GATA6 and TBX3 gene expressions analysis of indirect inguinal hernia sacs in children

Oguz Kizilkaya1, Mehmet Said Koprulu2, Hakan Gurkan3

  • 1Department of Pediatric Surgery, Faculty of Medicine, Trakya University, Edirne, Türkiye.

Insights

Altered expression of GATA6 and TBX3 genes in hernia sacs may contribute to indirect inguinal hernia (IIH) in children. This study examined gene expression and found significant changes in GATA6 and TBX3 levels in IIH patients.

Area of Science:

  • Pediatric Surgery
  • Molecular Biology
  • Genetics

Background:

  • Indirect inguinal hernia (IIH) is a common childhood surgical condition.
  • The precise etiology of IIH remains incompletely understood.
  • Understanding the molecular mechanisms underlying IIH is crucial for potential therapeutic targets.

Purpose of the Study:

  • To investigate the expression levels of GATA6 and TBX3 genes in hernia sacs of children with IIH.
  • To explore the role of these genes in the pathogenesis of indirect inguinal hernia.
  • To analyze single nucleotide polymorphisms (SNPs) in GATA6 and TBX3 genes in relation to IIH.

Main Methods:

  • Cross-sectional study comparing 20 boys with IIH to 20 controls.
  • Gene expression analysis of GATA6 and TBX3 in hernia sacs and prepuces.
  • DNA sequencing for GATA6 (rs1416421760, rs1040912117) and TBX3 (rs968910973) single nucleotide polymorphisms.
  • Statistical analysis using the Mann-Whitney U test.

Main Results:

  • GATA6 gene expression was significantly increased (p < 0.001) in the IIH group.
  • TBX3 gene expression was significantly decreased (p < 0.001) in the IIH group.
  • No statistically significant differences were observed in genotype or allele frequencies for the studied SNPs between groups.

Conclusions:

  • Dysregulation of GATA6 and TBX3 gene expression may play a role in the development of indirect inguinal hernia.
  • Altered apoptotic pathways mediated by GATA6 and TBX3 could contribute to IIH pathogenesis.
  • Further research is warranted to elucidate the precise molecular mechanisms involved in IIH development.
Abstract