Expression of epidermal keratins and the cornified envelope protein involucrin is influenced by permeability barrier disruption

被引:101
作者
Ekanayake-Mudiyanselage, S
Aschauer, H
Schmook, FP
Jensen, JM
Meingassner, JG
Proksch, E
机构
[1] Univ Kiel, Dept Dermatol, D-24105 Kiel, Germany
[2] Novartis Res Inst, Dept Chem & Pharmacol, Vienna, Austria
关键词
loricrin;
D O I
10.1046/j.1523-1747.1998.00318.x
中图分类号
R75 [皮肤病学与性病学];
学科分类号
100206 ;
摘要
In previous studies we have shown that experimental permeability barrier disruption leads to an increase in epidermal lipid and DNA synthesis. Here we investigate whether barrier disruption also influences keratins and cornified envelope proteins as major structural keratinocyte proteins, Cutaneous barrier disruption was achieved in hairless mouse skin by treatments with acetone +/- occlusion, sodium dodecyl sulfate, or tape-stripping. As a chronic model for barrier disruption, we used essential fatty acid deficient mice. Epidermal keratins were determined by one- and two-dimensional gel electrophoresis, immunoblots, and anti-keratin antibodies in biopsy samples. In addition, the expression of the cornified envelope proteins loricrin and involucrin after barrier disruption was determined by specific antibodies in human skin. Acute as well as chronic barrier disruption resulted in the induction of the expression of keratins K6, K16, and K17. Occlusion after acute disruption led to a slight reduction of keratin K6 and K16 expression, Expression of basal keratins K5 and K14 was reduced after both methods of barrier disruption. Suprabasal keratin K10 expression was increased after acute barrier disruption and K1 as well as K10 expression was increased after chronic barrier disruption. Loricrin expression in mouse and in human skin was unchanged after barrier disruption. In contrast, involucrin expression, which was restricted to the granular and upper spinous layers in normal human skin, showed an extension to the lower spinous layers 24 h after acetone treatment. In summary, our results document that acute or chronic barrier disruption leads to expression of keratins K6, K16, and K17 and to a premature expression of involucrin. We suggest that the coordinated regulation of Lipid, DNA, keratin, and involucrin synthesis is critical for epidermal permeability barrier function.
引用
收藏
页码:517 / 523
页数:7
相关论文
共 55 条
[1]  
Bavandi A, 1992, Exp Dermatol, V1, P199, DOI 10.1111/j.1600-0625.1992.tb00189.x
[2]   LORICRIN EXPRESSION IS COORDINATED WITH OTHER EPIDERMAL PROTEINS AND THE APPEARANCE OF LIPID LAMELLAR GRANNIES IN DEVELOPMENT [J].
BICKENBACH, JR ;
GREER, JM ;
BUNDMAN, DS ;
ROTHNAGEL, JA ;
ROOP, DR .
JOURNAL OF INVESTIGATIVE DERMATOLOGY, 1995, 104 (03) :405-410
[3]   THE GENETIC-BASIS OF EPIDERMOLYTIC HYPERKERATOSIS - A DISORDER OF DIFFERENTIATION-SPECIFIC EPIDERMAL KERATIN GENES [J].
CHENG, J ;
SYDER, AJ ;
YU, QC ;
LETAI, A ;
PALLER, AS ;
FUCHS, E .
CELL, 1992, 70 (05) :811-819
[4]   A LEUCINE-]PROLINE MUTATION IN THE H1 SUBDOMAIN OF KERATIN-1 CAUSES EPIDERMOLYTIC HYPERKERATOSIS [J].
CHIPEV, CC ;
KORGE, BP ;
MARKOVA, N ;
BALE, SJ ;
DIGIOVANNA, JJ ;
COMPTON, JG ;
STEINERT, PM .
CELL, 1992, 70 (05) :821-828
[5]  
CHOI JS, 1992, BIOLOGY OF THE EPIDERMIS : MOLECULAR AND FUNCTIONAL ASPECTS, P11
[6]  
DOWNING DT, 1992, J LIPID RES, V33, P301
[7]  
ELIAS PM, 1983, J INVEST DERMATOL, V80, P44, DOI DOI 10.1038/JID.1983.12)
[8]   ICHTHYOSIFORM DERMATOSES .3. STUDIES OF TRANSEPIDERMAL WATER LOSS [J].
FROST, P ;
WEINSTEIN, GD ;
BOTHWELL, JW ;
WILDNAUER, R .
ARCHIVES OF DERMATOLOGY, 1968, 98 (03) :230-+
[9]   Keratins and the skin [J].
Fuchs, E .
ANNUAL REVIEW OF CELL AND DEVELOPMENTAL BIOLOGY, 1995, 11 :123-153
[10]  
GRUBAUER G, 1989, J LIPID RES, V30, P323