This preprint is under consideration at Journal of Cardiothoracic Surgery. A preprint is 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.
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Background
Besides hematopoietic cells, miR-486 is also enriched in cardiac, skeletal, and smooth muscles. However, its roles in regulating the function of cardiomyocytes and tissue repair in myocardial infarction have not been explored yet.
Methods
We investigated the effects of miR-486 on the survival and hypoxic response of cardiomyocytes. Also, using adenovirus-mediated overexpression, we evaluated its therapeutic effects in myocardial repair in a rat acute myocardial infarct (AMI) model.
Results
Hypoxia treatment upregulated miR-486 in cardiomyocytes. Moreover, adenovirus-mediated overexpression of miR-486 reduced cell injury, increased cell viability, and decreased apoptosis in hypoxic conditions. In a rat AMI model, administration of Ad-miR-486 reduced infarct size and collagen deposition, increased vessel density, and improved cardiac function. Furthermore, in vivo data suggest that the protective effects of miR-486 in cardiomyocytes were related to its anti-apoptotic function.
Conclusion
miR-486 overexpression protects myocytes from hypoxia-induced apoptosis and has therapeutic potential in myocardial infarction.
Keywords
Rat acute myocardial model, MicroRNA-486, Adenovirus, Gene therapy
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Peer Review Timeline
CURRENT STATUS: Under Review
Version 1
Posted 04 Feb, 2021
No community comments so far
Editorial decision: Major revision
On 10 May, 2021
Review #4 received
Received 30 Apr, 2021
Reviewer #6 agreed
On 23 Apr, 2021
Review #3 received
Received 19 Apr, 2021
Review #2 received
Received 19 Apr, 2021
Reviewer #5 agreed
On 17 Apr, 2021
Reviewer #4 agreed
On 17 Apr, 2021
Reviewer #3 agreed
On 14 Apr, 2021
Reviewer #2 agreed
On 14 Apr, 2021
Review #1 received
Received 27 Mar, 2021
Reviewer #1 agreed
On 15 Mar, 2021
Reviews received
Received 15 Mar, 2021
Reviewers invited
Invitations sent on 14 Mar, 2021
Editor assigned
On 27 Jan, 2021
Submission checks complete
On 27 Jan, 2021
Editor invited
On 27 Jan, 2021
First submitted
On 27 Jan, 2021
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Cardiothoracic Surgery
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This preprint is under consideration at Journal of Cardiothoracic Surgery. A preprint is 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: Under Review
Version 1
Posted 04 Feb, 2021
No community comments so far
Editorial decision: Major revision
On 10 May, 2021
Review #4 received
Received 30 Apr, 2021
Reviewer #6 agreed
On 23 Apr, 2021
Review #3 received
Received 19 Apr, 2021
Review #2 received
Received 19 Apr, 2021
Reviewer #5 agreed
On 17 Apr, 2021
Reviewer #4 agreed
On 17 Apr, 2021
Reviewer #3 agreed
On 14 Apr, 2021
Reviewer #2 agreed
On 14 Apr, 2021
Review #1 received
Received 27 Mar, 2021
Reviewer #1 agreed
On 15 Mar, 2021
Reviews received
Received 15 Mar, 2021
Reviewers invited
Invitations sent on 14 Mar, 2021
Editor assigned
On 27 Jan, 2021
Submission checks complete
On 27 Jan, 2021
Editor invited
On 27 Jan, 2021
First submitted
On 27 Jan, 2021
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Cardiothoracic Surgery
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Background
Besides hematopoietic cells, miR-486 is also enriched in cardiac, skeletal, and smooth muscles. However, its roles in regulating the function of cardiomyocytes and tissue repair in myocardial infarction have not been explored yet.
Methods
We investigated the effects of miR-486 on the survival and hypoxic response of cardiomyocytes. Also, using adenovirus-mediated overexpression, we evaluated its therapeutic effects in myocardial repair in a rat acute myocardial infarct (AMI) model.
Results
Hypoxia treatment upregulated miR-486 in cardiomyocytes. Moreover, adenovirus-mediated overexpression of miR-486 reduced cell injury, increased cell viability, and decreased apoptosis in hypoxic conditions. In a rat AMI model, administration of Ad-miR-486 reduced infarct size and collagen deposition, increased vessel density, and improved cardiac function. Furthermore, in vivo data suggest that the protective effects of miR-486 in cardiomyocytes were related to its anti-apoptotic function.
Conclusion
miR-486 overexpression protects myocytes from hypoxia-induced apoptosis and has therapeutic potential in myocardial infarction.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
Figure 6
Figure 7
Figure 8
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