MicroRNAs take part in pathophysiology and pathogenesis of Male Pattern Baldness

Mol Biol Rep. 2009 Oct 10.
MicroRNAs take part in pathophysiology and pathogenesis of Male Pattern Baldness.
Goodarzi HR, Abbasi A, Saffari M, Tabei MB, Noori Daloii MR.

Department of Medical Genetics, Medical School, Tehran University of Medical Sciences, Poorsina Street, Tehran, Iran.

Male Pattern Baldness (MPB) or androgenetic alopecia is a common form of hair loss with androgens and genetics having etiological significance. Androgens are thought to pathophysiologically power on cascades of chronically dramatic alterations in genetically susceptible scalp dermal papillas, specialized cells in hair follicles in which androgens react, and finally resulting in a patterned alopecia. However, the exact mechanisms through which androgens, positive regulators of growth and anabolism in most body sites, paradoxically exert their effects on balding hair follicles, are not yet known. The role of microRNAs, a recently discovered class of non-coding RNAs, with a wide range of regulatory functions, has been documented in hair follicle formation and their deregulation in cancer of prostate, a target organ of androgens has also been delineated. Yet, there is a lack of knowledge in agreement with microRNAs' contribution in pathophysiology of MPB. To investigate the role of microRNAs in pathogenesis of MPB, we selected seven microRNAs, predicted bioinformatically on a reverse engineering basis, from previously published microarray gene expression data and analyzed their expression in balding relative to non-balding dermal papillas. We found for the first time upregulation of four microRNAs (miR-221, miR-125b, miR-106b and miR-410) that could participate in pathogenesis of MPB. Regarding microRNAs' therapeutic potential and accessibility of hair follicles for gene therapy, these microRNAs can be considered as good candidates for a new revolutionized generation of treatments.

I checked to see if either Curcumin, resveratrol or Sulforaphane, which are known to modulate some MicroRNAs in cancer and tumor growth, particularly in prostate cancer would effect these specific MicroRNAs: miR-221, miR-125b, miR-106b and miR-410.

So far, I've found nothing, but it doesn't mean they are not affected, so more research is needed. However, all three of the above help prevent androgen-dependent prostate cancer.

Here is more information on the connection between some MicroRNAs and prostate cancer. Notice that one of the for MPB is mentioned in this abstract below.

Cancer Res. 2009 Apr 15;69(:3356-63.
The role of microRNA-221 and microRNA-222 in androgen-independent prostate cancer cell lines.
Sun T, Wang Q, Balk S, Brown M, Lee GS, Kantoff P.

Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA 02115, USA.

Androgen-dependent prostate cancer typically progresses to castration-resistant prostate cancer (CRPC) after the androgen deprivation therapy. MicroRNAs (miR) are noncoding small RNAs (19-25nt) that play an important role in the regulation of gene expression. Recent studies have shown that miR expression patterns are significantly different in normal and neoplastic prostate epithelial cells. However, the importance of miRs in the development of CRPC has not yet been explored. By performing genome-wide expression profiling of miRs, we found that expression levels of several miRs, in particular miR-221 and miR-222, were significantly increased in CRPC cells (the LNCaP-derived cell line LNCaP-Abl), compared with those in the androgen-dependent prostate cancer cell line (LNCaP). Overexpression of miR-221 or miR-222 in LNCaP or another androgen-dependent cell line, LAPC-4, significantly reduced the level of the dihydrotestosterone (DHT) induced up-regulation of prostate-specific antigen (PSA) expression and increased androgen-independent growth of LNCaP cells. Knocking down the expression level of miR-221 and miR-222 with antagonist miRs in the LNCaP-Abl cell line restored the response to the DHT induction of PSA transcription and also increased the growth response of the LNCaP-Abl cells to the androgen treatment. Changing the expression level of p27/kip1, a known target of miR-221 and miR-222, alone in LNCaP cells affected the DHT-independent cell growth but did not significantly influence the response of PSA transcription to the DHT treatment. In conclusion, our data suggest the involvement of miR-221 and miR-222 in the development or maintenance of the CRPC phenotype.

MicroRNA-221 regulates high glucose-induced endothelial dysfunction.

http://www.ncbi.nlm.nih.gov/pubmed/19351599

Not a surprise here, miR-221 increases with high glucose. Also miR-221 is significantly up-regulated upon mast cell activation.

miR-125b maybe downregulated with sufficient vitamin D, but more research is needed. miR-125b is involved in psoriasis.

Bump. Now it's miR-22 that is thought to be implicated :

http://blogs.plos.org/biologue/2015/06/16/understanding-images-micrornas-contribute-to-hair-loss-and-follicle-regression/

CS: any idea of a miR-22 inhibitor? So far I found none.

CausticSymmetry wrote:MicroRNA-221 regulates high glucose-induced endothelial dysfunction.

http://www.ncbi.nlm.nih.gov/pubmed/19351599

Not a surprise here, miR-221 increases with high glucose.  Also miR-221 is significantly up-regulated upon mast cell activation.

miR-125b maybe downregulated with sufficient vitamin D, but more research is needed.  miR-125b is involved in psoriasis.