Whole transcriptome sequencing identifies increased CXCR2 expression in PNH granulocytes.
Kohei HosokawaSachiko KajigayaKeyvan KeyvanfarWangmin QiaoYanling XieAngelique BiancottoDanielle M TownsleyXingmin FengNeal S YoungPublished in: British journal of haematology (2017)
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-APs). This study applied RNA-sequencing to examine functional effects of the PIGA mutation in human granulocytes. CXCR2 expression was increased in GPI-AP- compared to GPI-AP+ granulocytes. Macrophage migration inhibitory factor, a CXCR2 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.
Keyphrases
- nuclear factor
- transcription factor
- single cell
- poor prognosis
- genome wide
- end stage renal disease
- toll like receptor
- newly diagnosed
- ejection fraction
- copy number
- protein kinase
- chronic kidney disease
- blood pressure
- gene expression
- adipose tissue
- rna seq
- obstructive sleep apnea
- prognostic factors
- immune response
- dna methylation
- electronic health record
- sleep apnea
- sleep quality
- induced pluripotent stem cells