2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) affects keratin 1 and keratin 17 gene expression and differentially induces keratinization in hairless mouse skin

Andrei A. Panteleyev, Renate Thiel, Reinhard Wanner, Juan Zhang, Vladmir S. Roumak, Ralf Paus, Diether Neubert, Beate M. Henz, Thomas Rosenbach

Research output: Contribution to journalArticle

34 Citations (Scopus)

Abstract

The environmental pollutant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) causes chloracne in humans by mechanisms that are as yet poorly understood. Because TCDD is known to affect keratinocyte differentiation in vitro, we have studied TCDD-dependent morphologic changes and the expression of murine keratin 1 (MK1; differentiation associated) and keratin 17 (MK17; presumably hyperproliferation associated) in HRS/J hr/hr hairless mouse skin. TCDD (0.2 μg in acetone) applied topically to the dorsal skin caused epidermal acanthosis and hyperkeratosis of the dermal cysts as well as an involution of the utricles and the sebaceous glands. By means of in situ hybridization with digoxigenin-labeled riboprobes of sections from untreated and vehicle (control)-treated skin, we localized MK1 mRNA to the epidermal spinous cell compartment. MK17 transcripts were detected only in the derivatives of the hair follicle-utricle epithelium and dermal cysts. No spatial overlap was observed between MK1 and MK17 expression. After TCDD application, MK17 was newly expressed in the upper spinous cell layers of the interfollicular epidermis, although it was suppressed in the involuting utricles. In contrast, MK1 expression in the interfollicular epidermis was not affected by TCDD. Furthermore, MK1 expression was induced in the epithelium of the utricle remnants and in some dermal cysts. These data suggest that increased keratinization of the part of the follicular epithelium corresponding to the dermal cyst epithelium of hairless mice most probably explains the pathogenesis of TCDD-induced chloracne. The results demonstrate, furthermore, that TCDD can differentially affect keratinocyte differentiation in vivo as well as in vitro.

Original languageEnglish (US)
Pages (from-to)330-335
Number of pages6
JournalJournal of Investigative Dermatology
Volume108
Issue number3
DOIs
StatePublished - Jan 1 1997
Externally publishedYes

Fingerprint

Keratin-17
Keratin-1
Hairless Mouse
Gene expression
Skin
Saccule and Utricle
Gene Expression
Cysts
Chloracne
Epithelium
Keratinocytes
Epidermis
Digoxigenin
Sebaceous Glands
Environmental Pollutants
Hair Follicle
Polychlorinated Dibenzodioxins
1,4-dioxin
Acetone
In Situ Hybridization

Keywords

  • chloracne
  • hair follicle
  • HRS
  • J mice

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Dermatology
  • Cell Biology

Cite this

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) affects keratin 1 and keratin 17 gene expression and differentially induces keratinization in hairless mouse skin. / Panteleyev, Andrei A.; Thiel, Renate; Wanner, Reinhard; Zhang, Juan; Roumak, Vladmir S.; Paus, Ralf; Neubert, Diether; Henz, Beate M.; Rosenbach, Thomas.

In: Journal of Investigative Dermatology, Vol. 108, No. 3, 01.01.1997, p. 330-335.

Research output: Contribution to journalArticle

Panteleyev, Andrei A. ; Thiel, Renate ; Wanner, Reinhard ; Zhang, Juan ; Roumak, Vladmir S. ; Paus, Ralf ; Neubert, Diether ; Henz, Beate M. ; Rosenbach, Thomas. / 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) affects keratin 1 and keratin 17 gene expression and differentially induces keratinization in hairless mouse skin. In: Journal of Investigative Dermatology. 1997 ; Vol. 108, No. 3. pp. 330-335.
@article{6993dd3a4c3e45638811573f82acb758,
title = "2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) affects keratin 1 and keratin 17 gene expression and differentially induces keratinization in hairless mouse skin",
abstract = "The environmental pollutant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) causes chloracne in humans by mechanisms that are as yet poorly understood. Because TCDD is known to affect keratinocyte differentiation in vitro, we have studied TCDD-dependent morphologic changes and the expression of murine keratin 1 (MK1; differentiation associated) and keratin 17 (MK17; presumably hyperproliferation associated) in HRS/J hr/hr hairless mouse skin. TCDD (0.2 μg in acetone) applied topically to the dorsal skin caused epidermal acanthosis and hyperkeratosis of the dermal cysts as well as an involution of the utricles and the sebaceous glands. By means of in situ hybridization with digoxigenin-labeled riboprobes of sections from untreated and vehicle (control)-treated skin, we localized MK1 mRNA to the epidermal spinous cell compartment. MK17 transcripts were detected only in the derivatives of the hair follicle-utricle epithelium and dermal cysts. No spatial overlap was observed between MK1 and MK17 expression. After TCDD application, MK17 was newly expressed in the upper spinous cell layers of the interfollicular epidermis, although it was suppressed in the involuting utricles. In contrast, MK1 expression in the interfollicular epidermis was not affected by TCDD. Furthermore, MK1 expression was induced in the epithelium of the utricle remnants and in some dermal cysts. These data suggest that increased keratinization of the part of the follicular epithelium corresponding to the dermal cyst epithelium of hairless mice most probably explains the pathogenesis of TCDD-induced chloracne. The results demonstrate, furthermore, that TCDD can differentially affect keratinocyte differentiation in vivo as well as in vitro.",
keywords = "chloracne, hair follicle, HRS, J mice",
author = "Panteleyev, {Andrei A.} and Renate Thiel and Reinhard Wanner and Juan Zhang and Roumak, {Vladmir S.} and Ralf Paus and Diether Neubert and Henz, {Beate M.} and Thomas Rosenbach",
year = "1997",
month = "1",
day = "1",
doi = "10.1111/1523-1747.ep12286478",
language = "English (US)",
volume = "108",
pages = "330--335",
journal = "Journal of Investigative Dermatology",
issn = "0022-202X",
publisher = "Nature Publishing Group",
number = "3",

