Whole transcriptome sequencing identifies increased   CXCR 2  expression in  PNH  granulocytes | Zendy

Hosokawa Kohei | Zendy; Kajigaya Sachiko | Zendy; Keyvanfar Keyvan | Zendy; Qiao Wangmin | Zendy; Xie Yanling | Zendy; Biancotto Angelique | Zendy; Townsley Danielle M. | Zendy; Feng Xingmin | Zendy; Young Neal S. | Zendy

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Whole transcriptome sequencing identifies increased CXCR 2 expression in PNH granulocytes

Author(s) -

Hosokawa Kohei,

Kajigaya Sachiko,

Keyvanfar Keyvan,

Qiao Wangmin,

Xie Yanling,

Biancotto Angelique,

Townsley Danielle M.,

Feng Xingmin,

Young Neal S.

Publication year - 2017

Publication title -

british journal of haematology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.907

H-Index - 186

eISSN - 1365-2141

pISSN - 0007-1048

DOI - 10.1111/bjh.14502

Subject(s) - transcriptome , downregulation and upregulation , mutation , microbiology and biotechnology , biology , phosphorylation , immunology , chemistry , gene expression , gene , biochemistry

Summary The aetiology of paroxysmal nocturnal haemoglobinuria ( PNH ) is a somatic mutation in the X‐linked phosphatidylinositol glycan class A gene ( PIGA ), resulting in global deficiency of glycosyl phosphatidylinositol–anchored proteins ( GPI ‐ AP s). This study applied RNA ‐sequencing to examine functional effects of the PIGA mutation in human granulocytes. CXCR 2 expression was increased in GPI ‐ AP ‐ compared to GPI ‐ AP + granulocytes. Macrophage migration inhibitory factor, a CXCR 2 agonist, was significantly higher in plasma of PNH patients. Nuclear factor‐κB phosphorylation was upregulated in GPI ‐ AP − compared with GPI ‐ AP + granulocytes. Our data suggest novel mechanisms in PNH , not obviously predicted by decreased production of the GPI moiety.

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