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MicroRNAs

MicroRNAs

MicroRNA (miRNA) are short, regulatory RNA transcribed from introns (non-coding regions of a gene) or intergenic regions (stretches of DNA present between genes). Several processing steps are required to form biologically active, mature miRNA. The initial transcript, called primary miRNA (pri-mRNA), base-pairs with itself, forming a stem-loop structure. Within the nucleus, an endonuclease enzyme, called Drosha, shortens the stem-loop structure into hairpin-shaped pre-miRNA. After the pre-miRNA...

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Updated: Dec 27, 2025

MicroRNA In situ Hybridization for Formalin Fixed Kidney Tissues

MicroRNA In situ Hybridization for Formalin Fixed Kidney Tissues

Published on: November 30, 2013

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

Shelby L Hemker^1,2, Débora M Cerqueira^1,2, Andrew J Bodnar^1,2

¹Division of Nephrology, Department of Pediatrics, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology

|March 7, 2020

Summary

This summary is machine-generated.

MicroRNA-210 plays a key role in kidney development. Its absence in mice led to a sex-specific reduction in nephron number, impacting kidney health.

Keywords:

apoptosis kidney development microRNA-210

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Last Updated: Dec 27, 2025

MicroRNA In situ Hybridization for Formalin Fixed Kidney Tissues

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Published on: November 30, 2013

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Published on: May 22, 2019

Area of Science:

Developmental Biology
Molecular Biology
Nephrology

Background:

Low nephron number increases the risk of hypertension and chronic kidney disease.
Intrauterine growth restriction, often due to placental insufficiency and fetal hypoxia, is linked to nephron deficit.
Hypoxia's impact on kidney development mechanisms remains unclear.

Purpose of the Study:

To investigate the role of microRNA-210 in kidney development.
To determine the effects of microRNA-210 deficiency on nephron formation and associated signaling pathways.

Main Methods:

Utilized a global microRNA-210 knockout mouse model.
Analyzed kidney development, nephron number, and gene expression profiles.
Examined Wnt/β-catenin signaling pathway components and apoptosis-related factors.

Main Results:

MicroRNA-210 knockout mice exhibited a male-specific 35% nephron deficit.
Misregulation of Wnt/β-catenin signaling was observed in male kidneys.
Increased expression of lymphoid enhancer binding factor 1 and caspase-8-associated protein 2 was noted.

Conclusions:

MicroRNA-210 is essential for normal kidney development.
The study reveals a sex-specific requirement for microRNA-210 in nephrogenesis.
Findings suggest microRNA-210 influences kidney development via Wnt/β-catenin signaling and apoptosis regulation.