RBM 28, a protein deficient in ANE syndrome, regulates hair follicle growth via miR‐203 and p63

• Published in: Experimental dermatology Vol. 24; no. 8; pp. 618 - 622
• Main Authors: Warshauer, Emily, Samuelov, Liat, Sarig, Ofer, Vodo, Dan, Bindereif, Albrecht, Kanaan, Moien, Gat, Uri, Fuchs‐Telem, Dana, Shomron, Noam, Farberov, Luba, Pasmanik‐Chor, Metsada, Nardini, Gil, Winkler, Eyal, Meilik, Benjamin, Petit, Isabelle, Aberdam, Daniel, Paus, Ralf, Sprecher, Eli, Nousbeck, Janna
• Format: Journal Article
• Language: English
• Published: 01.08.2015
• ISSN: 0906-6705; 1600-0625
• DOI: 10.1111/exd.12737

Abstract Alopecia–neurological defects–endocrinopathy ( ANE ) syndrome is a rare inherited hair disorder, which was shown to result from decreased expression of the RNA ‐binding motif protein 28 ( RBM 28 ). In this study, we attempted to delineate the role of RBM 28 in hair biology. First, we sought to obtain evidence for the direct involvement of RBM 28 in hair growth. When RBM 28 was downregulated in human hair follicle ( HF ) organ cultures, we observed catagen induction and HF growth arrest, indicating that RBM 28 is necessary for normal hair growth. We also aimed at identifying molecular targets of RBM 28. Given that an RBM 28 homologue was recently found to regulate mi RNA biogenesis in C. elegans and given the known pivotal importance of mi RNA s for proper hair follicle development, we studied global mi RNA expression profile in cells knocked down for RBM 28. This analysis revealed that RBM 28 controls the expression of miR‐203. miR‐203 was found to regulate in turn TP 63 , encoding the transcription factor p63, which is critical for hair morphogenesis. In conclusion, RBM 28 contributes to HF growth regulation through modulation of miR‐203 and p63 activity.