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Research article
Fen Zhu
Wuhan Third Hospital & Tongren Hospital of Wuhan University
Corresponding Author
ORCiD: https://orcid.org/0000-0002-8976-2786
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Background: Myocardial infarction is a serious representation of cardiovescular disease, however, ischemia–reperfusion (I/R) injury is an unpredictable complication of cardiovascular surgeries.
Methods: MiR-187 or DYRK2 was inhibited or overexpressed in cardiomyocytes H/R models by pretreatment with miR-187 mimic or inhibitor or DYRK2 inhibitor to confirm the function of miR-187 in H/R. A myocardium I/R mouse model was established using miR-187 transgenic mice. Circulating levels of miR-187 or DYRK2 was detected by quantitative realtime PCR and protein expression was detected by western blotting. The cell viability in all groups was determined by MTT assay and the apoptosis ratio was detected by flow cytometry after staining with Annexin V-FITC. The effect of miR-187 on cellular ROS generation was examined by DCFH-DA. The level of lipid peroxidation and SOD expression were determined by MDA and SOD assay.
Results: The findings indicated that miR-187 may be a possible regulator in the protective effect of H/R-induced cardiomyocyte apoptosis, cellular oxidative stress and leaded to DYRK2 suppression at a posttranscriptional level. Moreover, the improvement of miR-187 on H/R-induced cardiomyocyte injury contributed to the obstruction of DYRK2 expression. In addition, these results identified DYRK2 as the functional downstream target of miR-187 regulated myocardial infarction and oxidative stress.
Conclusions: These present work provided the first insight into the function of miR-187 in successfully protect cardiomyocyte both in vivo and in vitro, and such a protective effect were mediated through the regulation of DYRK2 expression.
Trial registration: Not Applicable.
Keywords
MiR-187, DYRK2, Cardiomyocyte, Myocardial infarction, Oxidative stress
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A new preprint design is coming!
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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.
Research article
Fen Zhu
Wuhan Third Hospital & Tongren Hospital of Wuhan University
Corresponding Author
ORCiD: https://orcid.org/0000-0002-8976-2786
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
History
CURRENT STATUS: Posted
Version 1
Posted 12 Mar, 2021
No community comments so far
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: Myocardial infarction is a serious representation of cardiovescular disease, however, ischemia–reperfusion (I/R) injury is an unpredictable complication of cardiovascular surgeries.
Methods: MiR-187 or DYRK2 was inhibited or overexpressed in cardiomyocytes H/R models by pretreatment with miR-187 mimic or inhibitor or DYRK2 inhibitor to confirm the function of miR-187 in H/R. A myocardium I/R mouse model was established using miR-187 transgenic mice. Circulating levels of miR-187 or DYRK2 was detected by quantitative realtime PCR and protein expression was detected by western blotting. The cell viability in all groups was determined by MTT assay and the apoptosis ratio was detected by flow cytometry after staining with Annexin V-FITC. The effect of miR-187 on cellular ROS generation was examined by DCFH-DA. The level of lipid peroxidation and SOD expression were determined by MDA and SOD assay.
Results: The findings indicated that miR-187 may be a possible regulator in the protective effect of H/R-induced cardiomyocyte apoptosis, cellular oxidative stress and leaded to DYRK2 suppression at a posttranscriptional level. Moreover, the improvement of miR-187 on H/R-induced cardiomyocyte injury contributed to the obstruction of DYRK2 expression. In addition, these results identified DYRK2 as the functional downstream target of miR-187 regulated myocardial infarction and oxidative stress.
Conclusions: These present work provided the first insight into the function of miR-187 in successfully protect cardiomyocyte both in vivo and in vitro, and such a protective effect were mediated through the regulation of DYRK2 expression.
Trial registration: Not Applicable.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
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