ArticleAngiogenesis2018
eNOS expression and NO release during hypoxia is inhibited by miR-200b in human endothelial cells.
Article in Angiogenesis, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
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Who cites it
39 citing papers in PubMed, 95 citations in OpenAlex.
- Clinical characteristics of patients with a risk of pulmonary artery hypertension secondary to ARDS in a high-altitude area.BMJ open respiratory research · 2023Trial
- Sodium Sulfite as an Oxygen-Depletion-Based Chemical Model of Tumor Hypoxia In Vitro.Applied biochemistry and biotechnology · 2026Article
- Pharmacological Blockade of Hypoxia-Driven Autophagy: A Therapeutic Strategy to Limit Endothelial Activation and Thrombosis.ACS pharmacology & translational science · 2026Article
- Temporal Coordination of Angiogenic, Nitric Oxide, and Endothelin Pathways in Vascular Adaptation to Hypoxia and Reoxygenation.Cardiovascular drugs and therapy · 2026Review
- The anticancer properties of dexmedetomidine in papillary thyroid cancer and its underlying mechanisms.Scientific reports · 2026Article
- Endothelial dysfunction in cardiovascular diseases: mechanisms and in vitro models.Molecular and cellular biochemistry · 2025Review
- Article
- Ginsenoside Rb1 Alleviated the AKI to CKD Transition by Targeting VEGFR2.Journal of cellular and molecular medicine · 2025Article
- Potential biomarker for screening nasopharyngeal carcinoma: three-microRNA panel in serum.Translational cancer research · 2025Article
- Hypoxia-Dependent Upregulation of VEGF Relies on β3-Adrenoceptor Signaling in Human Retinal Endothelial and Müller Cells.International journal of molecular sciences · 2025Article
- Endothelial MicroRNA-214 Confers Angiotensin II Hypertension by Targeting eNOS in Mice.Kidney & blood pressure research · 2025Article
- Metabolic alterations of endothelial cells under transient and persistent hypoxia: study using a 3D microvessels-on-chip model.Tissue barriers · 2025Article
- Subcellular Localization Guides eNOS Function.International journal of molecular sciences · 2024Review
- mir-605-3p prevents liver premetastatic niche formation by inhibiting angiogenesis via decreasing exosomal nos3 release in gastric cancer.Cancer cell international · 2024Article
- Endothelial cells signaling and patterning under hypoxia: a mechanistic integrative computational model including the Notch-Dll4 pathway.Frontiers in physiology · 2024Article
- Hypoxia Dysregulates the Transcription of Myoendothelial Junction Proteins Involved with Nitric Oxide Production in Brain Endothelial Cells.Biomedicines · 2023Article
- LDLR and PCSK9 3´UTR variants and their putative effects on microRNA molecular interactions in familial hypercholesterolemia: a computational approach.Molecular biology reports · 2023Article
- Big Things, Small Packages: An Update on Microalgae as Sustainable Sources of Nutraceutical Peptides for Promoting Cardiovascular Health.Global challenges (Hoboken, NJ) · 2023Review
- Article
- The transition from HIF-1 to HIF-2 during prolonged hypoxia results from reactivation of PHDs and HIF1A mRNA instability.Cellular & molecular biology letters · 2022Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
The nitric oxide (NO) secreted by vascular endothelium is required for the maintenance of cardiovascular homeostasis. Diminished release of NO generated by endothelial NO synthase contributes to endothelial dysfunction. Hypoxia and ischemia reduce endothelial eNOS expression via posttranscriptional mechanisms that result in NOS3 transcript destabilization. Here, we examine whether microRNAs contribute to this mechanism. We followed the kinetics of hypoxia-induced changes in NOS3 mRNA and eNOS protein levels in primary human umbilical vein endothelial cells (HUVECs). Utilizing in silico predictive protocols to identify potential miRNAs that regulate eNOS expression, we identified miR-200b as a candidate. We established the functional miR-200b target sequence within the NOS3 3'UTR, and demonstrated that manipulation of the miRNA levels during hypoxia using miR-200b mimics and antagomirs regulates eNOS levels, and established that miR-200b physiologically limits eNOS expression during hypoxia. Furthermore, we demonstrated that the specific ablation of the hypoxic induction of miR-200b in HUVECs restored eNOS-driven hypoxic NO release to the normoxic levels. To determine whether miR-200b might be the only miRNA that had this effect, we utilized Next Generation Sequencing (NGS) to follow hypoxia-induced changes in the miRNA levels in HUVECS and found 83 novel hypoxamiRs, with two candidate miRNAs besides miR-200b that could potentially influence eNOS levels. Taken together, the data establish miR-200b-eNOS regulation as a first hypoxamiR-based mechanism that limits NO bioavailability during hypoxia in endothelial cells, and show that hypoxamiRs could become useful therapeutic targets for cardiovascular diseases and other hypoxic-related diseases including various types of cancer.
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What OpenQuestion holds
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.