Editing MicroRNA (section)

===Kidney disease===
Targeted deletion of Dicer in the [[FOXD1|FoxD1]]-derived renal progenitor cells in a murine model resulted in a complex renal phenotype including expansion of [[Nephrology|nephron]] progenitors, fewer [[renin]] cells, smooth muscle [[arteriole]]s, progressive [[Mesangium|mesangial]] loss and glomerular aneurysms.<ref name="ReferenceB">{{cite journal | vauthors = Phua YL, Chu JY, Marrone AK, Bodnar AJ, Sims-Lucas S, Ho J | title = Renal stromal miRNAs are required for normal nephrogenesis and glomerular mesangial survival | journal = Physiological Reports | volume = 3 | issue = 10 | pages = e12537 | date = October 2015 | pmid = 26438731 | pmc = 4632944 | doi = 10.14814/phy2.12537 }}</ref> High throughput whole [[transcriptome]] profiling of the FoxD1-Dicer knockout mouse model revealed ectopic upregulation of pro-apoptotic gene, [[BCL2-like 1 (gene)|Bcl2L11]] (Bim) and dysregulation of the [[p53]] pathway with increase in p53 effector genes including [[Bcl-2-associated X protein|Bax]], [[TP53INP1|Trp53inp1]], Jun, [[P21|Cdkn1a]], [[MMP2|Mmp2]], and [[ARID3A|Arid3a]]. p53 protein levels remained unchanged, suggesting that FoxD1 stromal miRNAs directly repress p53-effector genes. Using a lineage tracing approach followed by [[Fluorescent-activated cell sorting]], miRNA profiling of the FoxD1-derived cells not only comprehensively defined the transcriptional landscape of miRNAs that are critical for vascular development, but also identified key miRNAs that are likely to modulate the renal phenotype in its absence. These miRNAs include miRs-10a, 18a, 19b, 24, 30c, 92a, 106a, 130a, 152, 181a, 214, 222, 302a, 370, and 381 that regulate Bcl2L11 (Bim) and miRs-15b, 18a, 21, 30c, 92a, 106a, 125b-5p, 145, 214, 222, 296-5p and 302a that regulate p53-effector genes. Consistent with the profiling results, ectopic [[apoptosis]] was observed in the cellular derivatives of the FoxD1 derived progenitor lineage and reiterates the importance of renal stromal miRNAs in cellular homeostasis.<ref name="ReferenceB"/>