Gene expression and regulation of nerve growth factor in atopic dermatitis mast cells and the human mast cell line-1

The gene expression and regulation of nerve growth factor (NGF) in atopic dermatitis (AD) and the human mast cell line (HMC)-1 was investigated at the molecular level. NGF-stimulation of HMC-1 cells resulted in increases in tryptase activity and histamine contents, paralleled by an increase of trypt...

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Published in:Journal of neuroimmunology 2005-04, Vol.161 (1), p.87-92
Main Authors: Groneberg, David A., Serowka, Frauke, Peckenschneider, Nora, Artuc, Metin, Grützkau, Andreas, Fischer, Axel, Henz, Beate M., Welker, Pia
Format: Article
Language:English
Subjects:
Atopic dermatitis
Cells, Cultured
Cytokines
Dermatitis, Atopic - blood
Dermatitis, Atopic - pathology
Enzyme-Linked Immunosorbent Assay - methods
Gene Expression Regulation - physiology
Histamine - metabolism
Humans
Immunohistochemistry
Immunohistochemistry - methods
Mast cells
Mast Cells - metabolism
Nerve Growth Factor - genetics
Nerve Growth Factor - metabolism
Neurotrophins
Reverse Transcriptase Polymerase Chain Reaction - methods
RNA, Messenger - biosynthesis
RT-PCR
Serine Endopeptidases - metabolism
Skin - cytology
Statistics, Nonparametric
Time Factors
Tryptases
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Summary:The gene expression and regulation of nerve growth factor (NGF) in atopic dermatitis (AD) and the human mast cell line (HMC)-1 was investigated at the molecular level. NGF-stimulation of HMC-1 cells resulted in increases in tryptase activity and histamine contents, paralleled by an increase of tryptase and histamine at the transcriptional level. Also, an increased expression of NGF was found in AD lesions, in association with increased systemic NGF plasma levels. Further cutaneous sources for increased NGF levels were keratinocytes and fibroblasts. These findings demonstrate an increased expression of NGF in AD and effects on tryptase and histamine. Mast cells may be major mediators of neurotrophin effects in AD.
ISSN:0165-5728
1872-8421
DOI:10.1016/j.jneuroim.2004.12.019