See the published version of this article at BMC Molecular and Cell Biology.
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
Xiwen Zhang
The Affiliated Huai’an No.1 People’s Hospital of Nanjing Medical University
Corresponding Author
License:
This work is licensed under a CC BY 4.0 License. Read Full License
View the published article at BMC Molecular and Cell Biology.
Background: Trace elements function as essential cofactors that are involved in various biochemical processes in mammals. Autophagy is vital for nutrient supplement, which is an important Zeitegber for the circadian homeostasis in heart. Here, we considered the possibility that autophagy, as well as the cardiomyocyte clock and glycolysis are interlinked. Detrimental effects were observed when cardiac system is exposed to bromine containing drugs. This study investigated the effects and mechanisms of bromide on the circadian clock and glycolytic metabolism of H9C2 cardiomyocytes.
Methods: H9C2 cardiomyocytes were incubated with sodium bromide at indicated doses for 24 hours, cell viability, mRNA expression of clock genes, glycolytic genes and autophagic genes were examined using various cellular and molecular approaches. Also, circadian oscillation rhythm of these genes was determined by serum shock with sodium bromide or equal amounts of sodium chloride.
Results: Bromide does not affect cell viability and apoptosis of H9C2 cardiomyocytes. Bromide dampens the clock and glycolytic ( Hk2 and Pkm2 ) gene expression rhythmicity in a dose-dependent manner. Additionally, bromide inhibits autophagic process in H9C2 cardiomyocytes. In contrast, rapamycin (an autophagy inducer) dramatically restores the inhibitory effect of NaBr on the mRNA expression levels of clock genes ( Bmal1 , Cry1 and Rorα ) and glycolytic genes ( Hk2 and Pkm2 ).
Conclusions: Our results reveal that bromide represses the clock and glycolytic gene expression patterns, partially through inhibition of autophagy.
Keywords
Bromide, H9C2, Circadian clock, Glycolysis, Autophagy
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
Figure 6
Loading...
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
Version 2
Posted 13 Apr, 2020
No comments provided
Editorial decision: Major revision
On 03 Mar, 2020
Review #2 received
Received 29 Feb, 2020
Reviewer #2 agreed
On 15 Feb, 2020
Review #1 received
Received 28 Jan, 2020
Reviewer #1 agreed
On 23 Jan, 2020
Reviewers invited
Invitations sent on 27 Nov, 2019
Editor assigned
On 20 Nov, 2019
Submission checks complete
On 19 Nov, 2019
Editor invited
On 19 Nov, 2019
First submitted
On 31 Oct, 2019
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Learn more about our company.
This preprint is under consideration at BMC Molecular and Cell Biology. 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
Xiwen Zhang
The Affiliated Huai’an No.1 People’s Hospital of Nanjing Medical University
Corresponding Author
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
Version 2
Posted 13 Apr, 2020
No comments provided
Editorial decision: Major revision
On 03 Mar, 2020
Review #2 received
Received 29 Feb, 2020
Reviewer #2 agreed
On 15 Feb, 2020
Review #1 received
Received 28 Jan, 2020
Reviewer #1 agreed
On 23 Jan, 2020
Reviewers invited
Invitations sent on 27 Nov, 2019
Editor assigned
On 20 Nov, 2019
Submission checks complete
On 19 Nov, 2019
Editor invited
On 19 Nov, 2019
First submitted
On 31 Oct, 2019
License:
This work is licensed under a CC BY 4.0 License. Read Full License
View the published article at BMC Molecular and Cell Biology.
Background: Trace elements function as essential cofactors that are involved in various biochemical processes in mammals. Autophagy is vital for nutrient supplement, which is an important Zeitegber for the circadian homeostasis in heart. Here, we considered the possibility that autophagy, as well as the cardiomyocyte clock and glycolysis are interlinked. Detrimental effects were observed when cardiac system is exposed to bromine containing drugs. This study investigated the effects and mechanisms of bromide on the circadian clock and glycolytic metabolism of H9C2 cardiomyocytes.
Methods: H9C2 cardiomyocytes were incubated with sodium bromide at indicated doses for 24 hours, cell viability, mRNA expression of clock genes, glycolytic genes and autophagic genes were examined using various cellular and molecular approaches. Also, circadian oscillation rhythm of these genes was determined by serum shock with sodium bromide or equal amounts of sodium chloride.
Results: Bromide does not affect cell viability and apoptosis of H9C2 cardiomyocytes. Bromide dampens the clock and glycolytic ( Hk2 and Pkm2 ) gene expression rhythmicity in a dose-dependent manner. Additionally, bromide inhibits autophagic process in H9C2 cardiomyocytes. In contrast, rapamycin (an autophagy inducer) dramatically restores the inhibitory effect of NaBr on the mRNA expression levels of clock genes ( Bmal1 , Cry1 and Rorα ) and glycolytic genes ( Hk2 and Pkm2 ).
Conclusions: Our results reveal that bromide represses the clock and glycolytic gene expression patterns, partially through inhibition of autophagy.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
Figure 6
Loading...