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Background: As the most frequent type of cyanotic congenital heart diseases (CHD), Tetralogy of Fallot (TOF) has a relatively poor prognosis without the corrective surgery. Circular RNA (circRNA) represents a novel class of endogenous noncoding RNAs that regulate target gene expression post-transcriptionally in heart development. Here, we investigate the potential role of ceRNA network in the pathogenesis of TOF.
Methods: To identify circRNAs expression profiles in Tetralogy of Fallot, microarrays were used to screen the differentially expressed circRNA between 3 TOF and 3 control human myocardial tissue samples. Then, a dysregulated circRNA- associated ceRNA network was constructed via using the established multi-step screening strategy.
Results: In summary, total 276 differentially expressed circRNAs were identified, including 214 up-regulated and 62 down-regulated ones in TOF samples. By constructing the circRNA-associated ceRNA network based on the bioinformatics data, a total of 19 key circRNAs, 9 key miRNAs and 34 key mRNAs were further screened. Moreover, by enlarging the samples size, the qPCR results validated that the positive correlations between hsa_circ_0007798 and HIF1A.
Conclusions: The findings in this study provide a comprehensive understanding of the ceRNA network involved in TOF biology, such as hsa_circ_0007798/miR-199b-
5p/HIF1A signal axis, and may offer candidate diagnostic biomarkers or potential therapeutic targets for TOF. In addtion, we propose that the ceRNA network regulates TOF progression.
Keywords
Disease progression, Gene Regulatory Networks, RNA, Small untranslated, Tetralogy of Fallot
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CURRENT STATUS: Under Revision
The most recent version of this article is available here.
No community comments so far
Editorial decision: Minor revision
On 05 Jan, 2021
Reviewer #2 agreed
On 07 Dec, 2020
Reviewer #1 agreed
On 07 Dec, 2020
Review #1 received
Received 07 Dec, 2020
Review #2 received
Received 07 Dec, 2020
Reviewers invited
Invitations sent on 24 Nov, 2020
Editor assigned
On 21 Nov, 2020
Submission checks complete
On 21 Nov, 2020
Editor invited
On 21 Nov, 2020
Version 1
Posted 06 Jul, 2020
No comments provided
Editorial decision: Major revision
On 22 Sep, 2020
Review #3 received
Received 19 Sep, 2020
Reviewer #3 agreed
On 01 Sep, 2020
Review #1 received
Received 06 Aug, 2020
Review #2 received
Received 06 Aug, 2020
Reviewer #2 agreed
On 20 Jul, 2020
Reviewer #1 agreed
On 18 Jul, 2020
Reviewers invited
Invitations sent on 09 Jul, 2020
Editor invited
On 02 Jul, 2020
Editor assigned
On 01 Jul, 2020
First submitted
On 30 Jun, 2020
Submission checks complete
On 30 Jun, 2020
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This preprint is under consideration at BMC Cardiovascular Disorders. 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 Revision
The most recent version of this article is available here.
No community comments so far
Editorial decision: Minor revision
On 05 Jan, 2021
Reviewer #2 agreed
On 07 Dec, 2020
Reviewer #1 agreed
On 07 Dec, 2020
Review #1 received
Received 07 Dec, 2020
Review #2 received
Received 07 Dec, 2020
Reviewers invited
Invitations sent on 24 Nov, 2020
Editor assigned
On 21 Nov, 2020
Submission checks complete
On 21 Nov, 2020
Editor invited
On 21 Nov, 2020
Version 1
Posted 06 Jul, 2020
No comments provided
Editorial decision: Major revision
On 22 Sep, 2020
Review #3 received
Received 19 Sep, 2020
Reviewer #3 agreed
On 01 Sep, 2020
Review #1 received
Received 06 Aug, 2020
Review #2 received
Received 06 Aug, 2020
Reviewer #2 agreed
On 20 Jul, 2020
Reviewer #1 agreed
On 18 Jul, 2020
Reviewers invited
Invitations sent on 09 Jul, 2020
Editor invited
On 02 Jul, 2020
Editor assigned
On 01 Jul, 2020
First submitted
On 30 Jun, 2020
Submission checks complete
On 30 Jun, 2020
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
License:
This work is licensed under a CC BY 4.0 License. Read Full License
The most recent version of this article is available here.
Background: As the most frequent type of cyanotic congenital heart diseases (CHD), Tetralogy of Fallot (TOF) has a relatively poor prognosis without the corrective surgery. Circular RNA (circRNA) represents a novel class of endogenous noncoding RNAs that regulate target gene expression post-transcriptionally in heart development. Here, we investigate the potential role of ceRNA network in the pathogenesis of TOF.
Methods: To identify circRNAs expression profiles in Tetralogy of Fallot, microarrays were used to screen the differentially expressed circRNA between 3 TOF and 3 control human myocardial tissue samples. Then, a dysregulated circRNA- associated ceRNA network was constructed via using the established multi-step screening strategy.
Results: In summary, total 276 differentially expressed circRNAs were identified, including 214 up-regulated and 62 down-regulated ones in TOF samples. By constructing the circRNA-associated ceRNA network based on the bioinformatics data, a total of 19 key circRNAs, 9 key miRNAs and 34 key mRNAs were further screened. Moreover, by enlarging the samples size, the qPCR results validated that the positive correlations between hsa_circ_0007798 and HIF1A.
Conclusions: The findings in this study provide a comprehensive understanding of the ceRNA network involved in TOF biology, such as hsa_circ_0007798/miR-199b-
5p/HIF1A signal axis, and may offer candidate diagnostic biomarkers or potential therapeutic targets for TOF. In addtion, we propose that the ceRNA network regulates TOF progression.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
Figure 6
This is a list of supplementary files associated with this preprint. Click to download.
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