New MicroRNA Research Announced “mIR-22”
Reddit Revelations
Last Wednesday morning, Zhengquan Yu of the China Agricultural University and Dr. Maksim Plikus of the University of California Irvine entertained an AMA (ask me anything) crowd on the social news website Reddit about their work involving hair follicles. Yu has just authored a paper titled “Post-transcriptional Regulation of Keratinocyte Progenitor Cell Expansion, Differentiation and Hair Follicle Regression by miR-22.” Plikus focuses on stem cell regulations in the hair follicle model. An interesting tidbit, Plikus was co-author of the Quorum-Sensing paper that garnered some attention online a few months ago.
The recent work done by Yu seemed to be the hot topic of the Reddit AMA. Yu and his co-authors discovered that a microRNA, known as mIR-22, plays an important roll in the regression of hair follicles. According to Yu’s research, increased levels of miR-22 resulted in the premature regression of hair follicles. I understand that the word “regression” refers to hair follicles moving out of the “anagen”, or growth, phase into the “catagen”, or transitional, phase. Therefore, by inhibiting mIR-22, it was found that the hair growth stage was prolonged. The studies done by Yu involving mIR-22 were done on mice.
The Highlight
Truth be told, there are a multitude of scientific papers published involving the hair follicle. Some appear extremely promising and gain more attention than others. They are all noteworthy and provide a piece of the puzzle, yet all of them will not make it onto this blog. The reason that this research has made it on to this blog is because of one single response that Zhengquan Yu made to a question posted on the AMA feed. Here’s the quote from Yu:
“In mouse model, we did find that loss of miR-22 retards hair follicle regression, which can prevent hair loss or prolong hair growth stage. We are testing this finding in human now.”
The magic words. Human trials.
It brings a whole new relevance to research to know that a group is moving forward with it and it is being studied in humans. Here’s another noteworthy quote from Yu that comments on an actual form of treatment that inhibits mIR-22:
“Yes. miR-22 antagomir or other anti-miR-22 oligonucletides could be used to inhibit miR-22 function, which would prevent hair loss or maintain prolonged follicle life.”
Follicle Thoughts
This mIR-22 finding reminds me of the PGD2(r) research in the sense that by suppressing either one of them, the result is elevated hair growth levels. It seems that the understanding of the microbiology of a hair follicle is multiplying at an astounding rate these days. Just like that we have another angle at hair regeneration. In fact, I just decided to visit Hair-GEL.net to plug in mIR-22 to the database and voila, there were the results. Now, I’m sitting here contemplating the gene levels of mIR-22 in the surrounding biology of a hair follicle. (laughs) Yes, it’s safe to say we are in a new unprecedented era of hair follicle understanding.
Here is another recent good research paper on microRNA and hair loss. Hopefully big potential to help us in the future.
MicroRNA-214 controls skin and hair follicle development by modulating the activity of the Wnt pathway
J Cell Biology 2014 Nov 24; 207(4): 549–567.
Authors: Mohammed I. Ahmed,1,* Majid Alam,1,* Vladimir U. Emelianov,2 Krzysztof Poterlowicz,1 Ankit Patel,1 Andrey A. Sharov,2 Andrei N. Mardaryev,1 and Natalia V. Botchkareva 1
Abstract:
Skin development is governed by complex programs of gene activation and silencing, including microRNA-dependent modulation of gene expression. Here, we show that miR-214 regulates skin morphogenesis and hair follicle (HF) cycling by targeting β-catenin, a key component of the Wnt signaling pathway. miR-214 exhibits differential expression patterns in the skin epithelium, and its inducible overexpression in keratinocytes inhibited proliferation, which resulted in formation of fewer HFs with decreased hair bulb size and thinner hair production. The inhibitory effects of miR-214 on HF development and cycling were associated with altered activities of multiple signaling pathways, including decreased expression of key Wnt signaling mediators β-catenin and Lef-1, and were rescued by treatment with pharmacological Wnt activators. Finally, we identify β-catenin as one of the conserved miR-214 targets in keratinocytes. These data provide an important foundation for further analyses of miR-214 as a key regulator of Wnt pathway activity and stem cell functions during normal tissue homeostasis, regeneration, and aging.