (COX5A) was determined by immunohistochemistry, western blotting (WB) and quantitative real time Polymerase Chain Reaction (qRT-PCR) techniques. Moreover, HSV-mediated COX5A over-expression virus was transducted into OGD neurons to explore the role of COX5A in-vitro, and the underlying mechanism was predicted by GeneMANIA, then verified by WB and qRT-PCR.
Results: HI induced a severe neurological dysfunction, brain infarction, and cell apoptosis as well as obvious neuron loss in neonatal rats, in corresponding to the decrease on the expression of COX5A in both sides of the brain. What’s more, COX5A over-expression significantly promoted the neuronal survival, reduced the apoptosis rate, and markedly increased the neurites length after OGD. Moreover, Triosephosephate isomerase (TPI) was predicted as physical interactions with COX5A, and COX5A over-expression largely increased the expressional level of TPI.
Conclusions: The present findings suggest that COX5A plays an important role in promoting neurological recovery after HI, and this process is related to TPI up-regulation.
Keywords
Neonatal hypoxic-ischemic encephalopathy, COX5A overexpression, neuronal survival, TPI
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CURRENT STATUS: Published
View the published article at BMC Neuroscience.
Version 3
Posted 15 Apr, 2020
No community comments so far
Submission checks complete
On 11 Apr, 2020
Editorial decision: Accept
On 11 Apr, 2020
No comments provided
Editorial decision: Minor revision
On 18 Mar, 2020
Review #2 received
Received 14 Mar, 2020
Review #1 received
Received 12 Mar, 2020
Reviewers invited
Invitations sent on 08 Mar, 2020
Reviewer #1 agreed
On 08 Mar, 2020
Reviewer #2 agreed
On 08 Mar, 2020
Editor assigned
On 02 Mar, 2020
Submission checks complete
On 01 Mar, 2020
Editor invited
On 01 Mar, 2020
No comments provided
Editorial decision: Minor revision
On 17 Jan, 2020
Review #1 received
Received 14 Jan, 2020
Review #2 received
Received 10 Jan, 2020
Reviewer #2 agreed
On 04 Jan, 2020
Reviewers invited
Invitations sent on 03 Jan, 2020
Reviewer #1 agreed
On 03 Jan, 2020
Editor assigned
On 31 Dec, 2019
Submission checks complete
On 30 Dec, 2019
Editor invited
On 30 Dec, 2019
Metrics
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See the published version of this preprint at BMC Neuroscience.
This is a preprint, a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Learn more about In Review
Research article
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
Peer Review Timeline
CURRENT STATUS: Published
View the published article at BMC Neuroscience.
Version 3
Posted 15 Apr, 2020
No community comments so far
Submission checks complete
On 11 Apr, 2020
Editorial decision: Accept
On 11 Apr, 2020
No comments provided
Editorial decision: Minor revision
On 18 Mar, 2020
Review #2 received
Received 14 Mar, 2020
Review #1 received
Received 12 Mar, 2020
Reviewers invited
Invitations sent on 08 Mar, 2020
Reviewer #1 agreed
On 08 Mar, 2020
Reviewer #2 agreed
On 08 Mar, 2020
Editor assigned
On 02 Mar, 2020
Submission checks complete
On 01 Mar, 2020
Editor invited
On 01 Mar, 2020
No comments provided
Editorial decision: Minor revision
On 17 Jan, 2020
Review #1 received
Received 14 Jan, 2020
Review #2 received
Received 10 Jan, 2020
Reviewer #2 agreed
On 04 Jan, 2020
Reviewers invited
Invitations sent on 03 Jan, 2020
Reviewer #1 agreed
On 03 Jan, 2020
Editor assigned
On 31 Dec, 2019
Submission checks complete
On 30 Dec, 2019
Editor invited
On 30 Dec, 2019
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
License:
This work is licensed under a CC BY 4.0 License. Read Full License
View the published article at BMC Neuroscience.
Background: Neonatal hypoxic-ischemic encephalopathy (HIE) represents as a major cause of neonatal morbidity and mortality. However, the underlying molecular mechanisms in brain damage are still not fully elucidated. This study was conducted to determine the specific potential molecular mechanism in the hypoxic-ischemic induced cerebral injury.
Methods: Here, hypoxic-ischemic (HI) animal models were established and primary cortical neurons were subjected to oxygen-glucose deprivation (OGD) to mimic HIE model in-vivo and in-vitro. The HI-induced neurological injury was evaluated by Zea-longa scores, Triphenyte-trazoliumchloride (TTC) staining the Terminal Deoxynucleotidyl Transferased Utp Nick End Labeling (TUNEL) and immunofluorescent staining. Then the expression of Cytochrome c oxidase subunit 5a (COX5A) was determined by immunohistochemistry, western blotting (WB) and quantitative real time Polymerase Chain Reaction (qRT-PCR) techniques. Moreover, HSV-mediated COX5A over-expression virus was transducted into OGD neurons to explore the role of COX5A in-vitro, and the underlying mechanism was predicted by GeneMANIA, then verified by WB and qRT-PCR.
Results: HI induced a severe neurological dysfunction, brain infarction, and cell apoptosis as well as obvious neuron loss in neonatal rats, in corresponding to the decrease on the expression of COX5A in both sides of the brain. What’s more, COX5A over-expression significantly promoted the neuronal survival, reduced the apoptosis rate, and markedly increased the neurites length after OGD. Moreover, Triosephosephate isomerase (TPI) was predicted as physical interactions with COX5A, and COX5A over-expression largely increased the expressional level of TPI.
Conclusions: The present findings suggest that COX5A plays an important role in promoting neurological recovery after HI, and this process is related to TPI up-regulation.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
Figure 6
Figure 7
This is a list of supplementary files associated with this preprint. Click to download.
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