Expression and modulation of S100A4 protein by human mast cells
•Tissue resident MCs stained positive to S100A4 in healthy, inflammatory and tumor samples.•Both human HMC-1 cell line and resting CD34+-derived MCs expressed S100A4.•S100A4 levels were differentially modulated upon MC activation.•Downregulation of the S100A4 protein resulted in alteration of MC phy...
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Published in: | Cellular immunology Vol. 332; pp. 85 - 93 |
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Main Authors: | , , , , , , , , , , , , , |
Format: | Journal Article |
Language: | English |
Published: |
Netherlands
Elsevier Inc
01-10-2018
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Subjects: | |
Online Access: | Get full text |
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Summary: | •Tissue resident MCs stained positive to S100A4 in healthy, inflammatory and tumor samples.•Both human HMC-1 cell line and resting CD34+-derived MCs expressed S100A4.•S100A4 levels were differentially modulated upon MC activation.•Downregulation of the S100A4 protein resulted in alteration of MC physiology.•S100A4 play a role in the MC life cycle and functions.
S100A4 protein is expressed in fibroblasts during tissue remodelling and in cancer stem cells and it induces the metastatic spread of tumor cells. In mast cells (MCs) S100A4 have been found in some pathological conditions, but its function in normal MCs remains to be described. The purpose of this study was to characterize the cellular localization of the S100A4 protein in MCs of human tissues with inflammatory or tumor disorders and, to determine the consequence of reducing its expression in MC response. We found that tissue resident MCs stained positive to S100A4. Both human HMC-1 cell line and resting CD34+-derived MCs expressed S100A4, whose levels were differentially modulated upon MC activation. Downregulation of the S100A4 protein resulted in MC growth inhibition, enhanced apoptosis and deregulation of MMP-1 and MMP-10 production. Our results suggest that S100A4 is also playing a role in the MC life cycle and functions. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0008-8749 1090-2163 |
DOI: | 10.1016/j.cellimm.2018.08.001 |