Glaucoma medication causes hair regrowth

Prostaglandin metabolism in human hair follicle.
Colombe L, Vindrios A, Michelet JF, Bernard BA.
Source
Centre Charles Zviak, L'Oreal Recherche, 90 rue du Général Roguet, Clichy Cedex, France. lcolombe@rd.loreal.com

Abstract
Prostaglandins regulate a wide number of physiological functions. Recently PGF(2alpha) analogue such as latanoprost was shown to have a real impact on hair regrowth. The aim of this study was to investigate and describe the expression profile in human hair follicle of prostaglandin metabolism key enzymes, i.e. carbonyl reductase-1 (CBR1), microsomal prostaglandin E synthase-1 (mPGES-1) and microsomal prostaglandin E synthase-2 (mPGES-2), cytosolic prostaglandin E synthase (cPGES), the aldoketoreductase AKR1C1 and the prostaglandin F synthase AKR1C3. Quantitative RT-PCR on plucked hair follicles revealed some sex-related differences, mPGES-2 and AKR1C3 expression levels being higher in women. Cell and hair follicle compartment specificity was investigated using Western blot, PGE(2) and PGF(2alpha) ELISA assays and immunohistochemistry. Most of the hair cell types were endowed with prostaglandin metabolism machinery and were thus able to produce PGE(2) and/or PGF(2alpha). The epithelial part of the hair bulb was identified by immunohistology and EIA assays as the main source of prostaglandin synthesis and interconversion. All these observations support the concept that prostaglandins might be involved in hair growth and differentiation control.

PGE2 alpha
The most common and most biologically active of the mammalian prostaglandins. It exhibits most biological activities characteristic of prostaglandins and has been used extensively as an oxytocic agent. The compound also displays a protective effect on the intestinal mucosa.

Chronic inflammatory disease is caused by the imbalance of non-inflammatory prostaglandins and inflammatory prostaglandins in the body. Cell membrane fatty acid profiles cause this imbalance, and it is the dietary sources or these fatty acids that is responsible for the cell membrane fatty acid make-up. Chronic inflammatory disease can be overcome by addressing the tissue fatty acid imbalance.

PGD2S LEVELS ARE ELEVATED IN BALD SCALP

http://www.wipo.int/pctdb/en/wo.jsp?ELEMENT_SET=F&LANGUAGE=ENG&KEY=07%2F149312&IA=07%2F149312&DISPLAY=DESC
"RESULTS

[ 00517 ] In addition to the above genes, levels of the lipocalin (brain) isoform prostaglandin D2 synthase (PGD2S) were elevated in bald scalp relative to haired scalp (Figure 7A). To confirm this finding, PGD2 levels were tested in bald and haired tissue from 3 patients. PGD2 was elevated in all bald samples, 15 at an average fold increase of 11.6 (Figure 7B). This increase in PGD2 was verified in 1 individual by mass spectrometry. PGD2 was detected at 17 pg/mg of tissue in haired scalp and 75.5 pg/mg in bald scalp, representing a 4.4 fold increase in bald tissue. PGF2a also was slightly elevated in bald scalp with 6.7 pg/mg in haired scalp and 15.9 pg/mg in bald scalp. PGE2, however, exhibited the reverse trend with PGE2 present at 22.7 pg/mg in the haired scalp and 12.0 pg/mg in the bald scalp (Figure 7C).

20 [ 00518 ] The RT-PCR results were further confirmed in 2 individuals not measured in the original array study by quantitative RT PCR, demonstrating a 5.23 and 10.7 fold increase of L-PGDS in bald scalp over haired scalp (Figure 7D). Immunohistochemical staining of L-PGDS revealed an increase in bald scalp, with L-PGDS appearing in the cells along the fibrous root sheath populated by dermal fibroblasts, as well as in scattered locations intrafollicularly. Given the lack of expression of L-PGDS in hematopoietic

25 cells, increases in L-PGDS were not from the sparse inflammatory cell infiltrate occasionally present in AGA.

[ 00519 ] Thus, PGD2 synthase and PGD2 are targets for ameliorating common baldness, e.g."