Allergic contact dermatitis induces upregulation of identical microRNAs in humans and mice

TY - JOUR

T1 - Allergic contact dermatitis induces upregulation of identical microRNAs in humans and mice

AU - Vennegaard, Marie T

AU - Bonefeld, Charlotte M

AU - Hagedorn, Peter

AU - Bangsgaard, Nannie

AU - Løvendorf, Marianne B

AU - Odum, Niels

AU - Woetmann, Anders

AU - Geisler, Carsten

AU - Skov, Lone

N1 - © 2012 John Wiley & Sons A/S.

PY - 2012/11

Y1 - 2012/11

N2 - Background. MicroRNAs are short, endogenous RNA molecules that can bind to parts of target mRNAs, thus inhibiting their translation and causing accelerated turnover or degradation of transcripts, thereby regulating gene expression. Several microRNAs have been found to be upregulated in atopic dermatitis and psoriasis, indicating a role in inflammatory skin diseases. However, there have been no studies on the expression of microRNAs in allergic contact dermatitis. Objectives. To investigate expression of microRNAs in allergic contact dermatitis. Methods. Lesional and non-lesional skin biopsies were collected from subjects with allergic responses to diphenylcyclopropenone (DPCP). Additional samples for profiling were collected from an experimental mouse model by use of the strong allergen dinitrofluorobenzene. RNA was purified from all samples, and locked nucleic acid microarray analysis was performed, followed by validation with quantitative polymerase chain reaction (PCR). Results. In humans sensitized with DPCP, we found significant upregulation of miR-21, miR-142-3p, miR-142-5p and miR-223 in challenged skin. The same microRNAs were significantly upregulated in the skin of mice in a mouse model of contact allergy. The upregulation of microRNA was confirmed by quantitative PCR. Conclusion. These are the first results indicating that microRNAs may be involved in the pathogenesis of allergic contact dermatitis, and they show that mouse models are valuable tools for further study of the involvement of microRNAs in allergic contact dermatitis.

AB - Background. MicroRNAs are short, endogenous RNA molecules that can bind to parts of target mRNAs, thus inhibiting their translation and causing accelerated turnover or degradation of transcripts, thereby regulating gene expression. Several microRNAs have been found to be upregulated in atopic dermatitis and psoriasis, indicating a role in inflammatory skin diseases. However, there have been no studies on the expression of microRNAs in allergic contact dermatitis. Objectives. To investigate expression of microRNAs in allergic contact dermatitis. Methods. Lesional and non-lesional skin biopsies were collected from subjects with allergic responses to diphenylcyclopropenone (DPCP). Additional samples for profiling were collected from an experimental mouse model by use of the strong allergen dinitrofluorobenzene. RNA was purified from all samples, and locked nucleic acid microarray analysis was performed, followed by validation with quantitative polymerase chain reaction (PCR). Results. In humans sensitized with DPCP, we found significant upregulation of miR-21, miR-142-3p, miR-142-5p and miR-223 in challenged skin. The same microRNAs were significantly upregulated in the skin of mice in a mouse model of contact allergy. The upregulation of microRNA was confirmed by quantitative PCR. Conclusion. These are the first results indicating that microRNAs may be involved in the pathogenesis of allergic contact dermatitis, and they show that mouse models are valuable tools for further study of the involvement of microRNAs in allergic contact dermatitis.

KW - Adult

KW - Animals

KW - Cyclopropanes

KW - Dermatitis, Allergic Contact

KW - Disease Models, Animal

KW - Female

KW - Humans

KW - Mice

KW - Mice, Inbred C57BL

KW - MicroRNAs

KW - Microarray Analysis

KW - Middle Aged

KW - Skin

KW - Up-Regulation

U2 - 10.1111/j.1600-0536.2012.02083.x

DO - 10.1111/j.1600-0536.2012.02083.x

M3 - Journal article

C2 - 22594804

SN - 1396-6669

VL - 67

SP - 298

EP - 305

JO - Contact Dermatitis. Supplement

JF - Contact Dermatitis. Supplement

IS - 5

ER -