Premium
Suppression of hyaluronan synthase 2 expression reflects the atrophogenic potential of glucocorticoids
Author(s) -
Averbeck Marco,
Gebhardt Carl,
Anderegg Ulf,
Simon Jan C.
Publication year - 2010
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1111/j.1600-0625.2010.01099.x
Subject(s) - hyaluronan synthase , calcineurin , human skin , glucocorticoid , in vitro , fibroblast , chemistry , pharmacology , endocrinology , biology , medicine , enzyme , biochemistry , transplantation , genetics
Please cite this paper as: Suppression of hyaluronan synthase 2 expression reflects the atrophogenic potential of glucocorticoids. Experimental Dermatology 2010; 19 : 757–759. Abstract: We recently demonstrated that dexamethasone, a strongly atrophogenic glucocorticoid (GC), downregulated hyaluronan (HA) production in human keratinocytes and fibroblasts in vitro and after topical application to human skin in vivo via suppression of hyaluronan synthase 2 (HAS2). To test whether HAS2 activity might discriminate the atrophogenic potential of other substances applied topically to skin, we compared the HA metabolism in cultured human fibroblasts following in vitro treatment with GCs and the non‐atrophogenic calcineurin inhibitor tacrolimus. GCs suppressed HAS2 mRNA expression and decreased HA as shown by qRT‐PCR or ELISA. Tacrolimus did not affect hyaluronan‐metabolizing enzymes nor total HA. Neither mometasone nor tacrolimus affected the expression of collagen mRNAs in human fibroblasts. In conclusion, suppression of HAS2 activity may represent an early process of GC‐induced skin atrophy that precedes the suppression of collagens. Analysis of HAS2 regulation may thus be of value to assess the atrophogenic potential of drugs being developed.