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Research article
Shouyan Zhang
Luoyang Central Hospital Affiliated to Zhengzhou University
Corresponding Author
ORCiD: https://orcid.org/0000-0003-4483-8131
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Background This study aimed to investigate the effect of miR-30c on myocardial ischemia reperfusion (IR) injury and its underlying molecular mechanisms.Methods In our study, rat myocardial IR injury model was established and hemodynamic examination was performed. Moreover, the myocardial infarct size was detected by TTC staining. The pathologic change of myocardial tissues was measured by HE staining. The myocardial cell apoptosis was measured by TUNEL staining and flow cytometry. The expression of miR-30c and Sirtuin 1 (SIRT1) was detected by qRT-PCR. The levels of IL-1β, IL-6 and TNF-α were detected by ELISA. The expressions of Bax, Bcl-2, caspase-3, p-IκBα, IκBα, p-NF-κB p65, NF-κB p65 and SIRT1 were detected by western blot. The luciferase activity was measured by dual luciferase reporter gene assay. Interaction between miR-30c and SIRT1 were analyzed by RNA immunoprecipitation assay.Results Our results showed that rat myocardial IR injury model was successfully established and IR injury induced myocardial injury in rats. miR-30c increased the levels of IL-1β, IL-6 and TNF-α and myocardial cell apoptosis by activating NF-κB pathway. In addition, we also confirmed that SIRT1 was the target gene of miR-30c. SIRT1 could reverse the effect of miR-30c on the process of inflammation and apoptosis, as well as the activation of NF-κB pathway in myocardial cells.Conclusions Our study demonstrated that miR-30c could promote myocardial ischemia reperfusion injury through activating SIRT1 mediating NF-κB pathway.
Keywords
myocardial ischemia reperfusion injury, miR-30c, inflammation, apoptosis, SIRT1, NF-κB pathway
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CURRENT STATUS: Published
View the published article at BMC Cardiovascular Disorders.
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On 08 May, 2020
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On 08 Apr, 2020
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Editor invited
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Editorial decision: Minor revision
On 01 Apr, 2020
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On 08 Mar, 2020
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On 07 Mar, 2020
Editor invited
On 07 Mar, 2020
No comments provided
Editorial decision: Minor revision
On 03 Mar, 2020
Reviewer #1 agreed
On 02 Mar, 2020
Review #1 received
Received 02 Mar, 2020
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Invitations sent on 01 Mar, 2020
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On 27 Feb, 2020
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On 26 Feb, 2020
Editor invited
On 26 Feb, 2020
No comments provided
Editorial decision: Major revision
On 14 Feb, 2020
Review #2 received
Received 07 Feb, 2020
Review #1 received
Received 07 Feb, 2020
Reviewer #1 agreed
On 24 Jan, 2020
Reviewer #2 agreed
On 24 Jan, 2020
Reviewers invited
Invitations sent on 23 Jan, 2020
Editor assigned
On 22 Jan, 2020
Submission checks complete
On 21 Jan, 2020
Editor invited
On 21 Jan, 2020
Version 1
Posted 30 Sep, 2019
No comments provided
Editorial decision: Major revision
On 22 Dec, 2019
Review #2 received
Received 02 Dec, 2019
Reviewer #2 agreed
On 18 Nov, 2019
Review #1 received
Received 08 Nov, 2019
Reviewer #1 agreed
On 11 Oct, 2019
Reviewers invited
Invitations sent on 09 Oct, 2019
Submission checks complete
On 24 Sep, 2019
Editor assigned
On 24 Sep, 2019
Editor invited
On 23 Sep, 2019
First submitted
On 20 Sep, 2019
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Subject Areas
Cardiac & Cardiovascular Systems
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A new preprint design is coming!
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See the published version of this preprint at BMC Cardiovascular Disorders.
