rss
Gut 2005;54:1776-1781 doi:10.1136/gut.2005.065144
  • Liver

Quantitative gene expression in Budd-Chiari syndrome: a molecular approach to the pathogenesis of the disease

  1. V Paradis1,
  2. I Bièche2,
  3. D Dargère3,
  4. D Cazals-Hatem4,
  5. I Laurendeau2,
  6. V Saada5,
  7. J Belghiti6,
  8. A Bezeaud5,
  9. M Vidaud2,
  10. P Bedossa1,
  11. D-C Valla7
  1. 1Service d’Anatomie Pathologique, Hôpital Beaujon, Clichy, France, and CNRS UMR 8149, Faculté de Pharmacie, Paris, France
  2. 2UPRES EA 3618, Faculté de Pharmacie, Paris, France
  3. 3CNRS UMR 8149, Faculté de Pharmacie, Paris V, France
  4. 4Service d’Anatomie Pathologique, Hôpital Beaujon, Clichy, France
  5. 5Service d’Hématologie, Hôpital Beaujon, Clichy, France
  6. 6Service de Chirurgie Hépatique, Hôpital Beaujon, Clichy, France
  7. 7Service d’Hépatologie, Hôpital Beaujon, Clichy, France
  1. Correspondence to:
    Dr V Paradis
    Service d’Anatomie Pathologique, Hôpital Beaujon, 110 bd du général Leclerc, 92118 Clichy Cedex, France; vparadisteaser.fr
  • Accepted 31 May 2005
  • Revised 18 May 2005
  • Published Online First 14 September 2005

Abstract

Background: Budd-Chiari syndrome (BCS) is associated with parenchymal changes leading to major architecture remodelling. In order to gain further insight into the pathogenesis of BCS, we investigated expression of a set of genes involved in the course of chronic liver diseases.

Methods: Quantitative expression of 35 selected genes involved in extracellular matrix regulation, growth factors, and angiogenesis was investigated in 13 cases of BCS and compared with 10 normal livers and 13 cirrhosis cases by real time reverse transcription-polymerase chain reaction. Differential gene expression was considered significant for genes showing at least a twofold variation, with p<0.05.

Results: Expression of 14 genes was significantly increased in BCS versus normal liver, with the highest increase in superior cervical ganglion 10 (SCG10) gene. BCS cases were classified according to their evolution and morphological pattern as either acute or chronic in six and seven cases, respectively. Unsupervised hierarchical clustering of acute and chronic BCS cases on the basis of similarity in gene expression pattern led to distinction between the two groups. Expression of three genes was significantly different in acute versus chronic BCS (increase in matrix metalloproteinase 7 and SCG10, decrease in thrombospondin-1 for chronic BCS). Seventeen and 10 genes, mainly involved in extracellular matrix and vascular remodelling, were significantly deregulated in acute BCS versus normal liver and cirrhosis, respectively.

Conclusion: These results show that BCS cases display a specific gene expression profile that is different from that of normal liver and cirrhosis; the molecular configuration of BCS can be readily distinguished by its evolution and morphological pattern.

Footnotes

  • Published online first 14 September 2005

  • Conflict of interest: None declared.

This Article

  1. Abstract
  2. Full text
  3. PDF
  4. All versions of this article:
    1. gut.2005.065144v1
    2. 54/12/1776 most recent

Register for free content

The full back archive is now available for all BMJ Journals. Institutional subscribers may access the entire archive as part of their subscription. Personal subscribers will also have access to all content when logged in. Non-subscribers who register have free access to all articles published before 2006 right back to volume 1 issue 1. Register here to access the free archive of all BMJ Journals.

Don't forget to sign up for content alerts so you keep up to date with all the articles as they are published.