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Published on: June 11, 2020
Lidocaine Administration Controls MicroRNAs Alterations Observed After Lung Ischemia-Reperfusion Injury
Lisa Rancan1, Carlos Simón, Emmeline Marchal-Duval
1From the *Department of Biochemistry and Molecular Biology III, Faculty of Medicine, Complutense University of Madrid, Spain; Departments of †Thoracic Surgery and ‡Anesthesiology, Hospital Gregorio Marañón, Madrid, Spain; and Departments of §Physiology and ‖Biostatistics and Operational Investigation, Faculty of Medicine, Complutense University of Madrid, Spain.
Background:
Ischemia-reperfusion injury (IRI) is associated with morbidity and mortality. MicroRNAs (miRNAs) have emerged as regulators of IRI, and they are involved in the pathogenesis of organ rejection. Lidocaine has proven anti-inflammatory activity in several tissues but its modulation of miRNAs has not been investigated. This work aims to investigate the involvement of miRNAs in lung IRI in a lung auto-transplantation model and to investigate the effect of lidocaine.
Methods:
Three groups (sham, control, and Lidocaine), each comprising 6 pigs, underwent a lung autotransplantation. All groups received the same anesthesia. In addition, animals of lidocaine group received a continuous intravenous administration of lidocaine (1.5 mg/kg/h) during surgery. Lung biopsies were taken before pulmonary artery clamp, before reperfusion, 30 minutes postreperfusion (Rp-30), and 60 minutes postreperfusion (Rp-60). Samples were analyzed for different miRNAs (miR-122, miR-145, miR-146a, miR-182, miR-107, miR-192, miR-16, miR-21, miR-126, miR-127, miR142-5p, miR152, miR155, miR-223, and let7) via the use of reverse-transcription quantitative polymerase chain reaction. Results were normalized with miR-103.
Results:
The expression of miR-127 and miR-16 did not increase after IRI. Let-7d, miR-21, miR-107, miR-126, miR-145, miR-146a, miR-182, and miR-192 significantly increased at the Rp-60 (control versus sham P < .001). miR-142-5p, miR-152, miR-155, and miR 223 significantly increased at the Rp-30 (control versus sham P < .001) and at the Rp-60 (control versus. sham P < .001). The administration of lidocaine was able to attenuate these alterations in a significant way (control versus Lidocaine P < .001).
Conclusions:
Lung IRI caused dysregulation miRNA. The administration of lidocaine reduced significantly miRNAs alterations.
Insights
Lung ischemia-reperfusion injury (IRI) alters microRNA (miRNA) expression. Lidocaine administration significantly reduced these miRNA changes, suggesting a therapeutic role in mitigating lung IRI.
Area of Science:
- Cardiovascular Science
- Pulmonary Medicine
- Molecular Biology
Background:
- Ischemia-reperfusion injury (IRI) is a significant cause of morbidity and mortality.
- MicroRNAs (miRNAs) are key regulators of IRI and organ rejection.
- Lidocaine's anti-inflammatory effects are known, but its impact on miRNA modulation in IRI is unexplored.
Purpose of the Study:
- To investigate miRNA involvement in lung IRI using a lung auto-transplantation model.
- To evaluate the therapeutic effect of lidocaine on miRNA dysregulation during lung IRI.
Main Methods:
- A lung auto-transplantation model in pigs (sham, control, lidocaine groups).
- Lung biopsies collected at multiple time points (pre-clamp, pre-reperfusion, 30, and 60 minutes post-reperfusion).
- Quantitative PCR analysis of 15 specific miRNAs, normalized to miR-103.
Main Results:
- Lung IRI significantly increased the expression of several miRNAs (miR-21, miR-107, miR-126, miR-145, miR-146a, miR-182, miR-192, miR-142-5p, miR-152, miR-155, miR-223) at 30 and 60 minutes post-reperfusion.
- Lidocaine administration significantly attenuated these IRI-induced miRNA alterations.
- miR-127 and miR-16 expression levels did not significantly increase post-IRI.
Conclusions:
- Lung IRI leads to significant miRNA dysregulation.
- Lidocaine effectively reduces miRNA alterations associated with lung IRI.
- These findings highlight lidocaine's potential as a therapeutic agent for lung IRI.
