Unknown

Dataset Information

0

Deletion of hypoxia-responsive microRNA-210 results in a sex-specific decrease in nephron number.


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.

SUBMITTER: Hemker SL 

PROVIDER: S-EPMC7136145 | biostudies-literature |

REPOSITORIES: biostudies-literature

Similar Datasets

| S-EPMC6027187 | biostudies-literature
| S-EPMC6093025 | biostudies-literature
| S-EPMC5413434 | biostudies-literature
| S-EPMC5406542 | biostudies-literature
| S-EPMC10095479 | biostudies-literature
| S-EPMC6556335 | biostudies-literature
| S-EPMC5655194 | biostudies-literature
| S-EPMC3996831 | biostudies-literature
| S-EPMC2759401 | biostudies-literature
| S-EPMC3259646 | biostudies-literature