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
Shouyan Zhang
Luoyang Central Hospital Affiliated to Zhengzhou University
Corresponding Author
ORCiD: https://orcid.org/0000-0003-4483-8131
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 Cardiovascular Disorders.
No community comments so far
Editorial decision: Accept
On 08 May, 2020
Editor assigned
On 08 Apr, 2020
Submission checks complete
On 07 Apr, 2020
Editor invited
On 07 Apr, 2020
No comments provided
Editorial decision: Minor revision
On 01 Apr, 2020
Editor assigned
On 08 Mar, 2020
Submission checks complete
On 07 Mar, 2020
Editor invited
On 07 Mar, 2020
No comments provided
Editorial decision: Minor revision
On 03 Mar, 2020
Reviewer #1 agreed
On 02 Mar, 2020
Review #1 received
Received 02 Mar, 2020
Reviewers invited
Invitations sent on 01 Mar, 2020
Editor assigned
On 27 Feb, 2020
Submission checks complete
On 26 Feb, 2020
Editor invited
On 26 Feb, 2020
No comments provided
Editorial decision: Major revision
On 14 Feb, 2020
Review #2 received
Received 07 Feb, 2020
Review #1 received
Received 07 Feb, 2020
Reviewer #1 agreed
On 24 Jan, 2020
Reviewer #2 agreed
On 24 Jan, 2020
Reviewers invited
Invitations sent on 23 Jan, 2020
Editor assigned
On 22 Jan, 2020
Submission checks complete
On 21 Jan, 2020
Editor invited
On 21 Jan, 2020
Version 1
Posted 30 Sep, 2019
No comments provided
Editorial decision: Major revision
On 22 Dec, 2019
Review #2 received
Received 02 Dec, 2019
Reviewer #2 agreed
On 18 Nov, 2019
Review #1 received
Received 08 Nov, 2019
Reviewer #1 agreed
On 11 Oct, 2019
Reviewers invited
Invitations sent on 09 Oct, 2019
Submission checks complete
On 24 Sep, 2019
Editor assigned
On 24 Sep, 2019
Editor invited
On 23 Sep, 2019
First submitted
On 20 Sep, 2019
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Cardiac & Cardiovascular Systems
License:
This work is licensed under a CC BY 4.0 License. Read Full License
View the published article at BMC Cardiovascular Disorders.
Background This study aimed to investigate the effect of miR-30c on myocardial ischemia reperfusion (IR) injury and its underlying molecular mechanisms.Methods In our study, rat myocardial IR injury model was established and hemodynamic examination was performed. Moreover, the myocardial infarct size was detected by TTC staining. The pathologic change of myocardial tissues was measured by HE staining. The myocardial cell apoptosis was measured by TUNEL staining and flow cytometry. The expression of miR-30c and Sirtuin 1 (SIRT1) was detected by qRT-PCR. The levels of IL-1β, IL-6 and TNF-α were detected by ELISA. The expressions of Bax, Bcl-2, caspase-3, p-IκBα, IκBα, p-NF-κB p65, NF-κB p65 and SIRT1 were detected by western blot. The luciferase activity was measured by dual luciferase reporter gene assay. Interaction between miR-30c and SIRT1 were analyzed by RNA immunoprecipitation assay.Results Our results showed that rat myocardial IR injury model was successfully established and IR injury induced myocardial injury in rats. miR-30c increased the levels of IL-1β, IL-6 and TNF-α and myocardial cell apoptosis by activating NF-κB pathway. In addition, we also confirmed that SIRT1 was the target gene of miR-30c. SIRT1 could reverse the effect of miR-30c on the process of inflammation and apoptosis, as well as the activation of NF-κB pathway in myocardial cells.Conclusions Our study demonstrated that miR-30c could promote myocardial ischemia reperfusion injury through activating SIRT1 mediating NF-κB pathway.
Figure 1
Figure 2
Figure 3
Figure 4
This is a list of supplementary files associated with this preprint. Click to download.
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