Expression profile of endothelin receptors (ETA and ETB) and microRNAs-155 and -199 in the corpus cavernosum of rats submitted to chronic alcoholism and diabetes mellitus

Gonçalves, Fernando Zapparoli; Neto, Fermino Sanches Lizarte; Novais, Paulo Cézar; Gattás, Daniela; Lourenço, Lilian; Carvalho, C.; Tirapelli, Daniela P.C.; Molina, C.; Tirapelli, Luís Fernando; Tucci, Sílvio

doi:10.1590/1414-431x20176329

Cited by 12 publications

(12 citation statements)

References 27 publications

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“…The ethanol consumption associated with DM have a pivotal role in the pathogenesis of ED that is explained by reduction in the turnover of ET A and ET B receptors of endothelin-1 that is a potent vasoconstrictor peptide in the corpus cavernosum 21 . Thus, based on these data and on our findings, we can suggest that apoptosis should be a mechanism that cooperates to the development of erectile dysfunction associated to DM.…”

Section: ■ Discussionmentioning

confidence: 99%

Chronic alcoholism associated with diabetes induced apoptosis in the corpus cavernosum of rats

Schimming

Cirino

Neto³

et al. 2020

Acta Cir. Bras.

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Section: ■ Discussionmentioning

confidence: 99%

Chronic alcoholism associated with diabetes induced apoptosis in the corpus cavernosum of rats

Schimming

Cirino

Neto³

et al. 2020

Acta Cir. Bras.

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“…The sample size in each group was defined considering previous studies that assessed genes and miRNAs expression in an animal model of diabetic and alcoholic rats. 19 , 20 …”

Section: Methodsmentioning

confidence: 99%

“… 25 Similarly, on the first day all rats were weighed and the diabetes was developed by 1 injection of alloxan (Sigma Aldrich Chemical - Saint Louis, MO, USA) (dissolved in 0.1 citrate buffer, 45 mg/kg) into the tail vein. 18 , 19 , 20 The control group received 1 injection of citrate buffer only into the tail vein and drinkable water replaced at the same time as did the others. Blood samples were drawn every week from a tail stab to measure the level of blood glucose using reagent strips (BM-Accutest and an auto-recorder, Accutrend, Boehring Mannheim, UK).…”

Section: Methodsmentioning

confidence: 99%

“… 19 The same research group also demonstrated that changes in the endothelinergic system (ETA and ETB) in the CSM that can play a role in the pathogenesis of ED. 20 miR-15b, miR-16, miR-138, miR-221, and miR-222 are miRNAs whose expressions have been related to endothelial cells, vascular physiology, angiogenesis, and vascular remodeling. 21 , 22 , 23 According to the MiRNA database and target prediction tool index (DIANA-miRPath v3.0), such miRNAs have also been related to regulatory pathways of angiogenesis, nitric oxide synthase activity and the mechanism of cell death by apoptosis.…”

Section: Introductionmentioning

confidence: 99%

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Expression of MicroRNAs (miR-15b, miR-16, miR-138, miR-221, and miR-222) as Biomarkers of Endothelial Corpus Cavernosum Dysfunction in a Diabetic Alcoholic Murine Model

