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11β-hydroxysteroid dehydrogenase type 1 is expressed in human sebaceous glands and regulates glucocorticoid-induced lipid synthesis and toll-like receptor 2 expression in SZ95 sebocytes.
Br J Dermatol. 2013 Jan; 168(1):47-55.BJ

Abstract

BACKGROUND

Glucocorticoids (GCs) affect the pathophysiology of sebaceous glands, causing development or exacerbation of acne. The availability of GCs is regulated by isoenzymes of 11β-hydroxysteroid dehydrogenase (11βHSD) at tissue-specific levels. 11βHSD type 1 (HSD11β1) is a reductase, catalysing the conversion of cortisone to active cortisol, and is highly expressed in liver and adipose tissue. Recently, HSD11β1 was observed in human skin in keratinocytes and fibroblasts.

OBJECTIVES

To investigate the expression of HSD11β1 in sebaceous glands of normal and acne-involved skin, and to examine the role of HSD11β1 in GC-induced lipid synthesis and toll-like receptor 2 (TLR2) expression in sebocytes.

METHODS

Expression of HSD11β1 was examined by immunohistochemistry in acne lesional skin and normal skin of healthy volunteers. The cultured SZ95 sebocytes were treated with dexamethasone, and the lipid synthesis and mRNA levels of sterol regulatory element binding protein 1 (SREBP-1) and TLR2 were determined. Use of an HSD11β1 inhibitor and the small interference RNA (siRNA) approach were used to investigate the role of HSD11β1 on the GC regulation of sebocyte functions.

RESULTS

HSD11β1 was expressed in human sebaceous glands and upregulated in acne lesional skin. HSD11β1 mRNA was enhanced by dexamethasone and cytokines in SZ95 sebocytes. Dexamethasone enhanced lipid synthesis, partially through the transcriptional induction of SREBP-1, and also by increasing TLR2 mRNA levels. Inhibition of HSD11β1 by PF-915275 or siRNA significantly inhibited the GC-induced lipid synthesis and the mRNA expression of SREBP-1 and TLR2.

CONCLUSIONS

Our results indicate that HSD11β1 plays a key role in the modulation of GC action on sebocytes, including sebum production and TLR2-mediated inflammation, thereby influencing the pathogenesis of acne.

Authors+Show Affiliations

Department of Dermatology, CHA Bundang Medical Center, CHA University, 351, Yatap-dong, Bundang-gu, Seongnam 463-712, Korea.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

22897663

Citation

Lee, S E., et al. "11β-hydroxysteroid Dehydrogenase Type 1 Is Expressed in Human Sebaceous Glands and Regulates Glucocorticoid-induced Lipid Synthesis and Toll-like Receptor 2 Expression in SZ95 Sebocytes." The British Journal of Dermatology, vol. 168, no. 1, 2013, pp. 47-55.
Lee SE, Kim JM, Jeong MK, et al. 11β-hydroxysteroid dehydrogenase type 1 is expressed in human sebaceous glands and regulates glucocorticoid-induced lipid synthesis and toll-like receptor 2 expression in SZ95 sebocytes. Br J Dermatol. 2013;168(1):47-55.
Lee, S. E., Kim, J. M., Jeong, M. K., Zouboulis, C. C., & Lee, S. H. (2013). 11β-hydroxysteroid dehydrogenase type 1 is expressed in human sebaceous glands and regulates glucocorticoid-induced lipid synthesis and toll-like receptor 2 expression in SZ95 sebocytes. The British Journal of Dermatology, 168(1), 47-55. https://doi.org/10.1111/bjd.12009
Lee SE, et al. 11β-hydroxysteroid Dehydrogenase Type 1 Is Expressed in Human Sebaceous Glands and Regulates Glucocorticoid-induced Lipid Synthesis and Toll-like Receptor 2 Expression in SZ95 Sebocytes. Br J Dermatol. 2013;168(1):47-55. PubMed PMID: 22897663.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - 11β-hydroxysteroid dehydrogenase type 1 is expressed in human sebaceous glands and regulates glucocorticoid-induced lipid synthesis and toll-like receptor 2 expression in SZ95 sebocytes. AU - Lee,S E, AU - Kim,J-M, AU - Jeong,M-K, AU - Zouboulis,C C, AU - Lee,S H, PY - 2012/8/18/entrez PY - 2012/8/18/pubmed PY - 2013/6/8/medline SP - 47 EP - 55 JF - The British journal of dermatology JO - Br. J. Dermatol. VL - 168 IS - 1 N2 - BACKGROUND: Glucocorticoids (GCs) affect the pathophysiology of sebaceous glands, causing development or exacerbation of acne. The availability of GCs is regulated by isoenzymes of 11β-hydroxysteroid dehydrogenase (11βHSD) at tissue-specific levels. 11βHSD type 1 (HSD11β1) is a reductase, catalysing the conversion of cortisone to active cortisol, and is highly expressed in liver and adipose tissue. Recently, HSD11β1 was observed in human skin in keratinocytes and fibroblasts. OBJECTIVES: To investigate the expression of HSD11β1 in sebaceous glands of normal and acne-involved skin, and to examine the role of HSD11β1 in GC-induced lipid synthesis and toll-like receptor 2 (TLR2) expression in sebocytes. METHODS: Expression of HSD11β1 was examined by immunohistochemistry in acne lesional skin and normal skin of healthy volunteers. The cultured SZ95 sebocytes were treated with dexamethasone, and the lipid synthesis and mRNA levels of sterol regulatory element binding protein 1 (SREBP-1) and TLR2 were determined. Use of an HSD11β1 inhibitor and the small interference RNA (siRNA) approach were used to investigate the role of HSD11β1 on the GC regulation of sebocyte functions. RESULTS: HSD11β1 was expressed in human sebaceous glands and upregulated in acne lesional skin. HSD11β1 mRNA was enhanced by dexamethasone and cytokines in SZ95 sebocytes. Dexamethasone enhanced lipid synthesis, partially through the transcriptional induction of SREBP-1, and also by increasing TLR2 mRNA levels. Inhibition of HSD11β1 by PF-915275 or siRNA significantly inhibited the GC-induced lipid synthesis and the mRNA expression of SREBP-1 and TLR2. CONCLUSIONS: Our results indicate that HSD11β1 plays a key role in the modulation of GC action on sebocytes, including sebum production and TLR2-mediated inflammation, thereby influencing the pathogenesis of acne. SN - 1365-2133 UR - https://www.unboundmedicine.com/medline/citation/22897663/11β_hydroxysteroid_dehydrogenase_type_1_is_expressed_in_human_sebaceous_glands_and_regulates_glucocorticoid_induced_lipid_synthesis_and_toll_like_receptor_2_expression_in_SZ95_sebocytes_ L2 - https://doi.org/10.1111/bjd.12009 DB - PRIME DP - Unbound Medicine ER -