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The microRNA network is considered to be a mediator of reductive stress in the heart

 Last Update: 2021-08-14
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Now, in the journal "Scientific Reports," researchers describe the putative molecular regulator of this pathological chronic reductive stress-a microRNA network
.

Redox balance is essential to health
.

For a long time, oxidative stress has been thought to be related to heart failure

Human microRNAs, or miRNAs, are short, non-coding RNAs, approximately 22 bases in length
.

They regulate gene expression through complementary pairing with the cell's specific messenger RNA

The current research is led by Dr.
Rajasekaran namakkar-soorappan, an associate professor in the UAB Department of Pathology, using mice that overexpress Nrf2 (pronounced "nerf-two") in cardiomyocytes to identify miRNA networks
.

Nrf2 is a major transcriptional regulator.
When cardiomyocytes produce reactive oxygen and nitrogen when blood flow is restored after a heart attack, it provides short-term protection by helping to express genes with antioxidant activity
.

However, sustained Nrf2 activation may paradoxically lead to restorative stress

Researchers recently discovered that Nrf2 deletion inhibits the expression of several miRNAs in the heart, which suggests that there is a correlation between Nrf2 expression and miRNAs
.

Therefore, they now decided to look for changes in miRNA levels in three mouse models-one is a normal Nrf2 model, and the other is a low or high level of Nrf2 overexpression model

Comparing the levels of miRNAs from the three models, a subset of miRNAs was found, which seems to be a direct and dose-dependent target of Nrf2, and is therefore presumed to be a regulator of reductive stress
.

namakkar-soorappan calls these mirna reductomiRs, pronounced "reducto-meers"

The researchers also found that there are dose-dependent genes that are differentially expressed in the hearts of mice overexpressing Nrf2
.

Because mirna silences gene expression at the post-transcriptional level, the researchers believe that this unique subset of genes can represent a negatively regulated target of reduced ir

Next, they sought to restore the connection between irs and genes
.

Under normal function, Nrf2 promotes the expression of genes, these genes contain a DNA sequence located near the promoter, called "antioxidant response element"

Then, they used bioinformatics tools to identify 19 mirna with complementary sequences to the seed sequence among 61 down-regulated differentially expressed genes
.

Therefore, these 19 mirna seem to be reducing irs that mediate the reduction stress of nrf2 responsive myocardium

Namakkal-Soorappan said that reductomiRs is just a hypothetical medium because the analysis in the current study comes from bioinformatics
.
He said that what is needed next is a mechanical study to confirm the function of the medium
.

"Identification of nrp2-responsive microRNA networks as hypothetical mediators of myocardial reduced stress" The co-first authors of this study are Justin M.
Quiles and Mark E.
Pepin, Department of Pathology, Department of Molecular and Cytopathology, UAB University
.

The co-author and corresponding author Namakkal-Soorappan are Nissani, Sandeep B.
Shelar, Anil K.
Challa and Adam R.
Wende, Department of Pathology, UAB; Brian Dalley and John R.
Hoidal, University of Utah; UAB School of Cardiovascular Medicine Steven M.
Pogwizd of the Comprehensive Center
.

Support from the National Institutes of Health 2HL118067, HL118067, AG042860, HL133011, HL007918 and HL137240; American Heart Association grants BGIA 0865015F; University of Utah Aging Research Center Pilot Fund; University of Utah; University of Alabama; and Alexander von Humboldt Foundation Postdoctoral Scholarship

Journal Reference :

Justin M.
Quiles, Mark E.
Pepin, Sini Sunny, Sandeep B.
Shelar, Anil K.
Challa, Brian Dalley, John R.
Hoidal, Steven M.
Pogwizd, Adam R.
Wende, Namakkal S.
Rajasekaran.
Identification of Nrf2- responsive microRNA networks as putative mediators of myocardial reductive stress .
Scientific Reports , 2021; 11 (1) DOI: 10.
1038/s41598-021-90583-y

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