Tomoregulin ectodomain shedding by proinflammatory cytokines |
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Authors: | Lin Hong Wada Ken Yonezawa Masaoki Shinoki Kei Akamatsu Tomonori Tsukui Taku Sakamoto Choitsu |
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Institution: | Third Department of Internal Medicine, Nippon Medical School, Tokyo, Japan. |
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Abstract: | The shedding mechanism for the tomoregulin (TR) ectodomain, which contains two follistatin modules and a single epidermal growth factor (EGF)-like domain, remains unclear. Our study provides the first evidence that proinflammatory cytokines, IL-1beta and TNF-alpha, induce TR-ectodomain shedding in cultured A172 human glioma cells, without affecting TR mRNA expression. In addition, it appears that this shedding process is induced via activation of the NF-kappaB signaling pathway; with consequent increase in the production of metalloproteinases. Furthermore, since due to erbB4 tyrosine phosphorylation TR may have functions similar to EGF/neuregulin (NRG) family growth factors, our results suggest that following inflammation-induced injury, increases in TR shedding may contribute to tissue growth and repair in the central nervous system. |
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