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Sulfonylurea receptor 1 in the germinal matrix of premature infants

J Marc Simard1, Rudolph J Castellani, Svetlana Ivanova

  • 1Department of Neurosurgery, University of Maryland School of Medicine, Baltimore, Maryland 21201, USA. msimard@smail.umaryland.edu

Pediatric Research
|August 6, 2008
PubMed

Insights

Germinal matrix hemorrhage (GMH) in preterm infants is linked to hypoxia-induced SUR1 channels. Targeting these channels may prevent cerebral palsy complications.

Area of Science:

  • Neuroscience
  • Neonatal Medicine
  • Vascular Biology

Background:

  • Germinal matrix hemorrhage (GMH) is a leading cause of mortality and cerebral palsy in premature infants.
  • GMH is often preceded by hypoxic-ischemic events, leading to the rupture of fragile germinal matrix veins.
  • Hypoxia up-regulates sulfonylurea receptor 1 (SUR1)-regulated NCCa-ATP channels in the central nervous system endothelium.

Purpose of the Study:

  • To investigate the hypothesis that SUR1-regulated NCCa-ATP channels are up-regulated in the germinal matrix of preterm infants at risk for GMH.
  • To examine the expression of SUR1 and its transcriptional factor, hypoxia-inducible factor 1 (HIF1), in relation to GMH.

Main Methods:

  • Studied postmortem germinal matrix and cortical tissues from premature infants with and without a history of GMH.
  • Analyzed the expression of HIF1 and SUR1 at both protein and mRNA levels.
  • Compared expression patterns in germinal matrix progenitor cells and veins.

Main Results:

  • Regionally specific up-regulation of HIF1 and SUR1 protein and mRNA was observed in germinal matrix tissues compared to cortical tissues.
  • SUR1 up-regulation was prominent in germinal matrix progenitor cells.
  • In germinal matrix veins, SUR1 expression was significantly higher in infants who had experienced GMH.

Conclusions:

  • The SUR1-regulated NCCa-ATP channel is implicated in the pathogenesis of germinal matrix hemorrhage in preterm infants.
  • Pharmacological inhibition of these channels presents a potential therapeutic strategy to reduce GMH incidence and associated morbidities.
  • Further research into targeting SUR1 channels could mitigate devastating complications of prematurity.

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