학술논문

Visualisation of tissue kallikrein, kininogen and kinin receptors in human skin following trauma and in dermal diseases
Document Type
research-article
Source
Biological Chemistry. 385(11):1069-1076
Subject
basalioma (basal cell carcinoma)
inflammation
kinin-B1 receptor upregulation
lichenificated atopic eczema
psoriasis
Highlight: Hiroshi Maeda – a life dedicated to research on infection, inflammation and cancer
Biochemistry
Molecular biology
Cellular biology
Language
English
ISSN
1437-4315
1431-6730
Abstract
During dermal injury and inflammation the serine proteases kallikreins cleave endogenous, multifunctional substrates (kininogens) to form bradykinin and kallidin. The actions of kinins are mediated by preferential binding to constitutively expressed kinin-B2 receptors or inducible kinin-B1 receptors. A feature of the kinin-B1 receptors is that they show low levels of expression, but are distinctly upregulated following tissue injury and inflammation. Because recent evidence suggested that kinin-B1 receptors may perform a protective role during inflammation, we investigated the specific occurrence of the kallikrein-kinin components in skin biopsies obtained from normal skin, patients undergoing surgery, basalioma, lichenificated atopic eczema, and psoriasis. The tissue was immunolabelled in order to determine the localisation of tissue pro-kallikrein, kallikrein, kininogen and kinin receptors. The kinin components were visualised in normal, diseased and traumatised skin, except that no labelling was observed for kininogen in normal skin. Of the five types of tissue examined, upregulation of kinin-B1 receptors was observed only in skin biopsies obtained following surgery. In essence, the expression of kinin-B1 receptors did not appear to be enhanced in the other biopsies. Within the multiple steps of the inflammatory cascade in wound healing, our results suggest an important regulatory role for kinin-B1 receptors during the first phase of inflammation following injury.