open access

Vol 45, No 1 (2014)
Prace oryginalne/Original research articles
Submitted: 2013-07-26
Published online: 2014-01-01
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Gene expression analysis in the pathogenesis of chronic immune thrombocytopenia in children

Monika Richert-Przygońska1, Bing Zhang2, James L. Zehnder2, Mariusz Wysocki1
DOI: 10.1016/j.achaem.2013.11.004
·
Acta Haematol Pol 2014;45(1):76-82.
Affiliations
  1. Klinika Pediatrii, Hematologii i Onkologii Collegium Medicum im. Ludwika Rydygiera, Uniwersytet Mikołaja Kopernika w Toruniu, Bydgoszcz, Polska
  2. Department of Pathology, School of Medicine, Stanford University, Stanford, CA, USA

open access

Vol 45, No 1 (2014)
Prace oryginalne/Original research articles
Submitted: 2013-07-26
Published online: 2014-01-01

Abstract

Background

A complex multifactorial dysregulation of immune system, including cytokines and autoantibodies production, and also proteins modification underlay the primary mechanism of immune thrombocytopenia (ITP). Specific genetic profile of ITP patients is presumed, especially those with a long and complex natural history of the disease.

Aim of the study

Gene expression analysis of VNN1 and PPARγ in children with immune thrombocytopenia.

Materials and methods

Candidate genes were identified with microarray cDNA procedure. For the validation of VNN1 and PPARγ expression changes we used qRT-PCR performed comparatively in samples of newly diagnosed ITP (ndITP, n=16), chronic ITP (cITP, n=8) and patients without thrombocytopenia (n=5).

Results

We analyzed the data of patients, followed for at least 12 months after ITP diagnosis. No significant differences of VNN1 expression profile were found in between groups (p>0.05). Lower signatures of mean PPARγ normalized expression values were noticed in chronic ITP patients in contrast to newly diagnosed ITP subjects (p=0.009). Differences between VNN1/PPARγ ratio values found in ndITP group comparing to subjects with progression to cITP were close to statistical significance (p=0.054).

Conclusions

Analysis of the VNN1 and PPARγ expression profiles utility in children diagnosed with ITP requires further investigation.

Abstract

Background

A complex multifactorial dysregulation of immune system, including cytokines and autoantibodies production, and also proteins modification underlay the primary mechanism of immune thrombocytopenia (ITP). Specific genetic profile of ITP patients is presumed, especially those with a long and complex natural history of the disease.

Aim of the study

Gene expression analysis of VNN1 and PPARγ in children with immune thrombocytopenia.

Materials and methods

Candidate genes were identified with microarray cDNA procedure. For the validation of VNN1 and PPARγ expression changes we used qRT-PCR performed comparatively in samples of newly diagnosed ITP (ndITP, n=16), chronic ITP (cITP, n=8) and patients without thrombocytopenia (n=5).

Results

We analyzed the data of patients, followed for at least 12 months after ITP diagnosis. No significant differences of VNN1 expression profile were found in between groups (p>0.05). Lower signatures of mean PPARγ normalized expression values were noticed in chronic ITP patients in contrast to newly diagnosed ITP subjects (p=0.009). Differences between VNN1/PPARγ ratio values found in ndITP group comparing to subjects with progression to cITP were close to statistical significance (p=0.054).

Conclusions

Analysis of the VNN1 and PPARγ expression profiles utility in children diagnosed with ITP requires further investigation.

Get Citation

Keywords

Immune thrombocytopenia; Genes; Expression; Children

About this article
Title

Gene expression analysis in the pathogenesis of chronic immune thrombocytopenia in children

Journal

Acta Haematologica Polonica

Issue

Vol 45, No 1 (2014)

Pages

76-82

Published online

2014-01-01

Page views

142

Article views/downloads

672

DOI

10.1016/j.achaem.2013.11.004

Bibliographic record

Acta Haematol Pol 2014;45(1):76-82.

Keywords

Immune thrombocytopenia
Genes
Expression
Children

Authors

Monika Richert-Przygońska
Bing Zhang
James L. Zehnder
Mariusz Wysocki

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