ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2020
Deletion of hypoxia-responsive microRNA-210 results in a sex-specific decrease in nephron number.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- Liquid Biopsy in Clear Cell Renal Cell Carcinoma: Diagnostic Potential of Urinary miRNAs.Cancers · 2026Article
- Sex differences in fetal kidney reprogramming: the case in the renin-angiotensin system.Pediatric nephrology (Berlin, Germany) · 2024Review
- MicroRNAs in kidney development and disease.JCI insight · 2022Review
- Chromatin accessibility and microRNA expression in nephron progenitor cells during kidney development.Genomics · 2022Article
- The miR-199a/214 Cluster Controls Nephrogenesis and Vascularization in a Human Embryonic Stem Cell Model.Stem cell reports · 2021Article
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Authors and funding
9 authors at 2 institutions in 1 country.
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Abstract
Low nephron number results in an increased risk of developing hypertension and chronic kidney disease. Intrauterine growth restriction is associated with a nephron deficit in humans, and is commonly caused by placental insufficiency, which results in fetal hypoxia. The underlying mechanisms by which hypoxia impacts kidney development are poorly understood. microRNA-210 is the most consistently induced microRNA in hypoxia and is known to promote cell survival in a hypoxic environment. In this study, the role of microRNA-210 in kidney development was evaluated using a global microRNA-210 knockout mouse. A male-specific 35% nephron deficit in microRNA-210 knockout mice was observed. Wnt/β-catenin signaling, a pathway crucial for nephron differentiation, was misregulated in male kidneys with increased expression of the canonical Wnt target lymphoid enhancer binding factor 1. This coincided with increased expression of caspase-8-associated protein 2, a known microRNA-210 target and apoptosis signal transducer. Together, these data are consistent with a sex-specific requirement for microRNA-210 in kidney development.
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