}

TY - JOUR

T1 - 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) affects keratin 1 and keratin 17 gene expression and differentially induces keratinization in hairless mouse skin

AU - Panteleyev, Andrei A.

AU - Thiel, Renate

AU - Wanner, Reinhard

AU - Zhang, Juan

AU - Roumak, Vladmir S.

AU - Paus, Ralf

AU - Neubert, Diether

AU - Henz, Beate M.

AU - Rosenbach, Thomas

PY - 1997/1/1

Y1 - 1997/1/1

N2 - The environmental pollutant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) causes chloracne in humans by mechanisms that are as yet poorly understood. Because TCDD is known to affect keratinocyte differentiation in vitro, we have studied TCDD-dependent morphologic changes and the expression of murine keratin 1 (MK1; differentiation associated) and keratin 17 (MK17; presumably hyperproliferation associated) in HRS/J hr/hr hairless mouse skin. TCDD (0.2 μg in acetone) applied topically to the dorsal skin caused epidermal acanthosis and hyperkeratosis of the dermal cysts as well as an involution of the utricles and the sebaceous glands. By means of in situ hybridization with digoxigenin-labeled riboprobes of sections from untreated and vehicle (control)-treated skin, we localized MK1 mRNA to the epidermal spinous cell compartment. MK17 transcripts were detected only in the derivatives of the hair follicle-utricle epithelium and dermal cysts. No spatial overlap was observed between MK1 and MK17 expression. After TCDD application, MK17 was newly expressed in the upper spinous cell layers of the interfollicular epidermis, although it was suppressed in the involuting utricles. In contrast, MK1 expression in the interfollicular epidermis was not affected by TCDD. Furthermore, MK1 expression was induced in the epithelium of the utricle remnants and in some dermal cysts. These data suggest that increased keratinization of the part of the follicular epithelium corresponding to the dermal cyst epithelium of hairless mice most probably explains the pathogenesis of TCDD-induced chloracne. The results demonstrate, furthermore, that TCDD can differentially affect keratinocyte differentiation in vivo as well as in vitro.

AB - The environmental pollutant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) causes chloracne in humans by mechanisms that are as yet poorly understood. Because TCDD is known to affect keratinocyte differentiation in vitro, we have studied TCDD-dependent morphologic changes and the expression of murine keratin 1 (MK1; differentiation associated) and keratin 17 (MK17; presumably hyperproliferation associated) in HRS/J hr/hr hairless mouse skin. TCDD (0.2 μg in acetone) applied topically to the dorsal skin caused epidermal acanthosis and hyperkeratosis of the dermal cysts as well as an involution of the utricles and the sebaceous glands. By means of in situ hybridization with digoxigenin-labeled riboprobes of sections from untreated and vehicle (control)-treated skin, we localized MK1 mRNA to the epidermal spinous cell compartment. MK17 transcripts were detected only in the derivatives of the hair follicle-utricle epithelium and dermal cysts. No spatial overlap was observed between MK1 and MK17 expression. After TCDD application, MK17 was newly expressed in the upper spinous cell layers of the interfollicular epidermis, although it was suppressed in the involuting utricles. In contrast, MK1 expression in the interfollicular epidermis was not affected by TCDD. Furthermore, MK1 expression was induced in the epithelium of the utricle remnants and in some dermal cysts. These data suggest that increased keratinization of the part of the follicular epithelium corresponding to the dermal cyst epithelium of hairless mice most probably explains the pathogenesis of TCDD-induced chloracne. The results demonstrate, furthermore, that TCDD can differentially affect keratinocyte differentiation in vivo as well as in vitro.

KW - chloracne

KW - hair follicle

KW - HRS

KW - J mice

UR - http://www.scopus.com/inward/record.url?scp=0031043421&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0031043421&partnerID=8YFLogxK

U2 - 10.1111/1523-1747.ep12286478

DO - 10.1111/1523-1747.ep12286478

M3 - Article

C2 - 9036934

AN - SCOPUS:0031043421

VL - 108

SP - 330

EP - 335

JO - Journal of Investigative Dermatology

JF - Journal of Investigative Dermatology

SN - 0022-202X

IS - 3

ER -