Biomedical Science Letters (대한의생명과학회지)

The Korean Society for Biomedical Laboratory Sciences (대한의생명과학회)
권호 표지
DOI QR코드

DOI QR Code

The Role of S100A8 and S100A9 in Differentiation of Human Eosinophilic Leukemia Cells, EoL-1

  • Kim, In Sik (Department of Senior Healthcare, BK21 plus program, Graduate School, Eulji University) ;
  • Gu, Ayoung (Department of Senior Healthcare, BK21 plus program, Graduate School, Eulji University) ;
  • Lee, Ji-Sook (Department of Clinical Laboratory Science, Wonkwang Health Science University)
  • Received : 2017.03.12
  • Accepted : 2017.04.03
  • Published : 2017.03.31
Download PDF
⟨ Previous Next ⟩

Abstract

S100A8 and S100A9 are associated with myeloid cell differentiation, chemotactic activities, adhesion of neutrophils, and apoptosis. In this study, we investigated the contribution of S100A8 and S100A9 to differentiation of the human eosinophilic leukemia cell line, EoL-1. S100A8 and S100A9 increased the number of vacuole per one cell and the protein expression of EPO and MBP. Rottlerin, an inhibitor of protein kinase C delta ($PKC{\delta}$), inhibited the EoL-1 cell differentiation induced by S100A8 and S100A9. These results suggest that S100A8 and S100A9 may regulate the differentiation of eosinophilic progenitors. Moreover, these findings may shed light on elucidation of eosinophil differentiation due to S100 proteins.

Keywords

References

  1. Chen B, Miller AL, Rebelatto M, Brewah Y, Rowe DC, Clarke L, Czapiga M, Rosenthal K, Imamichi T, Chen Y, Chang CS, Chowdhury PS, Naiman B, Wang Y, Yang D, Humbles AA, Herbst R, Sims GP. S100A9 induced inflammatory responses are mediated by distinct damage associated molecular patterns (DAMP) receptors in vitro and in vivo. PLoS One. 2015. 10: e0115828. https://doi.org/10.1371/journal.pone.0115828
  2. Gotlib J, Cools J, Malone JM 3rd, Schrier SL, Gilliland DG, Coutre SE. The FIP1L1-PDGFR alpha fusion tyrosine kinase in hypereosinophilic syndrome and chronic eosinophilic leukemia: implications for diagnosis, classification, and management. Blood. 2004. 103: 2879-2891. https://doi.org/10.1182/blood-2003-06-1824
  3. Goyette J, Geczy CL. Inflammation-associated S100 proteins: new mechanisms that regulate function. Amino Acids. 2011. 41: 821-842. https://doi.org/10.1007/s00726-010-0528-0
  4. Kerkhoff Cl, Voss A, Scholzen TE, Averill MM, Zanker KS, Bornfeldt KE. Novel insights into the role of S100A8/A9 in skin biology. Experimental Dermatology. 2012. 21: 822-826. https://doi.org/10.1111/j.1600-0625.2012.01571.x
  5. Lee JS, Kim IS. Leukotactin-1/CCL15 induces cell migration and differentiation of human eosinophilic leukemia EoL-1 cells through PKC delta activation. Molecular Biology Reports. 2010. 37: 2149-2156. https://doi.org/10.1007/s11033-009-9687-z
  6. Nam AR, Kim DH, Kim MJ, Lee JS, Yang SJ, Kim IS. S100A8 induces secretion of MCP-1, IL-6, and IL-8 via TLR4 in Jurkat T cells. Biomedical Science Letters. 2016. 22: 60-64. https://doi.org/10.15616/BSL.2016.22.2.60
  7. Nicolas E, Ramus C, Berthier S, Arlotto M, Bouamrani A, Lefebvre C, Morel F, Garin J, Ifrah N, Berger F, Cahn JY, Mossuz P. Expression of S100A8 in leukemic cells predicts poor survival in de novo AML patients. Leukemia. 2011. 25: 57-65. https://doi.org/10.1038/leu.2010.251
  8. Spijkers-Hagelstein JA, Schneider P, Hulleman E, de Boer J, Williams O, Pieters R, Stam RW. Elevated S100A8/S100A9 expression causes glucocorticoid resistance in MLL-rearranged infant acute lymphoblastic leukemia. Leukemia. 2012. 26: 1255-1265. https://doi.org/10.1038/leu.2011.388
  9. Steinberg SF. Structural basis of protein kinase C isoform function. Physiological Reviews. 2008. 88: 1341-1378. https://doi.org/10.1152/physrev.00034.2007
  10. Tefferi A, Patnaik MM, Pardanani A. Eosinophilia: secondary, clonal and idiopathic. British Journal of Haematology. 2006. 133: 468-492. https://doi.org/10.1111/j.1365-2141.2006.06038.x
  11. Wang L, Luo H, Chen X, Jiang Y, Huang Q. Functional characterization of S100A8 and S100A9 in altering monolayer permeability of human umbilical endothelial cells. PLoS One. 2014. 9: e90472. https://doi.org/10.1371/journal.pone.0090472