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The healing skin wound: a novel site of action of the chemokine C10
Authors:Kaesler Susanne  Regenbogen Johannes  Durka Silke  Goppelt Andreas  Werner Sabine
Institution:1. Institute of Cell Biology, ETH Zürich, Hönggerberg, CH-8093, Zürich, Switzerland;2. Switch Biotech AG, Fraunhoferstrasse 10, D-82152, Martinsried, Germany;1. Department of Pharmacognosy, Graduate School of Pharmaceutical Sciences, Nagoya City University, 3-1 Tanabe-Dori, Mizuho-ku, Nagoya, Aichi, 467-8603, Japan;2. Kuki Sangyo Co., Ltd., 11 Onoe-cho, Yokkaichi-shi, Mie, 510-0059, Japan;1. Department of Pharmacy, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, No.3 Qingchun East Road, Hangzhou 310016, China;2. Core Facilities, School of Medicine, Zhejiang University, 866 Yuhang Tang Road, Hangzhou 310058, China;3. College of Pharmaceutical Sciences, Zhejiang University, 866 Yuhang Tang Road, Hangzhou 310058, China;1. Department of Gastroenterology and Hepatology, Ghent University, Belgium;2. Laboratory of Myeloid Cell Ontogeny and Functional Specialization, VIB-UGent Center for Inflammation Research, Ghent, Belgium;3. Department of Biomedical Molecular Biology, Ghent University, Ghent, Belgium;4. Centre for Immunobiology, Institute of Infection, Immunity and Inflammation, College of Medicine, Veterinary Medicine and Life Sciences, University of Glasgow, UK;1. Department of Biomedical Sciences, University of North Dakota School of Medicine and Health Sciences, Grand Forks, ND, USA;2. Department of Pathology, University of North Dakota School of Medicine and Health Sciences, Grand Forks, ND, USA;3. Laboratory for Proteolytic Neuroscience, RIKEN Center for Brain Science, Wako-shi, Saitama, Japan
Abstract:To gain insight into the molecular mechanisms underlying the wound repair process, we searched for genes that are regulated by skin injury. For this purpose we generated a subtractive cDNA library from normal mouse back skin and 1-day full-thickness excisional wounds. One of the differentially expressed genes encodes the chemokine C10. Using Northern blotting, RNase protection assay and Western blotting, we confirmed the injury-induced expression of C10 at the mRNA and protein level. Maximal levels of C10 mRNA and protein were seen at day 1 after wounding, and expression levels subsequently declined. In situ hybridization and immunohistochemistry revealed expression of C10 in macrophages of the clot and the granulation tissue as well as in keratinocytes of the epidermis and the hair follicles at the wound edge. Since C10 is a potent chemoattractant for macrophages, our results suggest that this chemokine contributes to the strong macrophage influx observed in the healing skin wound.
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