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Expression of wild‐type, but not mutant, loricrin causes programmed cell death in HaCaT keratinocytes
Author(s) -
YONEDA Kozo,
DEMITSU Toshio,
MANABE Motomu,
IGARASHI Junsuke,
KOSAKA Hiroaki,
INAGAKI Nobuya,
TAKAHASHI Hidetoshi,
KON Atsushi,
KAKURAI Maki,
KUBOTA Yasuo
Publication year - 2010
Publication title -
the journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.9
H-Index - 65
eISSN - 1346-8138
pISSN - 0385-2407
DOI - 10.1111/j.1346-8138.2010.00932.x
Subject(s) - loricrin , hacat , keratinocyte , transfection , biology , immunoelectron microscopy , microbiology and biotechnology , mutant , cell culture , genetics , involucrin , immunology , gene , immunohistochemistry
The epidermal cornified cell envelope is a complex protein–lipid composite that replaces the plasma membrane of corneocytes and is crucial for epidermal barrier function. Loricrin is a major constituent of the epidermal cornified cell envelope, contributing approximately 70% by mass. In order to explore novel function of wild‐type (WT) loricrin other than the major component of the epidermal cornified cell envelope, we transiently expressed construct encoding human WT and mutant loricrin (730insG) in HaCaT keratinocytes. HaCaT cells transfected with WT or mutant loricrin were at differentiation level. WT loricrin in the transfected cells was seen diffusely in the cytoplasm and nuclei. Positive transferase deoxytidyl uridine end labeling staining was observed in the nuclei of WT loricrin‐transfected HaCaT keratinocytes. Data from the DNA fragmentation assay showed that only WT loricrin induced DNA ladders compared with that of mutant loricrin. WT loricrin‐transfected HaCaT keratinocytes were susceptible to programmed cell death (PCD). Activation of caspase‐14 was also seen. In contrast, PCD or activation of caspase‐14 did not occur in mutant loricrin‐transfected HaCaT cells. These results suggest that the expression of WT loricrin facilitates induction of PCD in HaCaT keratinocytes.