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Various peroxisome proliferator‐activated receptor ( PPAR )‐ γ agonists differently induce differentiation of cultured human keratinocytes
Author(s) -
Yan Yan,
Furumura Minao,
Numata Sanae,
Teye Kwesi,
Karashima Tadashi,
Ohyama Bungo,
Tanida Norifumi,
Hashimoto Takashi
Publication year - 2015
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/exd.12571
Subject(s) - troglitazone , ciglitazone , rosiglitazone , pioglitazone , loricrin , peroxisome proliferator activated receptor , endocrinology , thiazolidinedione , medicine , chemistry , filaggrin , telmisartan , receptor , involucrin , keratinocyte , pharmacology , immunology , in vitro , biochemistry , atopic dermatitis , blood pressure , type 2 diabetes , diabetes mellitus
Peroxisome proliferator‐activated receptors (PPARs) are potentially useful for the treatment of skin diseases, because they stimulate keratinocyte differentiation, exert anti‐inflammatory effects and improve barrier function. We examined five PPAR‐ γ agonists, including four thiazolidinediones (ciglitazone, troglitazone, rosiglitazone and pioglitazone) and an angiotensin‐II receptor blocker (telmisartan), for their ability to upregulate filaggrin and loricrin expression at both mRNA and protein levels in cultured normal human keratinocytes (NHKs). Troglitazone, rosiglitazone, pioglitazone and telmisartan significantly increased filaggrin expression at both mRNA and protein levels in calcium‐induced differentiated NHKs. Rosiglitazone and pioglitazone, but not troglitazone nor telmisartan, also significantly increased loricrin expression at both mRNA and protein levels in differentiated NHKs. These effects were not found in undifferentiated NHKs nor differentiated NHKs treated with ciglitazone. This study revealed differential effects of various PPAR‐ γ agonists on epidermal differentiation, and the most potent of those are rosiglitazone and pioglitazone.