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Title: Chemoattraction of macrophage, by secretory molecules derived from cells expressing the signal peptide of eosinophil cationic protein
Authors: Yu-Shu Liu
Pei-Wen Tsai
Yong Wang
Tan-chi Fan
Chia-Hung Hsieh
Margaret Dah-Tsyr Chang
Tun-Wen Pai
Chien-Fu Huang
Chung-Yu Lan
Hao-Teng Chang
Contributors: 國立臺灣海洋大學:資訊工程學系
Keywords: Cell migration
Signal peptide
Eosinophil cationic protein (ECP)
Functional linkage network
Date: 2012
Issue Date: 2017-01-16T05:50:43Z
Publisher: BMC Systems Biology
Abstract: Abstract

Eosinophil cationic protein is a clinical asthma biomarker that would be released into blood, especially gathered in bronchia. The signal peptide of eosinophil cationic protein (ECPsp) plays an important role in translocating ECP to the extracellular space. We previously reported that ECPsp inhibits microbial growth and regulates the expression of mammalian genes encoding tumor growth factor-α (TGF-α) and epidermal growth factor receptor (EGFR).

In the present study, we first generated a DNA microarray dataset, which showed that ECPsp upregulated proinflammatory molecules, including chemokines, interferon-induced molecules, and Toll-like receptors. The levels of mRNAs encoding CCL5, CXCL10, CXCL11, CXCL16, STAT1, and STAT2 were increased in the presence of ECPsp by 2.07-, 4.21-, 7.52-, 2.6-, 3.58-, and 1.67-fold, respectively. We then constructed a functional linkage network by integrating the microarray dataset with the pathway database of Kyoto Encyclopedia of Genes and Genomes (KEGG). Follow-up analysis revealed that STAT1 and STAT2, important transcriptional factors that regulate cytokine expression and release, served as hubs to connect the pathways of cytokine stimulation (TGF-α and EGFR pathways) and inflammatory responses. Furthermore, integrating TGF-α and EGFR with the functional linkage network indicated that STAT1 and STAT2 served as hubs that connect two functional clusters, including (1) cell proliferation and survival, and (2) inflammation. Finally, we found that conditioned medium in which cells that express ECPsp had been cultured could chemoattract macrophages. Experimentally, we also demonstrated that the migration of macrophage could be inhibited by the individual treatment of siRNAs of STAT1 or STAT2. Therefore, we hypothesize that ECPsp may function as a regulator for enhancing the migration of macrophages through the upregualtion of the transcriptional factors STAT1 and STAT2.

The increased expression and release of various cytokines triggered by ECPsp may attract macrophages to bronchia to purge damaged cells. Our approach, involving experimental and computational systems biology, predicts pathways and potential biological functions for further characterization of this novel function of ECPsp under inflammatory conditions.
Relation: 6(105)
URI: http://ntour.ntou.edu.tw:8080/ir/handle/987654321/40208
Appears in Collections:[資訊工程學系] 期刊論文

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