Tiraboschi¹,

Neto

Tirapelli

et al. 2021

Sexual Medicine

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Introduction MicroRNAs (miRNAs) are short noncoding RNA molecules that regulate gene expression and are related to endothelial dysfunction (EnD). Recently, miRNAs have also been explored as potential biomarkers and target molecular therapy of erectile dysfunction (ED). Could the miRNAs be the tip of the iceberg of chronic arterial disease foreshadowed by the ED? Aim To investigate the expression of miR-15b, miR-16, miR-138, miR-221, and miR-222 in corpus cavernosum (CC) and peripheral blood in a rat model of endothelium dysfunction secondary to diabetes (DM) and alcohol consumption to assess potential endothelial lesion biomarkers. Methods Twenty males Wistar rats were divided into 4 groups: control group (C), alcohol consumption group (A), diabetic group (D), diabetic-alcohol consumption group (D + A). DM was alloxan-induced and alcohol consumption was through progressive increase of ethanol concentration in drinkable water. After 7 weeks, miRNAs expressions from CC and blood sample were evaluated by real-time PCR. Functional assessment of CC was performed in an acetylcholine endothelium-dependent relaxation pharmacological study. Main Outcome Measure miRNA expression in CC and blood were evaluated; pharmacological study in CC strips was conducted to validate EnD. Results We found that 3 miRNAs (miR-16, miR-221, and miR-222) were downregulated in the CC in the D+A group, while all 5 miRNAs were downregulated in the blood of D and D + A groups. The endothelium-dependent relaxation induced by acetylcholine was significantly decreased in groups A, D, and D + A. Diagnostic accuracy estimated by AUC, to discriminating groups A, D, and D + A from controls, was superior to >0.9 in all plasmatic miRNAs. Conclusion miRNAs downregulation was identified in both CC and blood notably in DM associated with alcohol consumption animals (D + A), the greatest endothelial injury potential group. Serum miRNAs have also demonstrated high diagnostic accuracy properties in predicting CC relaxation dysfunction labeling EnD. RB Tiraboschi, FSL Neto, DP da Cunha Tirapelli, et al. Expression of MicroRNAs (miR-15b, miR-16, miR-138, miR-221, and miR-222) as Biomarkers of Endothelial Corpus Cavernosum Dysfunction in a Diabetic Alcoholic Murine Model. Sex Med 2021;9:100326.

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“…The function of miRNAs is modulated by binding to the 3 0 -UTR of target mRNAs, resulting in degeneration of mRNA and prohibition of translation (11). Previous studies have revealed that various miRNAs regulate the development of diabetes (12,13). Downregulation of miR-15a in the retina of patients with diabetes was found to counteract inflammation and generation of vessels (14).…”

Section: Introductionmentioning

confidence: 99%

Inhibition of miR-383 suppresses oxidative stress and improves endothelial function by increasing sirtuin 1

Gong

2020

Braz J Med Biol Res

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Previous research has shown that suppression of miR-383 can prevent inflammation of the endothelium, as well as postpone the development of atherosclerosis. However, the role of miR-383 in endothelial cell apoptosis in diabetes remains unclear. The aim of this study was to investigate the function of miR-383 in high glucose-induced apoptosis and oxidative stress in endothelial cells. A series of experiments involving qualitative polymerase chain reaction, cell transfection, luciferase assay, assessment of cell death, detection of catalase and superoxide dismutase concentrations, detection of intracellular reactive oxygen species (ROS), and western blot analysis were performed in this study. We found that miR-383 expression was promoted, while NAD +-dependent deacetylase and sirtuin 1 (SIRT1) expressions were suppressed in the endothelium of the aorta in db/db mice as well as in human umbilical vein endothelial cells, which were treated with high glucose (HG). Increased expression of miR-383 decreased expression of SIRT1, while suppression of miR-383 promoted expression of SIRT1 in human umbilical vein endothelial cells (HUVECs). Furthermore, suppression of miR-383 following transfection with miR-383 suppressor repressed cell death and generation of ROS in HUVECs. SIRT1 knockdown by siRNA-SIRT1 reversed the suppressive effect of miR-383 inhibition on ROS production and cell apoptosis induced by HG treatment. Overall, the findings of our research suggested that suppression of miR-383 repressed oxidative stress and reinforced the activity of endothelial cells by upregulation of SIRT1 in db/db mice, and targeting miR-383 might be promising for effective treatment of diabetes.

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Expression profile of endothelin receptors (ETA and ETB) and microRNAs-155 and -199 in the corpus cavernosum of rats submitted to chronic alcoholism and diabetes mellitus

Cited by 12 publications

References 27 publications

Chronic alcoholism associated with diabetes induced apoptosis in the corpus cavernosum of rats

Chronic alcoholism associated with diabetes induced apoptosis in the corpus cavernosum of rats

Expression of MicroRNAs (miR-15b, miR-16, miR-138, miR-221, and miR-222) as Biomarkers of Endothelial Corpus Cavernosum Dysfunction in a Diabetic Alcoholic Murine Model

Inhibition of miR-383 suppresses oxidative stress and improves endothelial function by increasing sirtuin 1

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