The association of eNOS gene polymorphism with avascular necrosis of femoral head

PLoS One. 2014 Feb 3;9(2):e87583. doi: 10.1371/journal.pone.0087583. eCollection 2014.

Abstract

Objectives: Necrosis of femoral head is a severe pathological state with multiple etiologies. This study investigated the association of the 27-bp repeat polymorphism in intron 4 and G894T polymorphism in exon 7 of the endothelial nitric oxide synthase (eNOS) gene with the pathogenesis of avascular necrosis of femoral head (ANFH).

Methods: A total of 125 non-traumatic ANFH patients and 126 healthy controls were recruited for this study. The 27-bp repeat polymorphisms in intron 4 were analyzed by polymerase chain reaction (PCR) and sequencing. The G894T polymorphisms in exon 7 were analyzed by PCR- restriction fragment length polymorphism (PCR-RFLP) analysis.

Results: All alleles were observed in non-traumatic ANFH patients and control subjects. Both ANFH patients and idiopathic subgroup of ANFH patients showed higher frequency of the 4a/b genotype than controls (p = 0.001 and p = 0.020, respectively). Significantly higher frequency of G/T genotype was observed in ANFH patients and idiopathic subgroup of ANFH patients compared to controls (p = 0.009 and p = 0.035, respectively).

Conclusion: eNOS gene polymorphisms may be a risk factor for ANFH. The 27-bp repeat polymorphism in intron 4, G894T polymorphism in exon 7, and subsequently reduced eNOS activity may be involved in the etiology of idiopathic ANFH.

MeSH terms

  • Adult
  • Aged
  • Base Sequence
  • DNA Mutational Analysis
  • Exons / genetics
  • Female
  • Femur Head Necrosis / genetics*
  • Gene Frequency
  • Genetic Predisposition to Disease / genetics*
  • Genotype
  • Humans
  • Male
  • Middle Aged
  • Nitric Oxide Synthase Type III / genetics*
  • Polymerase Chain Reaction
  • Polymorphism, Genetic*
  • Polymorphism, Restriction Fragment Length
  • Polymorphism, Single Nucleotide
  • Repetitive Sequences, Nucleic Acid / genetics
  • Risk Factors

Substances

  • NOS3 protein, human
  • Nitric Oxide Synthase Type III

Grants and funding

The authors have no support or funding to report.