Oncotarget

Research Papers: Immunology:

P2Y6 contributes to ovalbumin-induced allergic asthma by enhancing mast cell function in mice

Jue-ping Shi, Shao-ying Wang, Li-li Chen, Xiao-yu Zhang, Yi-han Zhao, Bing Du, Wen-zheng Jiang, Min Qian and Hua Ren _

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Oncotarget. 2016; 7:60906-60918. https://doi.org/10.18632/oncotarget.11758

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Abstract

Jue-ping Shi1, Shao-ying Wang1, Li-li Chen1, Xiao-yu Zhang1, Yi-han Zhao1, Bing Du1, Wen-zheng Jiang1, Min Qian1 and Hua Ren1

1 Shanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences and School of Life Sciences, East China Normal University, Shanghai, P.R.China

Correspondence to:

Hua Ren, email:

Keywords: P2Y6; asthma; mast cell; UDP; migration; Immunology and Microbiology Section; Immune response; Immunity

Received: May 27, 2016 Accepted: August 25, 2016 Published: August 31, 2016

Abstract

Extracelluar nucleotides have been identified as regulatory factors in asthmatic pathogenesis by activating purinergic receptors. This research aimed to investigate the function of the purinergic receptor P2Y6 in mediating airway inflammation in allergic asthma. Wild-type (WT) and P2Y6-deficient mice were stimulated with ovalbumin (OVA) to construct asthmatic mouse models. Overexpression of P2Y6 and uridine 5’-diphosphate (UDP)-releasing were demonstrated in lung tissues in ovalbumin-induced asthmatic mice. The release of the cytokine IL-4, mast cell invasion, and the airway remodeling phenotypes were more severe following the application of UDP in asthmatic mice. However, P2Y6 deficiency reduced these asthmatic pathogeneticsymptoms markedly in a mouse model. In vitro, we found that P2Y6 in purified mast cells enhanced the functions of mast cells in the inflammatory response in the asthmatic process by triggering their capability for migration, cytokine secretion and granule release. Moreover, P2Y6 stimulated the function of mast cells through activation of the AKT signaling pathway. Our data provides evidence that P2Y6 contributes to allergic airway inflammation and remodeling by enhancing the functions of mast cells in ovalbumin-induced asthmatic mice.


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