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Research article
Shengkai Gong
The first affiliated hospital of Zhengzhou University
Corresponding Author
ORCiD: https://orcid.org/0000-0003-2593-8508
License:
This work is licensed under a CC BY 4.0 License. Read Full License
The aim of the study was to explore the function and mechanism of lincRNA PADNA in bupivacaine-induced neurotoxicity. Mouse DRG neurons were cultured in vitro and treated with bupivacaine to establish the neurotoxicity model. Caspase3 activity, cell viability, tunel assay were analyzed to assess the role of lincRNA PADNA. Dual-luciferase reporter assay was used to determine the binding target of lincRNA PANDA. The expression of lincRNA PADNA was significantly increased with the increasing concentration of bupivacaine. Functional analysis revealed that knockdown of lincRNA PADNA accelerated the caspase3 activity and inhibited the cell viability. Western blot showed that knockdown of lincRNA PADNA promoted the occurrence of cleaved-caspase3. We also proved that lincRNA PADNA may bind with miR-194. Overexpression of miR-194 could rescued the function of lincRNA PADNA, suggesting that lincRNA PADNA may sponge miR-194. In addition, we provided new evidences that lincRNA PADNA/miR-194/FBXW7 axis play an important role in the neurotoxicity process. We performed comprehensive experiments to verify the function and mechanism of lincRNA PADNA in bupivacaine-induced neurotoxicity. Our study provided new evidences and clues for prevention of neurotoxicity.
Keywords
lincRNA, PADNA, miR-194, FBXW7
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View the published article at Molecular Medicine.
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Review #1 received
Received 02 Aug, 2020
Editorial decision: Accept
On 02 Aug, 2020
Editor assigned
On 24 Jul, 2020
Reviewers invited
Invitations sent on 24 Jul, 2020
Reviewer #1 agreed
On 24 Jul, 2020
Submission checks complete
On 23 Jul, 2020
Editor invited
On 23 Jul, 2020
Version 1
Posted 29 May, 2020
No comments provided
Review #2 received
Received 16 Jun, 2020
Editorial decision: Major revision
On 16 Jun, 2020
Review #1 received
Received 15 Jun, 2020
Reviewer #2 agreed
On 11 Jun, 2020
Reviewer #1 agreed
On 06 Jun, 2020
Editor assigned
On 04 Jun, 2020
Reviewers invited
Invitations sent on 04 Jun, 2020
Editor invited
On 03 Jun, 2020
Submission checks complete
On 26 May, 2020
First submitted
On 21 May, 2020
Metrics
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Subject Areas
Molecular Genetics
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A new preprint design is coming!
We have improved readability, clarity, accessibility, and opportunities for engagement.
See the published version of this preprint at Molecular Medicine.
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
Shengkai Gong
The first affiliated hospital of Zhengzhou University
Corresponding Author
ORCiD: https://orcid.org/0000-0003-2593-8508
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 Molecular Medicine.
No community comments so far
Review #1 received
Received 02 Aug, 2020
Editorial decision: Accept
On 02 Aug, 2020
Editor assigned
On 24 Jul, 2020
Reviewers invited
Invitations sent on 24 Jul, 2020
Reviewer #1 agreed
On 24 Jul, 2020
Submission checks complete
On 23 Jul, 2020
Editor invited
On 23 Jul, 2020
Version 1
Posted 29 May, 2020
No comments provided
Review #2 received
Received 16 Jun, 2020
Editorial decision: Major revision
On 16 Jun, 2020
Review #1 received
Received 15 Jun, 2020
Reviewer #2 agreed
On 11 Jun, 2020
Reviewer #1 agreed
On 06 Jun, 2020
Editor assigned
On 04 Jun, 2020
Reviewers invited
Invitations sent on 04 Jun, 2020
Editor invited
On 03 Jun, 2020
Submission checks complete
On 26 May, 2020
First submitted
On 21 May, 2020
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Molecular Genetics
License:
This work is licensed under a CC BY 4.0 License. Read Full License
View the published article at Molecular Medicine.
The aim of the study was to explore the function and mechanism of lincRNA PADNA in bupivacaine-induced neurotoxicity. Mouse DRG neurons were cultured in vitro and treated with bupivacaine to establish the neurotoxicity model. Caspase3 activity, cell viability, tunel assay were analyzed to assess the role of lincRNA PADNA. Dual-luciferase reporter assay was used to determine the binding target of lincRNA PANDA. The expression of lincRNA PADNA was significantly increased with the increasing concentration of bupivacaine. Functional analysis revealed that knockdown of lincRNA PADNA accelerated the caspase3 activity and inhibited the cell viability. Western blot showed that knockdown of lincRNA PADNA promoted the occurrence of cleaved-caspase3. We also proved that lincRNA PADNA may bind with miR-194. Overexpression of miR-194 could rescued the function of lincRNA PADNA, suggesting that lincRNA PADNA may sponge miR-194. In addition, we provided new evidences that lincRNA PADNA/miR-194/FBXW7 axis play an important role in the neurotoxicity process. We performed comprehensive experiments to verify the function and mechanism of lincRNA PADNA in bupivacaine-induced neurotoxicity. Our study provided new evidences and clues for prevention of neurotoxicity.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
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