The pro-apoptotic protein Bim is a microRNA target in kidney progenitors.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 21546576.
- Also identified by DOI 10.1681/ASN.2010080841 and PMC identifier 3103725.
- No licence information is recorded for this record.
- Because redistribution is not established, this page shows the abstract only. Follow the links below for the full text.
Abstract
Understanding the mechanisms that regulate nephron progenitors during kidney development should aid development of therapies for renal failure. MicroRNAs, which modulate gene expression through post-transcriptional repression of specific target mRNAs, contribute to the differentiation of stem cells, but their role in nephrogenesis is incompletely understood. Here, we found that the loss of miRNAs in nephron progenitors results in a premature depletion of this population during kidney development. Increased apoptosis and expression of the pro-apoptotic protein Bim accompanied this depletion. Profiling of miRNA expression during nephrogenesis identified several highly expressed miRNAs (miR-10a, miR-106b, miR-17-5p) in nephron progenitors that are either known or predicted to target Bim. We propose that modulation of apoptosis by miRNAs may determine congenital nephron endowment. Furthermore, our data implicate the pro-apoptotic protein Bim as a miRNA target in nephron progenitors.
Medical subject headings
- Apoptosis Regulatory Proteins
- Kidney
- Membrane Proteins
- MicroRNAs
- Proto-Oncogene Proteins
- Stem Cells