ArticlePhysiological genomics2013
miR-222 contributes to sex-dimorphic cardiac eNOS expression via ets-1.
Article in Physiological genomics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
15 citing papers in PubMed, 29 citations in OpenAlex.
- Epigenetic regulation of sex dimorphism in cardiovascular health.Canadian journal of physiology and pharmacology · 2024Review
- miR-222 regulates cell growth, apoptosis, and autophagy of interstitial cells of Cajal isolated from slow transit constipation rats by targeting c-kit.Indian journal of gastroenterology : official journal of the Indian Society of Gastroenterology · 2021Article
- What microRNAs could tell us about the human X chromosome.Cellular and molecular life sciences : CMLS · 2020Review
- Sex disparity in cancer: roles of microRNAs and related functional players.Cell death and differentiation · 2018Review
- miRNA as a New Regulatory Mechanism of Estrogen Vascular Action.International journal of molecular sciences · 2018Review
- Role of miRNA in the Regulatory Mechanisms of Estrogens in Cardiovascular Ageing.Oxidative medicine and cellular longevity · 2018Review
- MiR-222 in Cardiovascular Diseases: Physiology and Pathology.BioMed research international · 2017Review
- Sex differences in response to miRNA-34a therapy in mouse models of cardiac disease: identification of sex-, disease- and treatment-regulated miRNAs.The Journal of physiology · 2016Article
- Recent exposure to ultrafine particles in school children alters miR-222 expression in the extracellular fraction of saliva.Environmental health : a global access science source · 2016Article
- Report of the National Heart, Lung, and Blood Institute Working Group on Sex Differences Research in Cardiovascular Disease: Scientific Questions and Challenges.Hypertension (Dallas, Tex. : 1979) · 2016Review
- Characterization of the sex-dependent myocardial S-nitrosothiol proteome.American journal of physiology. Heart and circulatory physiology · 2016Article
- Association of Common Variants in eNOS Gene with Primary Open Angle Glaucoma: A Meta-Analysis.Journal of ophthalmology · 2016Article
- Transgenic Expression of miR-222 Disrupts Intestinal Epithelial Regeneration by Targeting Multiple Genes Including Frizzled-7.Molecular medicine (Cambridge, Mass.) · 2015Article
- Medicinal facilities to B16F10 melanoma cells for distant metastasis control with a supramolecular complex by DEAE-dextran-MMA copolymer/paclitaxel.Drug delivery and translational research · 2015Article
- Estrogen regulation of protein expression and signaling pathways in the heart.Biology of sex differences · 2014Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
It is well recognized that there is sex-dimorphic expression of mRNA and protein in the heart; however, the underlying mechanism is poorly understood. Endothelial nitric oxide synthase (eNOS) is an important regulator of cardiac function, and the expression levels of eNOS differ between male and female hearts. The aim of this study was to examine whether expression of specific microRNA (miRNA, miR) in males and females contributes to changes in the expression of eNOS. miRNA was extracted from the myocardium of male and female C57BL/6 mice and subjected to an Affymetrix miRNA array. Decreased expression of miR-222 was discovered in females and confirmed by qRT-PCR from whole heart or isolated cardiomyocytes. The transcription factor V-ets erythroblastosis virus E26 oncogene homolog-1 (ets-1) was identified as a potential target of miR-222 using TargetScan, and fivefold increased ets-1 protein expression in females was confirmed by Western blot. Targeting of ets-1 by miR-222 was determined in HEK293 cells overexpressing luciferase under regulation of either the ets-1 3'-UTR, a null 3'-UTR control, or a scrambled ets-1 3'-UTR and treated with a small molecule miR-222 mimic or inhibitor. Additionally qRT-PCR confirmed that mRNA levels of the ets-1 transcriptional target, eNOS, were 25% higher in females. Compared with untreated myocyte controls, 50% inhibition of eNOS expression was achieved by treatment with a miR-222 mimic, compared with a 25% increase due to miR-222 inhibitor. Our findings indicate that sex-dependent miR-222 regulation alters the expression of the cardiac regulatory protein eNOS.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.