Email this article Expression proteaseinhibitors receptor PAR-2 on neutrophils peripheral blood of patients with atopic dermatitis and their relation with heat shock proteins HSP90
- Authors: Elistratova I.V1, Morozov S.G.2, Zakharova I.A2
-
Affiliations:
- Main Military Clinical Hospital of Internal Troops of the Ministry of Internal Affairs of Russia
- Institute of General Pathology and Pathophysiology
- Issue: Vol 19, No 1 (2016)
- Pages: 53-58
- Section: Articles
- URL: https://journals.rcsi.science/1560-9588/article/view/37138
- DOI: https://doi.org/10.18821/1560-9588-2016-19-1-53-58
- ID: 37138
Cite item
Full Text
Abstract
Expression ofprotease-activated receptors PAR-2 has been investigated on neutrophils isolated from atopic dermatitis patient peripheral blood and has been analyzed with index SCORAD. The simultaneous expression of both, PAR-2 receptors and heat shock protein 90 (HSP90) was measured on neutrophils at the first week of acute phase of atopic dermatitis. Methods. Peripheral blood neutrophils were isolated on the Percoll gradient. Cells were stained with antibodies to PAR-2 receptor and HSP90 followed by the flow cytometry. Results. The PAR-2 receptors have been shown to be expressed on the plasma membrane of neutrophils obtained from patients with atopic dermatitis. The percentage of PAR-2+ neutrophils was positive correlated with diseases severity. HSP90 was found to be elevated simultaneously with PAR-2 receptors on neutrophils at the acute phase of atopic relapse. Conclusions. Atopic dermatitis patients have the higher level of PAR-2 receptor expression compared with healthy donors. Percentage of PAR-2+ neutrophils is elevated with the increasing of disease severity. Simultaneous elevation of PAR-2 receptors and HSP90 was found at the first week of acute atopic dermatitis.
Full Text
##article.viewOnOriginalSite##About the authors
I. V Elistratova
Main Military Clinical Hospital of Internal Troops of the Ministry of Internal Affairs of Russia143915, Balashiha, Russia
Sergey G. Morozov
Institute of General Pathology and Pathophysiology
Email: biopharm@list.ru
Doctor of Medical Sciences, Professor, Corresponding Member of Russian Academy of Sciences, deputy director for scientific work 125315, Moscow, Russia
I. A Zakharova
Institute of General Pathology and Pathophysiology125315, Moscow, Russia
References
- Lee S., Jeong S., Lee S. Protease and protease-activated receptor-2 signaling in the pathogenesis of atopic Dermatitis. Yonsei. Med. J. 2010; 51(6): 808-22.
- Nakagawa H., Hiura A. Four possible itching pathways related to the TRPV1 channel, histamine, PAR-2 and serotonin. Malays. J. Med. Sci. 2013; 20(4): 5-12.
- Kempkes C., Buddenkotte J., Cevikbas F., Buhl T., Steinhoff M. Role of PAR-2 in Neuroimmune Communication and Itch. Frontiers in Neuroscience: Carstens E., Akiyama T. editors; Itch: Mechanisms and Treatment. Boca Raton (FL): CRC Press; 2014. Chapter 11.
- Yau M., Liu L., Fairlie D. Toward drug for protease-activated receptor 2 (PAR2). J. Med. Chem. 2013; 56(19): 7477-97.
- Rothmeier A., Ruf W. Protease-activated receptor 2 signaling in inflammation. Semin. Immunopathol. 2012; 34(1): 133-49.
- Yamaguchi R., Yamamoto T., Sakamoto A., Ishimaru Y., Narahara S., Sugiuchi H., et al. Mechanism of interleukin-13 production by granulocyte-macrophage colony-stimulating factor-dependent macrophages via protease-activated receptor-2. Blood Cells Mol. Dis. 2015; 55(1): 21-6.
- Post S., Heijink I., Petersen A., de Bruin H., van Oosterhourt A., Nawijn M. Protease-activated receptor-2 activation contributes to house dust mite-induced IgE responses in mice. PLOS One. 2014; 9(3): e91206.
- Zhu Z.,, Stricker R., Li R., Zündorf G., Reiser G. The intracellular carboxyl tail of the PAR-2 receptor controls intracellular signaling and cell death. Cell Tissue Res. 2015; 359(3): 817-27.
- Botham A., Guo X., Xiao Y., Morice A., Compton S., Sadofsky L. Palmitoylation of human proteinase-activated receptor-2 differentially regulates receptor-triggered ERK1/2 activation, calcium signalling and endocytosis. Biochem. J. 2011; 438(2): 359-67.
- Zhao P., Lieu T., Barlow N., Sostegni S., Haerteis S., Korbmacher C., et al. Neutrophil elastase activates protease-activated receptor-2 (PAR2) and transient teceptor potential vanilloid 4 (TRPV4) to cause inflammation and pain. J Biol. Chem. 2015; 290(22): 13875-87.
- Helyes Z., Sándor K., Borbély E., Tékus V., Pintér E., Elekes K., et al. Involvement of transient receptor potential vanilloid 1 receptors in protease-activated receptor-2-induced joint inflammation and nociception. Eur. J. Pain. 2010; 14(4): 351-8.
- Dai Y., Wang S., Tominaga M., Yamamoto S., Fukuoka T., Higashi T., et al. Sensitization of TRPA1 by PAR2 contributes to the sensation of inflammatory pain. J. Clin. Invest. 2007; 117(7): 1979-87.
- Takei-Taniguchi R., Imai Y., Ishikawa C., Sakaguchi Y., Nakagawa N., Tsuda T., et al. Interleukin-17- and protease-activated receptor 2-mediated production of CXCL1 and CXCL8 modulated by cyclosporine A, vitamin D3 and glucocorticoids in human keratinocytes. J. Dermatol. 2012; 39(7): 625-31.
- Kim J., Kim do Y., Son H., Kim Y., Oh S. Protease-activated receptor-2 activates NQO-1 via Nrf2 stabilization in keratinocytes. J. Dermatol. Sci. 2014; 74(1): 48-55.
- St-Onge M., Lagarde S., Laflamme C., Rollet-Labelle E., Marois L., Naccache P., Pouliot M. Proteinase-activated receptor-2 up-regulation by Fcgamma-receptor activation in human neutrophils. FASEB J. 2010; 24(6): 2116-25.
- Bzowska M., Hamczyk M., Skalniak A., Guzik K. Rapid decrease of CD16 (FcγRIII) expression on heat-shocked neutrophils and their recognition by macrophages. J. Biomed. Biotechnol. 2011; 2011: 284759.
