Isoflurane and low-level carbon monoxide exposures increase expression of pro-survival miRNA in neonatal mouse heart

Anesthetics such as isoflurane are known to cause apoptosis in the developing mammalian brain. However, isoflurane may have protective effects on the heart via relieving ischemia and downregulating genes related to apoptosis. Ischemic preconditioning, e.g. through the use of low levels of carbon mon...

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Bibliographic Details
Published in:Cell stress & chaperones Vol. 26; no. 3; pp. 541 - 548
Main Authors: Logan, Samantha M., Gupta, Aakriti, Wang, Aili, Levy, Richard J., Storey, Kenneth B.
Format: Journal Article
Language:English
Published: Dordrecht Springer Science + Business Media 01.05.2021
Springer Netherlands
Springer Nature B.V
Subjects:
Anesthesia
Anesthetics
Animals
Animals, Newborn
Apoptosis
Apoptosis - genetics
Autophagy
Biochemistry
Biomedical and Life Sciences
Biomedicine
Cancer Research
Carbon monoxide
Carbon Monoxide - metabolism
Cell Biology
Cell death
Contraction
Energy balance
Exposure
Gene Expression - drug effects
Heart
Heart - drug effects
Hypertrophy
Hypoxia
Immunology
Injury prevention
Ischemia
Isoflurane
Isoflurane - pharmacology
Mice, Inbred C57BL
MicroRNAs
MicroRNAs - metabolism
miRNA
Mortality
Myocardial Reperfusion Injury - drug therapy
Myocardial Reperfusion Injury - metabolism
Neonates
Neurosciences
ORIGINAL PAPER
Oxidative stress
Phagocytosis
Preconditioning
Reperfusion
Up-Regulation
Oxidative stress
MicroRNA
Cardioprotective
Anesthetic
Apoptosis
Mus musculus
ISSN:1355-8145, 1466-1268, 1466-1268
Online Access:Get full text
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Summary:Anesthetics such as isoflurane are known to cause apoptosis in the developing mammalian brain. However, isoflurane may have protective effects on the heart via relieving ischemia and downregulating genes related to apoptosis. Ischemic preconditioning, e.g. through the use of low levels of carbon monoxide (CO), has promise in preventing ischemia-reperfusion injury and cell death. However, it is still unclear how it either triggers the stress response in neonatal hearts. For this reason, thirty-three microRNAs (miRNAs) known to be differentially expressed following anesthesia and/or ischemic or hypoxic heart damage were investigated in the hearts from neonatal mice exposed to isoflurane or low level of CO, using an air-exposed control group. Only miR-93-5p increased with isoflurane exposure, which may be associated with the suppression of cell death, autophagy, and inflammation. By contrast, twelve miRNAs were differentially expressed in the heart following CO treatment. Many miRNAs previously shown to be responsible for suppressing cell death, autophagy, and myocardial hypertrophy were upregulated (e.g., 125b-3p, 19-3p, and 21a-5p). Finally, some miRNAs (miR-103-3p, miR-1a-3p, miR-199a-1-5p) which have been implicated in regulating energy balance and cardiac contraction were also differentially expressed. Overall, this study demonstrated that CO-mediated miRNA regulation may promote ischemic preconditioning and cardioprotection based on the putative protective roles of the differentially expressed miRNAs explored herein and the consistency of these results with those that have shown positive effects of CO on heart viability following anesthesia and ischemia-reperfusion stress.
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ISSN:1355-8145
1466-1268
1466-1268
DOI:10.1007/s12192-021-01199-0